Skip to main content
Download PDF

Strategies to prevent, diagnose and treat kidney disease related to systemic arterial hypertension: a narrative review from the Mexican Group of Experts on Arterial Hypertension

BMC Nephrology volume 25, Article number: 24 (2024) Cite this article

Abstract

This narrative review highlights strategies proposed by the Mexican Group of Experts on Arterial Hypertension endorsed to prevent, diagnose, and treat chronic kidney disease (CKD) related to systemic arterial hypertension (SAH). Given the growing prevalence of CKD in Mexico and Latin America caused by SAH, there is a need for context-specific approaches to address the effects of SAH, given the diverse population and unique challenges faced by the region. This narrative review provides clinical strategies for healthcare providers on preventing, diagnosing, and treating kidney disease related to SAH, focusing on primary prevention, early detection, evidence-based diagnostic approaches, and selecting pharmacological treatments. Key-strategies are focused on six fundamental areas: 1) Strategies to mitigate kidney disease in SAH, 2) early detection of CKD in SAH, 3) diagnosis and monitoring of SAH, 4) blood pressure targets in patients living with CKD, 5) hypertensive treatment in patients with CKD and 6) diuretics and Non-Steroidal Mineralocorticoid Receptor Inhibitors in Patients with CKD. This review aims to provide relevant strategies for the Mexican and Latin American clinical context, highlight the importance of a multidisciplinary approach to managing SAH, and the role of community-based programs in improving the quality of life for affected individuals. This position paper seeks to contribute to reducing the burden of SAH-related CKD and its complications in Mexico and Latin America.

Peer Review reports

Introduction

Chronic kidney disease (CKD) is a growing public health concern globally, with an estimated prevalence of 13.4% worldwide and 10% in Latin America [1, 2]. Systemic Arterial Hypertension is a leading cause of CKD, contributing to approximately 30% of all CKD cases. In Mexico and Latin America, the burden of systemic arterial hypertension and its complications – including CKD – is substantial and increasing [3]. The escalating prevalence of CKD in the region can be attributed to multiple factors, such as an aging population, increased prevalence of diabetes and obesity, and inadequate access to healthcare services [4]. Early identification and management of systemic arterial hypertension are essential to prevent or delay the progression of kidney damage and reduce associated morbidity and mortality. It is essential to formulate context-specific approaches to address the effects of systemic arterial hypertension in Mexico and Latin America, considering the vast and diverse population of the region. These strategies should be tailored to tackle the unique challenges faced by the region, considering the socioeconomic, cultural, and healthcare system factors that lead to disparities in systemic arterial hypertension and CKD care [5]. In this narrative review, we seek to offer a comprehensive and context-specific guide for healthcare providers on the prevention, diagnosis, and treatment of kidney damage related to systemic arterial hypertension in Mexico and Latin America. For this purpose, we followed the Delphi technique to identify and address six specific topics related to primary prevention, early detection, evidence-based diagnostic approaches, and selecting pharmacological treatments [6]. By addressing topics, we aim to reduce the burden of systemic arterial hypertension-related CKD and its complications in the region. Emphasizing the importance of a multidisciplinary approach and the role of community-based programs, this review seeks to improve the quality of life for millions of affected individuals. In Fig. 1, we summarize and synthesize these strategies for clinical scenarios.

Fig. 1
figure 1

Summary of strategies for managing kidney disease related to systemic arterial hypertension in Mexico and Latin America. Abbreviations: SAH: Systemic Arterial Hypertension; CKD: Chronic Kidney Disease; eGFR: Estimated Glomerular Filtration Rate; BP: Blood Pressure; SGLT2: Sodium-glucose Cotransporter-2; RAAS: Renin–Angiotensin–Aldosterone System; ACEIs: Angiotensin-Converting Enzyme; ARBs: Angiotensin II Receptor Blocker; nsMRA: Non-Steroidal Mineralocorticoid Receptor Antagonists

Full size image

Section 1: strategies to mitigate kidney disease

Systemic arterial hypertension and kidney disease (KD) are interlinked through complex pathophysiological pathways; these relationships position the kidney as both a target and a causative factor in hypertension. Disentangling the precise pathogenic role of moderate hypertension in kidney damage is challenging, as other risk factors or associated morbidities often coexist. In the United States, systemic arterial hypertension and impaired kidney function (glomerular filtration rate, [GFR], between 60–89 mL/min/1.73 m2) prevalence have been consistently increasing, reaching 28.9% and 51.2%, respectively [7]. From 1999 to 2004, the occurrence of CKD with GFR < 60 mL/min/1.73 m2 rose to 8%. Once KD is evident with the onset of albuminuria, the progression of CKD accelerates; this is particularly relevant when systemic arterial hypertension is accompanied by diabetes, hyperuricemia, or another KD. Considering these challenges, it is essential to create strategies to mitigate systemic arterial hypertension in patients living with CKD.

Question 1.1: can kidney damage and the development of CKD be prevented in patients with primary systemic arterial hypertension?

Preventing KD caused primarily by systemic arterial hypertension involves preventing its onset. The main etiological factors of systemic arterial hypertension include inherited hypertension phenotypes, epigenetic inheritance, and acquired or environmental factors. Although genetic factors cannot currently be altered, it may be possible to modify epigenetic and environmental factors related to systemic arterial hypertension onset [4]. Overall, lifestyle and dietary changes, along with the effects of specific drugs, contribute to lowering blood pressure levels and promote nephroprotection, which may hinder or delay systemic arterial hypertension onset in some individuals [8]. A second measure consists in providing adequate control of blood pressure levels in patients with systemic arterial hypertension to reduce macro- and micro-vascular complications associated with systemic arterial hypertension. In this regard, choosing and monitoring antihypertensive medications is crucial to reducing systemic arterial hypertension-associated complications. In the context of Mexico and Latin America, the following prevention measures are endorsed for both the general population and susceptible individuals:

  1. 1.

    National information campaigns and increased physician awareness: Early detection of systemic arterial hypertension is essential for preventing systemic arterial hypertension-related kidney damage. National campaigns should raise awareness regarding abdominal obesity, which has been demonstrated to be a main contributor to the development of cardiometabolic diseases, including systemic arterial hypertension [9]. Additionally, all healthcare personnel should prioritize systemic arterial hypertension awareness and detection for the general population, from medical schools to practicing doctors, including internists, endocrinologists, neurologists, cardiologists, and nephrologists.

  2. 2.

    Behavioral lifestyle modifications for patients living with systemic arterial hypertension: Three interventions have been proven to reduce the risk of systemic arterial hypertension-related outcomes: the DASH diet, reducing salt intake to < 5 g/day (2 g of sodium), and weight loss. These three interventions lower blood pressure in both normotensive and hypertensive individuals, preventing kidney damage onset and progression. Additionally, it is important to warn against the potential harm of high-protein diets and supplements, as intake of > 0.8 g of protein/kg of ideal weight, along with obesity and excess salt consumption, can cause hyperfiltration and glomerular hypertension [10,11,12].

  3. 3.

    Caution regarding nephrotoxic agents: Physicians should aim to educate the general population and susceptible individuals regarding the potential nephrotoxic risks of medications, which can lead to hyperfiltration, tubular and cortical toxicity, interstitial nephritis, crystalline nephropathy, and papillary necrosis. These include non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics (including neomycin, kanamycin, paromomycin, bacitracin, polymyxin B, colistin, and amphotericin B), anticancer drugs, and more. Awareness about the nephrotoxic risks of off-label herbal substances such as licorice, aloe, and ephedra should also be raised [13].

  4. 4.

    Continuous medical follow-up using accessible biochemical biomarkers: Follow-up of patients living with systemic arterial hypertension should include evaluations of serum creatinine or cystatin C (where available) at the point of first evaluation and clinical care and with subsequent follow-up visits. Furthermore, all patients should be assessed for estimated GFR (eGFR) using the CKD-EPI 2021 equation and albuminuria (using nephelometry or turbidimetry techniques), as well as casual and morning urinary albumin-to-creatinine ratio assessments (ACR index). It is important to note that an eGFR < 60 mL/min/1.73 m2 and an ACR index > 30 mg/g are indicative of CKD-related damage in systemic arterial hypertension [14,15,16].

  5. 5.

    Consider the nephroprotective role of antihypertensive drugs: Systemic arterial hypertension-related kidney damage may be caused by several mechanisms, including vascular injury, hyperfiltration, and glomerular hypertension, amongst others. Because of its effects in improving endothelial dysfunction and reducing vascular injury, all antihypertensive drugs offer some level of nephroprotection. However, not all antihypertensive agents have positive and significant effects in ameliorating hyperfiltration and glomerular hypertension. Hyperfiltration depends on afferent arteriolar vasodilation and efferent vasoconstriction, which can result from impairments in the renin–angiotensin–aldosterone system (RAAS) often observed in diabetes, obesity, excess sodium, and protein intake. Angiotensin-converting enzyme (ACE) inhibitor and angiotensin II receptor blocker (ARBs) use leads to post-capillary, efferent arteriolar vasodilation, increasing glomerular flow without increasing glomerular pressure or filtration [17].

Section 2: strategies for early detection of kidney disease

CKD is diagnosed when a decrease in eGFR < 60 ml/minute/1.73m2 is documented or with the onset of albuminuria ≥ 30 mg/g (3 mg/mmol), hematuria of glomerular-origin, kidney transplant, or any documented structural alteration through laboratory or imaging tests, which persists for at least three months [18]. CKD is a global public health issue, as it is associated with high mortality rates and is a significant risk factor for cardiovascular mortality. In Mexico, KD-related mortality currently stands amongst the top ten causes of death among individuals ≥ 45 years [19]. In 2021, there were 14,376 deaths due to kidney failure in Mexico, with CKD accounting for 71.8% (10,316 deaths) of these cases [20]. Additionally, CKD poses a significant economic challenge to the healthcare sector due to the prohibitive costs of treating end-stage KD (ESKD), its cardiovascular consequences, and the years lost due to premature mortality [21]. Therefore, early diagnosis and prevention of CKD and delaying its progression should be a priority to reduce complications and improve patient outcomes.

Question 2.1: does the determination of proteinuria have the same prognostic value for kidney function and the development of cardiovascular complications as albuminuria?

Albuminuria is an independent risk factor for both all-cause and cardiovascular disease (CVD) mortality, and its detection should rely on quantitative measures such as the albumin-to-creatinine (ACR) ratio [22, 23]. As a crucial marker for progression to ESKD, identifying albuminuria as the earliest indicator of renal damage progression could be helpful in establishing therapeutic approaches which minimize the burden of adverse outcomes in patients living with systemic arterial hypertension. In the context of Mexico and Latin America, the following clinical strategies aim to estimate impaired kidney function based on albuminuria and eGFR:

  1. 1.

    Determination of albuminuria and eGFR in all patients living with systemic arterial hypertension: All patients with risk factors for developing CKD (> 60 years, diabetes, hypertension, overweight or obesity, previous CVD, use of nephrotoxic drugs, hereditary/familial history KD or hypertensive disease in pregnancy) should have frequent albuminuria and eGFR determinations [24]. Physicians should schedule follow-up visits and new evaluations, using albuminuria as the primary marker for predicting CKD progression, and refer patients to a nephrology specialist when necessary [25, 26]. In Fig. 2, we append the risk stratification of KD based on albuminuria and eGFR according to the KDIGO guidelines [24].

  2. 2.

    Albuminuria and proteinuria are metrics of renal structural damage: Albuminuria and endogenous proteinuria should not be used as equivalents to decreased kidney function, as they are not markers of kidney function but only indicators of structural damage within the kidney [27].

  3. 3.

    Estimate the risk of CKD progression and CVD using the KDIGO calculator: Although albuminuria is a strong predictor of CKD progression and CVD, some traditional risk estimations, such as the Framingham Risk Prediction Score, are not accurate in patients with CKD [28, 29]. To address this issue, KDIGO clinical guidelines have developed a CVD risk stratification score based on eGFR and albuminuria, which improves risk prediction, particularly given that the magnitude of albuminuria in CKD predicts a higher risk of CVD [24]. Additionally, this calculator estimates the probability of initiating renal replacement therapy (RRT) for patients with CKD in clinical practice (http://ckdpcrisk.org/lowgfrevents/) [30]. This KDIGO calculator has been developed for risk prediction of RRT, risk of death, and CVD in patients with CKD, using eGFR and albuminuria as two of the evaluated criteria.

  4. 4.

    Use treatments based on ACE inhibitors or ARBs: ACE inhibitors and ARBs can reduce initial albuminuria by 30–52%, preserving kidney function and decreasing the incidence of CVD events, which are the leading cause of death in patients living with CKD [31, 32]. However, controversy persists over whether reducing albuminuria or blood pressure as a single strategy can effectively reduce the risk of progression to CKD in patients living with systemic arterial hypertension.

Fig. 2
figure 2

Staging and prognosis of chronic kidney disease according to estimated Glomerular Filtration Rate (eGFR) and albuminuria categories based on the KDIGO guidelines

Full size image

Question 2.2: what is the ideal formula to estimate eGFR in non-dialysis patients?

The eGFR is an essential tool for diagnosing CKD and determining its prevalence, as it helps assess KD progression, CVD risk, and related complications. eGFR also guides decisions on drug limitations, dosing, RRT initiation, and certain procedures’ feasibility. While invasive methods can precisely determine eGFR, they are not routinely used in clinical practice. Instead, estimation equations based on serum creatinine levels and clinical data serve as the primary method for eGFR determination [33]. However, serum creatinine concentrations can vary depending on factors such as age, gender, muscle mass, and diet. The most widely used eGFR equations are the Cockcroft-Gault (CG), MDRD, and CKD-EPI equations, with the most recent 2021 equation removing the race coefficient [34,35,36]. These eGFR equations are critical in establishing CKD diagnoses and stratifying patients using the KDIGO guidelines, evaluating disease progression, and determining appropriate treatments. However, these equations may underestimate or overestimate CKD, depending on the clinical scenario and target population where they are incorporated [37]. In the context of Mexico and Latin America, the following strategies to estimate eGFR based on formulas are endorsed:

  1. 1.

    Standardize plasma creatinine determinations: It is necessary to standardize plasma creatinine determinations across different equipment and manufacturers to improve reproducibility and reduce classification errors, especially around 60 ml/min/1.73 m2 [38].

  2. 2.

    Facilitate digital access to eGFR calculation tools: Develop and promote electronic calculators that provide results for multiple equations (CG, MDRD, CKD-EPI 2009 and 2021) so that physicians can choose the most appropriate equation for each patient’s clinical context.

  3. 3.

    Promote awareness and availability of cystatin C-based equations: These approaches can be used as alternatives to creatinine-based equations, especially when creatinine production is abnormal (decreased muscle mass, diet, elderly, liver disease). Cystatin C could improve CKD diagnosis, screening, and monitoring and be a useful alternative in specific patient populations.

  4. 4.

    Individualize the use of eGFR equations according to the patient’s needs: Based on the individual patient’s characteristics, prioritize formulas that consider specific clinical scenarios, such as those in patients using anticoagulation medications or drugs that can modify creatinine clearance. Understand the limitations and benefits of each equation and apply them specifically [39].

  5. 5.

    Specify the eGFR equation in algorithmic calculators: Explicitly mention the equation used for eGFR estimation in different risk assessment tools, such as QRISK-SCORE 3 (cardiovascular risk calculator that considers CKD and requests eGFR with MDRD 4), MEHRAN SCORE (contrast-induced nephropathy risk calculator after PCI that requests eGFR with MDRD 4), and CRUSADE SCORE (hospital bleeding risk calculator after myocardial infarction that requests eGFR with Cockcroft-Gault).

Choosing the right eGFR equation is crucial for diagnosing and managing CKD. Standardizing creatinine measurements, facilitating digital access to eGFR calculators, conducting studies for local reference values, promoting alternative markers like cystatin C, and individualizing the use of eGFR formulas based on patient needs can improve CKD diagnosis and management in Mexico and Latin America.

Question 2.3: what is the recommended technique for detecting albuminuria in patients with systemic arterial hypertension?

Proteinuria, characterized by elevated levels of urinary proteins, is a marker for KD progression and is associated with CVD morbidity and mortality [40, 41]. In contrast, albuminuria enables earlier CKD diagnosis and assists in the extrarenal diagnosis of systemic complications. Current guidelines advise annual screening for CKD in at-risk populations by assessing eGFR and albuminuria using three determinations [24]. The 2012 KDIGO guideline for managing CKD recommends stratification based on the urinary ACR, preferably from the first-morning urine sample, as it strongly correlates with values measured in 24-h urine samples [18]. Furthermore, regular screening for urinary albumin is recommended for individuals living with systemic arterial hypertension based on the following factors:

  1. 1.

    When significant albuminuria is present when two out of three samples collected over at least three months show increased values.

  2. 2.

    When patients are diagnosed with CKD and albuminuria (ACR > 300 mg/g or > 30 mg/mmol), monitoring can be performed using the urinary protein/creatinine ratio (PR/CR).

  3. 3.

    The protein-to-creatinine in urine is recommended for patients with suspected renal interstitial pathology since proteinuria in these contexts stems from low molecular weight tubular proteins, distinct from albumin.

Accurate interpretation of results guides treatment response and prognosis, with changes in proteinuria/albuminuria levels serving as a “therapeutic target” and being associated with CKD progression or regression. Moreover, a reduction in ACR implies a decreased risk of needing RRT. As albuminuria is the earliest and most cost-effective marker of CKD, its use should be widely adopted in daily clinical practice for diagnosis, disease classification, therapeutic targeting, analysis of therapeutic outcomes (progression or regression), and prognosis for cardiovascular complications and the need for RRT [42, 43]. In the context of Mexico and Latin America, the following strategies for estimating albuminuria are proposed:

  1. 1.

    Health personnel training is crucial for accurate interpretation. Digital algorithms can be developed to guide the action based on ACR monitoring.

  2. 2.

    Encourage all clinicians to estimate both eGFR and urine ACR: This will provide primary care physicians with both diagnostic criteria for KD and allow subsequent studies to observe values over time, increasing KD diagnosis graphically. Confirming KD diagnosis will ensure timely patient referral to nephrology as these are strong predictors of mortality in patients living with CKD, even in the initial stages of the disease [44].

  3. 3.

    Consider including albuminuria in primary cardiovascular risk scores: This will have a direct impact on physician care, promoting early initiation of proteinuria-reducing treatments (e.g., ACEIs/ARBs, sodium-glucose cotransporter 2 inhibitors [SGLT2i]/ non-dihydropyridine calcium channel blockers [CCBs]).

  4. 4.

    Monitor patients to assess the possibility of residual albuminuria: Persistent albuminuria is defined as when albuminuria is present after six months of treatment with maximum pharmacological doses of ACEIs/ARBs, low-protein diet, and lipid-lowering agents). Residual albuminuria has been shown to have a linear relationship with subsequent risk of KD, just as initial, untreated albuminuria has a higher likelihood of progressing to CKD and maintaining elevated CVD risk [45].

In line with the strategies mentioned above, it is essential to develop a “guided search” for albuminuria when a patient at risk of developing CKD (e.g., patients with hypertension, type 2 diabetes, previous CVD, ≥ 60 years, obesity, patients on nephrotoxic drugs, etc.).

Section 3: strategies for diagnose and monitor systemic arterial hypertension

Office-based blood pressure (BP) measurement continues to be a valid and useful systemic arterial hypertension screening and diagnosis method. However, out-of-office BP monitoring, including ambulatory BP monitoring (ABPM) and home BP monitoring (HBPM), provides alternative approaches that are linked to predicting systemic arterial hypertension-mediated organ damage, major CVD events, and mortality [46]. In the context of patients with CKD, BP monitoring poses a challenge due to masked systemic arterial hypertension, white-coat hypertension, and 24-h variability patterns at either ABPM or office-based BP measurements. Accurate monitoring and continuous vigilance of BP in systemic arterial hypertension are crucial for ensuring proper treatment and preventing progression to end-stage CKD. Therefore office-based BP measurements alone are insufficient, and it is essential to complement them with methods such as ABPM and/or HBPM in patients living with CKD.

Question 3.1: which of the different techniques for measuring BP outside the office is ideal for patients living with CKD?

CKD without dialysis

Achieving proper control and diagnosis of systemic arterial hypertension in patients living with CKD can be challenging. This is partly due to the high prevalence of conditions such as white coat hypertension, which affects approximately 30% of CKD patients submitted to RRT [47]. Additionally, masked systemic arterial hypertension is observed in 8–20% of the general population [48]. Cupisti et al. demonstrated the superiority of HBPM over office-based BP measurements in identifying the white coat effect in 62.5% of patients and masked systemic arterial hypertension in 22.7% of patients with stage 3–5 CKD [49]. Furthermore, the relationship between elevated BP and CVD is significant; notably, patients with high BP variability exhibit increased rates of CVD and mortality [50,51,52]. In a cohort of 1,219 patients living with CKD, high BP was independently correlated with organ damage [53]; similarly, Drawz et al., also demonstrated in a cohort of 1,492 patients with CKD an independent association between masked systemic arterial hypertension and end-organ damage [54]. Consequently, the association between uncontrolled high BP and clinical outcomes in patients with systemic arterial hypertension and CKD is significant.

In patients with CKD who are not receiving RRT, a stronger correlation has been observed between HBPM or ABPM and a decline in eGFR and/or need for RRT, compared to office-based BP measurements [55]. Moreover, ABPM outperformed office-based measurements in predicting composite events of all-cause mortality and the need for RRT, though it did not demonstrate superiority over HBPM [56]. In a cohort study by Borelli et al., which included 906 CKD patients, factors most strongly associated with an increased risk of fatal and non-fatal CVD events and kidney function deterioration were the absence of nocturnal dipping and systolic BP exceeding the ABPM target (> 135 mmHg during the day or > 120 mmHg at night) [57]. Consequently, for CKD patients without dialysis, ABPM is the recommended method for BP measurement.

CKD on dialysis

Diagnosing and monitoring systemic arterial hypertension in patients undergoing RRT, particularly hemodialysis (HD), is a considerable challenge. Mansoor and White reported that almost 80% of adults on HD were classified with systemic arterial hypertension, yet only 30% achieved BP goals [58]. Additionally, studies have shown that when a 44-h interdialytic ABPM was conducted, only 33% of the population met the criteria for systemic arterial hypertension, highlighting the difficulty of managing systemic arterial hypertension in RRT settings. In patients submitted to dialysis, nighttime BP measurements strongly predict overall outcomes [59]; a study performed by Tripepi et al. identified the night/day BP ratio as a prognostic factor for clinical outcomes in these patients [60]. Similarly, Ekart R. et al. described that 48-h ABPM, rather than office-based BP measurements, were independent predictors of CVD death in HD patients [61]. Finally, Alborzi et al. associated HBPM with CVD mortality and all-cause mortality [62]. Therefore, both night/day BP ratios and HBPM are superior predictors of CVD events compared to office-based or peridialytic period BP measurements. These findings emphasize the importance of utilizing appropriate diagnostic and monitoring tools for managing systemic arterial hypertension in patients on RRT.

For patients with systemic arterial hypertension and CKD, substantial evidence supports the superiority of both ABPM and HBPM over office-based BP measurement in accurately diagnosing systemic arterial hypertension, predicting major CVD events, kidney function decline, and CVD and all-cause mortality. Considering the context of Mexico and Latin America, the following strategies for out-of-office BP measurement in patients with CKD are proposed:

  1. 1.

    ABPM should be the method for diagnosing systemic arterial hypertension: Consistent with existing evidence, ABPM offers relevant prognostic value due to its ability to assess nighttime compared to daytime BP. Moreover, ABPM has the most significant impact on a patient’s clinical prognosis in the context of CKD.

  2. 2.

    If ABPM is unavailable, HBPM is an excellent alternative: HBPM is a superior option for identifying masked and white coat arterial hypertension, as it demonstrates a better correlation with CVD, KD, and mortality compared to office-based BP measurements.

  3. 3.

    Office-based BP measurement should be used for screening and detecting systemic arterial hypertension: Given the evidence highlighting the superiority of both ABPM and HBPM for accurate diagnosis and prognosis, office-based BP measurements should be primarily employed for screening in patients with CKD and systemic arterial hypertension.

Section 4: strategies to achieve BP Targets in patients living with CKD

In patients living with CKD, systemic arterial hypertension prevalence increases with KD progression, reaching 90% prevalence in patients classified with CKD stage 5 [63]. The key mechanisms related to systemic arterial hypertension in patients living with CKD include volume overload, sympathetic hyperactivity, salt retention, endothelial dysfunction, and alterations in BP-regulating hormone systems [64]. Moreover, in kidney transplant recipients, systemic arterial hypertension etiology is multifactorial, depending on the recipient and donor characteristics and transplant-specific causes (e.g., immunosuppressive medications, allograft dysfunction, and surgical complications like transplant artery stenosis) [65]. High BP is an independent risk factor for CVD morbidity-mortality and adverse KD outcomes, making BP control a crucial goal for adequate clinical management. However, optimal BP goals in hypertensive CKD patients, specifically kidney transplant recipients, remain controversial [66].

Question 4.1: what are the risks/benefits of key-strategies in patients living with CKD who survive stage 3 KDIGO?

Target BP in patients with CKD without dialysis

The ideal BP targets in patients with CKD without dialysis vary widely across systemic arterial hypertension guidelines. The American College of Cardiology/American Heart Association (ACC/AHA) recommends a BP target of < 130/80 mmHg for stage 5 CKD patients. This goes in line with threshold recommendations by the European Society of Cardiology/European Society of Hypertension (ESC/ESH), which also suggest a BP target < 130–139 mmHg for the same population [67, 68]. Conversely, the updated National Institute for Health and Care Excellence (NICE) guidelines recommend a BP target of < 140/90 mmHg for patients with ACR < 70 mmol/mol and systolic BP (SBP) of 130 mmHg and BP < 130/80 mmHg (considering lower SBP of 120 mmHg) for those with CKD and ACR > 70 mmol/mol [69].

The 2021 KDIGO Clinical Practice Guideline for BP management in CKD recommends treating patients not receiving RRT using an SBP threshold of < 120 mmHg [70]. This strategy is primarily based on the SPRINT study subgroup analysis of CKD patients, which demonstrated a 25% risk reduction in major adverse CVD events using this threshold. However, for patients with eGFR < 45 ml/min/1.73m2, no reduction in CVD risk was observed with these SBP targets, although reductions in all-cause mortality and mild cognitive impairment were observed [71, 72]. Nevertheless, it has been further questioned whether an SBP target < 120 mmHg is the ideal threshold as it has been associated with increased risks of adverse outcomes, including hypotension, syncope, electrolyte abnormalities, and acute kidney injury or failure. A sub-analysis of the ACCORD trial compared intensive SBP control (SBP < 120 mmHg) with standard control (SBP < 140 mmHg) in patients living with diabetes and found no overall benefit of intensive BP control, except for a reduced risk of non-fatal stroke [73]. Recently, three systematic reviews and meta-analyses examined the benefits of intensive BP control in patients living with CKD. The first meta-analysis performed by Tsai et al. found no additional benefit of intensive BP control compared to standard control on KD outcomes [74]. Conversely, a second meta-analysis showed that intensive BP reduction was associated with significantly lower mortality risk compared to less intensive BP control [75]. The last meta-analysis found no differences in death, cardiovascular death, or heart failure when comparing various SBP targets. However, lower BP targets were associated with higher adverse effects at follow-up [76]. Based on this evidence, we suggest that patients living with CKD without dialysis should have SBP targets of < 130 mmHg, as this threshold could lead to an optimal balance between efficacy and safety.

Target blood pressure in patients with CKD with dialysis

The 2021 KDIGO Guideline recommends a BP target of < 130/80 mmHg for kidney transplant recipients [70]. This recommendation is based on expert opinion, as no clinical trials have investigated the relationship between this BP target and adverse clinical outcomes. Nevertheless, it has been reported that lower BP has been associated with eGFR decline, CKD progression, and acute kidney injury events in kidney transplant recipients [76]. A more conservative target is suggested, as kidney transplant recipients with a single kidney may be more vulnerable to these adverse effects. This recommendation aligns with the 2017 ACC/AHA guideline on hypertension, which also proposes a BP target of ≤ 130/80 mmHg for kidney transplant recipients [68].

Considering the context of Mexico and Latin America, the following strategies for BP goals in patients with CKD are proposed:

  1. 1.

    Adopt standardized BP measurement according to KDIGO guidelines: This strategy is based on ensuring accurate and consistent BP readings for patients living with CKD, considering factors such as resting, avoiding caffeine, exercising, and smoking before BP measurement.

  2. 2.

    Address challenges in performing standardized BP measurements in clinical practice: Due to time constraints and institution-specific clinical policies, it may be difficult to perform standardized BP measurements; however, it is essential to prioritize accurate BP readings for patients living with CKD.

  3. 3.

    Recognize the white coat effect on office BP readings: Non-standardized office BP readings can be significantly higher than standardized BP measurements, which can affect treatment decisions for patients living with CKD. In this context, home BP monitoring can help to eliminate the “white coat” effect by providing a more accurate assessment of BP levels.

  4. 4.

    Be cautious when applying SBP targets to non-standardized BP measurements: As previously discussed, applying an SBP target of < 120 mmHg can lead to overtreatment and increased adverse events in patients living with CKD. Therefore, most patients living with CKD should achieve and maintain BP levels < 130/80 mmHg as this target ensures a well-tolerated BP for most patients [77].

  5. 5.

    Implement improved BP measurement methods in clinical settings: Creating specialized areas for standardized BP measurement and employing trained nursing staff can ensure accurate BP readings for patients with CKD in clinical settings [78].

  6. 6.

    Involve health authorities in promoting health goals and continuous training: Health authorities should support the achievement of health goals, reduce long-term expenditure, and provide continuous training for medical professionals to ensure the best possible care for patients living with CKD.

Given the lack of strong evidence, the current SBP target of < 120 mmHg for patients with CKD recommended by KDIGO is inappropriate for most patients and may even be harmful to those with CKD stages 4 and 5, diabetes, glomerulopathies, polycystic KD, and proteinuria. Based on previous evidence, we endorse an SBP target of < 130/80 as this goal is more reasonable and well tolerated.

Section 5: hypertensive treatment strategies in patients living with CKD

CVD is the leading cause of mortality in patients living with CKD in Mexico [79]. Consequently, BP control is the main pillar to mitigate the burden of complications related to systemic arterial hypertension and CKD. Nevertheless, several risk factors have been found to be associated with difficult-to-control BP, including albuminuria, volume overload, and sympathetic nervous system hyperactivity with circadian rhythm alterations [79]. As kidney function declines, cardiovascular health deteriorates, and the risk of adverse outcomes increases [80, 81]. Therefore, cardio-nephroprotection from the early stages of KD is crucial. Current guidelines propose that managing systemic arterial hypertension in patients with CKD should begin with RAAS inhibitors due to their demonstrated efficacy in reducing various markers of KD progression. Second-line drugs, such as CCBs, have also positively affected albuminuria, eGFR preservation, and circadian rhythm BP variability. However, there are specific considerations when using RAAS inhibitors and CCBs in clinical practice.

Question 5.1: can we expect the same results on CKD progression and CVD outcomes for all RAAS inhibitors?

ACEIs and ARBs

ACEIs and ARBs are indispensable for treating systemic arterial hypertension in patients living with CKD [81]. Their use is also well-established in treating albuminuria, heart failure with reduced ejection fraction, and acute myocardial infarction. In Table 1, we present the results of two primary meta-analyses comparing different pharmacological groups of RAAS inhibitors and their clinical use for adverse outcomes. Both studies found that using ACEIs and ARBs in patients living with CKD reduces the risk of renal failure and CVD events. Additionally, ACEIs have been shown to decrease all-cause mortality and may be superior to ARBs in reducing CVD death. This suggests that ACEIs could be the first therapeutic option for this population [82]. However, some authors, such as Strippoli et al., concluded in a Cochrane systematic review that there are no significant differences in overall mortality when comparing ACEIs versus ARBs [83]. The debate continues, but the main strategy emphasize using the maximum tolerable dose of ACEIs to optimize and manage CKD-related outcomes.

Table 1 Studies comparing the effect of ARBs and ACE inhibitors for kidney disease and cardiovascular outcomes in patients with chronic kidney disease
Full size table

Calcium channel blockers

CCBs play a key role in treating systemic arterial hypertension in patients living with CKD. The main evidence stems primarily from the ACCOMPLISH study, which found that the benazepril-amlodipine combination was superior to benazepril-hydrochlorothiazide in reducing CVD events and slowing CKD progression [84]. Subsequently, several meta-analyses and systematic reviews have been conducted to clarify the potential benefits of CCBs. The primary results of three meta-analyses are presented in Table 2. The first study, conducted by Fu et al., provides evidence that initiating RAAS inhibitors compared to CCBs offers renal benefits in patients with CKD and similar cardiovascular protection [85]. This study shows that the benefits continue with ACEIs and ARBs in ESKD patients. Another study by Lin et al. found a similar long-term effect on BP control, mortality, heart failure, stroke events, and kidney function in patients with stage 3–5 CKD with systemic arterial hypertension using CCBs and RAAS inhibitors [86]. Finally, Zhao et al. conclude that the best therapeutic option combines RAAS inhibitors with CCB [87]. In summary, using CCBs is an excellent therapeutic option when combined with another RAAS inhibitor. In the case of patients where ACEIs/ARBs are not well-tolerated, non-dihydropyridines CCB (e.g., Diltiazem) have been demonstrated to have beneficial effects on BP management and the time course of blood pressure [88, 89].

Table 2 Studies comparing the effect of RAAS inhibitors drugs versus CCBs in renal and cardiovascular outcomes in patients with kidney disease
Full size table

Question 5.2: what are the safe therapeutic strategies to reduce BP and albuminuria, and control the circadian rhythm BP variability in stage 4–5 CKD?

Albuminuria

Pharmacological RAAS blockade using ACEIs, and ARBs is still the treatment of choice for reducing albuminuria, as showed by Lambers et al. in a meta-analysis examining the effects of pharmacological proteinuria reduction and nephroprotection. The analysis primarily included studies with RAAS inhibitors, which showed an average albuminuria reduction of 19.2% and significant differences compared to the control group. A crucial association was found, showing that for every 30% reduction in albuminuria, the risk of end-stage KD decreases by 23.7% [90]. In this context, new evidence has emerged about the benefits of reducing albuminuria linked to the use of CCBs. In a study by Abraham et al., they suggest that dihydropyridine CCBs can be used as a first-line treatment in non-proteinuric CKD, but when combined with RAAS inhibitors, they have a more significant impact on proteinuric CKD [91]. Additionally, CCBs that act on L/N and L/T channels also have a substantial effect on decreasing albuminuria and intraglomerular pressure, improving renal hemodynamics, and producing a more significant reduction in proteinuria, even in patients already treated with RAAS inhibitors. Additionally, CCBs inhibit aldosterone secretion, improve endothelial dysfunction, and reduce oxidative stress [92]. An association between CCBs and an increase in the glomerular filtration rate has been observed, thereby delaying the onset of KD. Consequently, CCBs could present an alternative for treating systemic arterial hypertension in patients living with CKD, although more long-term studies are needed to confirm its impact on clinical outcomes.

Sodium-glucose cotransporter 2 inhibitors

A new pharmacological group of interest for cardio-renal protection and reduction of albuminuria are SGLT2i. Developed for the treatment of type 2 diabetes, SGLT2i works by inhibiting proximal glucose reabsorption. Additionally, recent evidence has discovered the pleiotropic effects of SGLT2i, such as natriuresis, intravascular volume contraction, and intra-renal hemodynamics modification, contributing to the beneficial effects on BP, body weight, and albuminuria. Evidence from the EMPA-REG and studies show a reduction in adverse CVD events with the use of SGLT2i compared to placebo [93, 94]. Similarly, the CREDENCE study found a significant reduction in albuminuria and CVD events with SGLT2i [95]. A substantial reduction in adverse events is evident in the decrease of heart failure and progression of KD with SGLT2i. To evaluate outcomes in patients with stage 3–4 CKD, Li et al. conducted a meta-analysis and found that the use of SGLT2i effectively reduced the risk of primary CVD outcomes by 26%, with reductions of 30% in patients with stage 3a CKD, 23% in stage 3b CKD, and 29% in stage 4 CKD. The results were similar for the reduction of heart failure with reduced ejection fraction in patients with KD and patients with arteriosclerosis [96]. This evidence shows the increasing potential benefits of adding SGLT2i for decreasing the progression and managing systemic arterial hypertension in patients living with CKD.

Circadian rhythm BP variability

CCBs are useful for controlling circadian rhythm BP variability. The action time of dihydropyridine CCBs, such as amlodipine, has been seen to control BP for 24 h, thereby minimizing BP variability. This decrease in variability results in a reduction of kidney function deterioration and CVD complications [91]. The ASCOT-BPLA (Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm) study evaluated the treatment with CCBs in combination with or without ACEI, beta-blockers, and diuretics [97]. The findings revealed that treatment with amlodipine was superior to beta-blockers, showing a reduction in BP variability and prevention of CVD events.

Risk of hyperkalemia and kidney function deterioration

Although it is well established that using RAAS inhibitors slows the progression of CKD, some studies suggest discontinuing it when CKD advances due to potential kidney function deterioration. Bhandari and colleagues published a multicenter study and found no differences between the control group and the group using RAAS inhibitors in terms of KD outcomes. The study concluded that discontinuing RAAS inhibitors is not associated with a decline in eGFR in the long term [98].

In summary, ACEI and ARBs have similar effectiveness in managing KD and CVD outcomes in CKD patients, with a preference for ACEI. Combining a RAAS inhibitor with a dihydropyridine CCB is suggested for optimal results. Controlling albuminuria and BP variability is essential, for which SGLT2i shows promising results in reducing CVD and KD adverse events. Nevertheless, there is a need for affordable and accessible medications to improve treatment adherence and implementation of multidisciplinary management, which are crucial for effectively treating patients living with CKD.

Section 6: strategies of usage of diuretics and non-steroidal mineralocorticoid receptor inhibitors in patients with CKD

For patients with CKD, thiazide and loop diuretics are highly recommended. Thiazides lower BP by increasing urinary sodium excretion, which leads to a decrease in extracellular volume. Thiazides have been proven to improve CVD outcomes, including stroke, heart failure, coronary events, and CVD death. When used in combination with other pharmacological groups, such as ACEI, ARBs, and CCBs, thiazides enhance antihypertensive and cardioprotective effects [99]. Conversely, for patients with CKD and eGFR < 30 ml/min/1.73 m2, the use of thiazide has shown less effectiveness [100]. In these patients, loop diuretics positively impact reducing volume overload and improving functional class, although their antihypertensive effects are limited [101]. Diuretics should be avoided in patients with CKD secondary to polycystic KD, as they increase cyst size and promote the loss of tubular excretory function [102].

Question 6.1: what is the utility of Diuretics and Non-Steroidal Mineralocorticoid Receptor Antagonists (nsMRAs) in treating systemic arterial hypertension with CKD?

Mineralocorticoid receptor antagonists

The RAAS plays a crucial role in BP control, extracellular fluid volume regulation, and serum potassium levels. Persistent activation of mineralocorticoid receptors significantly affects cardiomyocytes, fibroblasts, podocytes, and endothelial cells, leading to ventricular hypertrophy, fibrosis, and proinflammatory activity [103]. The first MRA, spironolactone, was a non-selective agent. Highly selective nsMRAs such as finerenone, esaxerenone, and apararenone are available as nsMRAs have demonstrated better anti-inflammatory and antifibrotic activity without significant antihypertensive effects [104].

nsMRAs are effective in managing resistant systemic arterial hypertension, which is uncontrolled hypertension, despite full-dose use of three or more antihypertensive drugs, including a diuretic [105]. These antagonists carry the risk of causing hyperkalemia or reversible kidney function impairment, primarily in those with an eGFR < 30 ml/min/1.73 m2. neMRAs have shown benefits in the cardiorenal sphere; the FIDELIO study documented mild to moderate antihypertensive effects and an increased risk of hyperkalemia. In controlled clinical trials involving patients with type 2 diabetes mellitus, CKD, and systemic arterial hypertension, finerenone significantly reduces albuminuria [106].

New strategies for hyperkalemia management

Hyperkalemia is one of the most frequent complications in the context of RAAS inhibitors used in patients living with CKD. Various results show that nsMRAs such as finerenone pose a lower risk of hyperkalemia due to the drug’s distribution in the heart and kidney, compared to steroidal MARs (spironolactone and eplerenone) [107]. Risk factors for hyperkalemia include decreased eGFR combined with RAAS inhibitor use. Other risk factors include heart failure, diabetes mellitus, resistant systemic arterial hypertension, acute myocardial infarction, and drugs (heparin, NSAIDs, trimethoprim, and pentamidine).

Therapeutic approaches for patients with hyperkalemia begin with identifying risk factors and periodically checking potassium levels. The frequency of monitoring depends on the patient’s comorbidities and the combination of the mentioned risk factors. Persistent hyperkalemia management includes loop diuretics and thiazides, changing the dose of RAAS inhibitors, and finding enhancing drugs. However, RAAS-modulating drugs are essential in patients with CVD, predisposing them to hyperkalemia. In this circumstance, potassium-binding agents can benefit by limiting hyperkalemia [108, 109]. Potassium-binding drugs prevent intestinal potassium absorption and promote fecal excretion. The most commonly used molecules are kayexalate, patiromer, and sodium zirconium cyclosilicate. Initiating these pharmacological agents could be considered in patients with persistent hyperkalemia. Patiromer’s utility was proven in controlled clinical trials involving patients with hyperkalemia, CKD, and heart failure under treatment with RAAS inhibitors [110]. In these patients, escalating oral doses of patiromer between 8.4 g and 25.2 g every 12 h managed to attenuate serum potassium levels by up to 1 mEq/L. Sodium zirconium cyclosilicate is a recently approved potassium-binding agent for patients with chronic hyperkalemia. Clinical studies of its effectiveness come from patients with CKD, heart failure, and/or diabetes who have needed RAAS-modulating drugs. These studies have shown the utility of 5–10 g per day, with a decrease in potassium levels within the first 48 h [111].

Conclusion

In conclusion, in this narrative review, we extensively analyzed strategies endorsed by the Mexican Group of Experts on Arterial Hypertension to prevent, diagnose, and treat CKD related to systemic arterial hypertension within the Mexican and Latin American context. Our review underscores the importance of multidisciplinary management of systemic arterial hypertension and the crucial role community-based programs play in improving the quality of life for affected individuals. By providing these tailored strategies, we aim to reduce the burden of systemic arterial hypertension related to CKD and its complications in Mexico and Latin America, ultimately benefiting millions of people across the region. Future efforts should be directed towards continuously evaluating and updating these strategies, incorporating new evidence as it emerges, and promoting their dissemination and implementation in healthcare settings throughout the region. In addition, further research should focus on identifying and addressing barriers to adopting these strategies and evaluating their real-world effectiveness in improving patient outcomes and reducing the impact of systemic arterial hypertension related to CKD in Mexico and Latin America.

Availability of data and materials

Not applicable.

Abbreviations

ABPM:

Ambulatory BP Monitoring

ACC/AHA:

American College of Cardiology/American Heart Association

ACR:

Albumin-to-Creatinine

AICEs:

Angiotensin-Converting Enzyme

ARBs:

Angiotensin II Receptor Blocker

BP:

Blood Pressure

CCBs:

Calcium Channel blockers

CG:

Cockcroft-Gault

CKD-EPI:

Chronic Kidney Disease Epidemiology Collaboration

CKD:

Chronic Kidney Disease

CVD:

Cardiovascular Disease

eGFR:

Estimated Glomerular Filtration Rate

ESC/ESH:

European Society of Cardiology/European Society of Hypertension

ESKD:

End-Stage Kidney Disease

HBPM:

Home Blood Pressure Monitoring

HD:

Hemodialysis

KD:

Kidney Disease

KDIGO:

Kidney Disease: Improving Global Outcomes

MDRD:

Modification of Diet in Renal Disease

nsMRAs:

Non-Steroidal Mineralocorticoid Receptor Antagonists

NICE:

National Institute for Health and Care Excellence

NSAID:

Non-Steroidal Anti-Inflammatory Drugs

RAAS:

Renin–Angiotensin–Aldosterone System

RRT:

Renal Replacement Therapy

SBP:

Systolic Blood Pressure

SGLT2i:

Sodium-glucose Cotransporter-2 Inhibitors

References

  1. Wainstein M, Bello AK, Jha V, Harris DCH, Levin A, Gonzalez-Bedat MC, et al. International society of nephrology global kidney health atlas: structures, organization, and services for the management of kidney failure in Latin America. Kidney Int Suppl. 2021;11(2):e35-46.

    Article  Google Scholar 

  2. Kovesdy CP. Epidemiology of chronic kidney disease: an update 2022. Kidney Int Suppl. 2022;12(1):7–11.

    Article  Google Scholar 

  3. Georgianos PI, Agarwal R. Hypertension in chronic Kidney Disease (CKD): diagnosis, classification, and therapeutic targets. Am J Hypertens. 2021;34(4):318–26.

    Article  PubMed  Google Scholar 

  4. Oparil S, Acelajado MC, Bakris GL, Berlowitz DR, Cífková R, Dominiczak AF, et al. Hypertens Nat Rev Dis Primer. 2018;4:18014.

    Article  Google Scholar 

  5. Pecoits-Filho R, Sola L, Correa-Rotter R, Claure-Del Granado R, Douthat WG, Bellorin-Font E, et al. Kidney Disease in Latin America: current status, challenges, and the role of the ISN in the development of nephrology in the region. Kidney Int. 2018;94(6):1069–72.

    Article  PubMed  Google Scholar 

  6. Shang Z. Use of Delphi in health sciences research: a narrative review. Med (Baltim). 2023;102(7):e32829.

    Article  Google Scholar 

  7. Li L, Astor BC, Lewis J, Hu B, Appel LJ, Lipkowitz MS, et al. Longitudinal progression trajectory of GFR among patients with CKD. Am J Kidney Dis. 2012;59(4):504–12.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Kunes J, Zicha J. The interaction of genetic and environmental factors in the etiology of Hypertension. Physiol Res. 2009;58(Suppl 2):33–42.

    Article  Google Scholar 

  9. Valenzuela PL, Carrera-Bastos P, Castillo-García A, Lieberman DE, Santos-Lozano A, Lucia A. Obesity and the risk of cardiometabolic Diseases. Nat Rev Cardiol. 2023;20(7):475–94.

    Article  PubMed  Google Scholar 

  10. He FJ, Li J, Macgregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. 2013;346: f1325.

    Article  PubMed  Google Scholar 

  11. Filippou CD, Tsioufis CP, Thomopoulos CG, Mihas CC, Dimitriadis KS, Sotiropoulou LI, et al. Dietary approaches to stop Hypertension (DASH) Diet and blood pressure reduction in adults with and without Hypertension: a systematic review and Meta-analysis of Randomized controlled trials. Adv Nutr Bethesda Md. 2020;11(5):1150–60.

    Article  Google Scholar 

  12. Hall ME, Cohen JB, Ard JD, Egan BM, Hall JE, Lavie CJ, et al. Weight-loss strategies for Prevention and Treatment of Hypertension: A Scientific Statement from the American Heart Association. Hypertens Dallas Tex 1979. 2021;78(5):e38-50.

    CAS  Google Scholar 

  13. Awdishu L, Mehta RL. The 6R’s of drug induced nephrotoxicity. BMC Nephrol. 2017;18:124.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Inoue K, Streja E, Tsujimoto T, Kobayashi H. Urinary albumin-to-creatinine ratio within normal range and all-cause or cardiovascular mortality among U.S. adults enrolled in the NHANES during 1999–2015. Ann Epidemiol. 2021;55:15–23.

    Article  PubMed  Google Scholar 

  15. Mensah GA, Croft JB, Giles WH. The heart, kidney, and brain as target organs in Hypertension. Curr Probl Cardiol. 2003;28(2):156–93.

    Article  PubMed  Google Scholar 

  16. Inker LA, Eneanya ND, Coresh J, Tighiouart H, Wang D, Sang Y, et al. New Creatinine- and cystatin C-Based equations to Estimate GFR without Race. N Engl J Med. 2021;385(19):1737–49.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Cravedi P, Ruggenenti P, Remuzzi G. Which antihypertensive Drugs are the most nephroprotective and why? Expert Opin Pharmacother. 2010;11(16):2651–63.

    Article  CAS  PubMed  Google Scholar 

  18. Stevens PE, Levin A, Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline Development Work Group Members. Evaluation and management of chronic Kidney Disease: synopsis of the Kidney Disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013;158(11):825–30.

    Article  PubMed  Google Scholar 

  19. Agudelo-Botero M, Valdez-Ortiz R, Giraldo-Rodríguez L, González-Robledo MC, Mino-León D, Rosales-Herrera MF, et al. Overview of the burden of chronic Kidney Disease in Mexico: secondary data analysis based on the global burden of Disease Study 2017. BMJ Open. 2020;10(3): e035285.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Mexico - Estadísticas. de Defunciones Registradas 2021. Available from: https://www.inegi.org.mx/rnm/index.php/catalog/822. Cited 2023 May 1.

  21. Figueroa-Lara A, Gonzalez-Block MA, Alarcon-Irigoyen J. Medical expenditure for chronic Diseases in Mexico: the case of selected diagnoses treated by the Largest Care Providers. PLoS ONE. 2016;11(1): e0145177.

    Article  PubMed  PubMed Central  Google Scholar 

  22. Gerstein HC, Mann JF, Yi Q, Zinman B, Dinneen SF, Hoogwerf B, et al. Albuminuria and risk of cardiovascular events, death, and Heart Failure in diabetic and nondiabetic individuals. JAMA. 2001;286(4):421–6.

    Article  CAS  PubMed  Google Scholar 

  23. Romundstad S, Holmen J, Kvenild K, Hallan H, Ellekjaer H. Microalbuminuria and all-cause mortality in 2,089 apparently healthy individuals: a 4.4-year follow-up study. The Nord-Trøndelag Health Study (HUNT), Norway. Am J Kidney Dis off J Natl Kidney Found. 2003;42(3):466–73.

    Article  Google Scholar 

  24. Kidney Disease. Improving global outcomes (KDIGO) blood pressure Work Group. KDIGO 2021 Clinical Practice Guideline for the management of blood pressure in chronic Kidney Disease. Kidney Int. 2021;99(3S):1–87.

    Google Scholar 

  25. Borch-Johnsen K, Feldt-Rasmussen B, Strandgaard S, Schroll M, Jensen JS. Urinary albumin excretion. An Independent predictor of Ischemic Heart Disease. Arterioscler Thromb Vasc Biol. 1999;19(8):1992–7.

    Article  CAS  PubMed  Google Scholar 

  26. Zoppini G, Targher G, Chonchol M, Ortalda V, Negri C, Stoico V, et al. Predictors of estimated GFR decline in patients with type 2 Diabetes and preserved kidney function. Clin J Am Soc Nephrol CJASN. 2012;7(3):401–8.

    Article  CAS  PubMed  Google Scholar 

  27. Levey AS, Becker C, Inker LA. Glomerular filtration rate and Albuminuria for detection and staging of Acute and chronic Kidney Disease in adults: a systematic review. JAMA. 2015;313(8):837–46.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Weir MR. Microalbuminuria and Cardiovascular Disease. Clin J Am Soc Nephrol CJASN. 2007;2(3):581–90.

    Article  PubMed  Google Scholar 

  29. Chen SC, Su HM, Tsai YC, Huang JC, Chang JM, Hwang SJ, et al. Framingham risk score with cardiovascular events in chronic Kidney Disease. PLoS ONE. 2013;8(3): e60008.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Grams ME, Sang Y, Ballew SH, Carrero JJ, Djurdjev O, Heerspink HJL, et al. Predicting timing of clinical outcomes in patients with chronic Kidney Disease and severely decreased glomerular filtration rate. Kidney Int. 2018;93(6):1442–51.

    Article  PubMed  PubMed Central  Google Scholar 

  31. Xu R, Sun S, Huo Y, Yun L, Huang S, Li G, et al. Effects of ACEIs Versus ARBs on Proteinuria or Albuminuria in primary Hypertension. Med (Baltim). 2015;94(39):e1560.

    Article  CAS  Google Scholar 

  32. Chu CD, Powe NR, McCulloch CE, Banerjee T, Crews DC, Saran R, et al. Angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use among hypertensive US adults with Albuminuria. Hypertens Dallas Tex 1979. 2021;77(1):94–102.

    CAS  Google Scholar 

  33. Levey AS, Inker LA. Assessment of Glomerular Filtration Rate in Health and Disease: a state of the Art Review. Clin Pharmacol Ther. 2017;102(3):405–19.

    Article  CAS  PubMed  Google Scholar 

  34. Levey AS, Stevens LA, Schmid CH, Zhang Y (Lucy), Castro AF, Feldman HI. A New Equation to Estimate Glomerular Filtration Rate, et al. editors. Ann Intern Med. 2009;150(9):604–12.

  35. Beauvieux MC, Le Moigne F, Lasseur C, Raffaitin C, Perlemoine C, Barthe N, et al. New predictive equations improve monitoring of kidney function in patients with Diabetes. Diabetes Care. 2007;30(8):1988–94.

    Article  PubMed  Google Scholar 

  36. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med. 1999;130(6):461–70.

    Article  CAS  PubMed  Google Scholar 

  37. Rule AD, Rodeheffer RJ, Larson TS, Burnett JC, Cosio FG, Turner ST, et al. Limitations of estimating glomerular filtration rate from serum creatinine in the general population. Mayo Clin Proc. 2006;81(11):1427–34.

    Article  CAS  PubMed  Google Scholar 

  38. Piéroni L, Bargnoux AS, Cristol JP, Cavalier E, Delanaye P. Did Creatinine Standardization give benefits to the evaluation of glomerular filtration rate? EJIFCC. 2017;28(4):251–7.

    PubMed  PubMed Central  Google Scholar 

  39. Alaini A, Malhotra D, Rondon-Berrios H, Argyropoulos CP, Khitan ZJ, Raj DSC, et al. Establishing the presence or absence of chronic Kidney Disease: uses and limitations of formulas estimating the glomerular filtration rate. World J Methodol. 2017;7(3):73–92.

    Article  PubMed  PubMed Central  Google Scholar 

  40. Zhang A, Huang S. Progress in pathogenesis of proteinuria. Int J Nephrol. 2012;2012:314251.

    Article  PubMed  PubMed Central  Google Scholar 

  41. Bello AK, Hemmelgarn B, Lloyd A, James MT, Manns BJ, Klarenbach S, et al. Associations among estimated glomerular filtration rate, proteinuria, and adverse cardiovascular outcomes. Clin J Am Soc Nephrol CJASN. 2011;6(6):1418–26.

    Article  PubMed  Google Scholar 

  42. Coresh J, Heerspink HJL, Sang Y, Matsushita K, Arnlov J, Astor BC, et al. Change in albuminuria and subsequent risk of end-stage Kidney Disease: an individual participant-level consortium meta-analysis of observational studies. Lancet Diabetes Endocrinol. 2019;7(2):115–27.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Inker LA, Levey AS, Pandya K, Stoycheff N, Okparavero A, Greene T, et al. Early change in proteinuria as a surrogate end point for Kidney Disease progression: an individual patient meta-analysis. Am J Kidney Dis off J Natl Kidney Found. 2014;64(1):74–85.

    Article  Google Scholar 

  44. Association of estimated. Glomerular filtration rate and albuminuria with mortality and end-stage renal Disease: a collaborative meta-analysis of Kidney Disease cohorts. Kidney Int. 2011;79(12):1331–40.

    Article  Google Scholar 

  45. de Zeeuw D, Remuzzi G, Parving HH, Keane WF, Zhang Z, Shahinfar S, et al. Proteinuria, a target for renoprotection in patients with type 2 diabetic Nephropathy: lessons from RENAAL. Kidney Int. 2004;65(6):2309–20.

    Article  PubMed  Google Scholar 

  46. Cepeda M, Pham P, Shimbo D. Status of ambulatory blood pressure monitoring and home blood pressure monitoring for the diagnosis and management of Hypertension in the US: an up-to-date review. Hypertens Res. 2023;46(3):620–9.

    Article  PubMed  PubMed Central  Google Scholar 

  47. Waeber B. What stands behind masked Hypertension? J Hypertens. 2008;26(9):1735–7.

    Article  CAS  PubMed  Google Scholar 

  48. Thakkar HV, Pope A, Anpalahan M. Masked Hypertension: a systematic review. Heart Lung Circ. 2020;29(1):102–11.

    Article  PubMed  Google Scholar 

  49. Cupisti A, Ghiadoni L, Zullo C, Marchini M, Varricchio E, Puntoni A, et al. Home blood pressure measurement as a systematic tool for clinical practice in CKD patients: a real-world picture. Panminerva Med. 2018;60(1):1–7.

    Article  PubMed  Google Scholar 

  50. Wang C, Zhang J, Liu X, Li C, Ye Z, Peng H, et al. Reversed dipper blood-pressure pattern is closely related to severe renal and cardiovascular damage in patients with chronic Kidney Disease. PLoS ONE. 2013;8(2): e55419.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Verdecchia P, Angeli F. How can we use the results of ambulatory blood pressure monitoring in clinical practice? Hypertens Dallas Tex 1979. 2005;46(1):25–6.

    CAS  Google Scholar 

  52. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Pede S, Porcellati C. Ambulatory pulse pressure: a potent predictor of total cardiovascular risk in Hypertension. Hypertens Dallas Tex 1979. 1998;32(6):983–8.

    CAS  Google Scholar 

  53. Wang C, Zhang J, Deng W, Gong W, Liu X, Ye Z, et al. Nighttime Systolic blood-pressure load is correlated with target-organ damage Independent of ambulatory blood-pressure level in patients with non-diabetic chronic Kidney Disease. PLoS ONE. 2015;10(7): e0131546.

    Article  PubMed  PubMed Central  Google Scholar 

  54. Drawz PE, Alper AB, Anderson AH, Brecklin CS, Charleston J, Chen J, et al. Masked Hypertension and elevated Nighttime blood pressure in CKD: Prevalence and Association with Target Organ damage. Clin J Am Soc Nephrol CJASN. 2016;11(4):642–52.

    Article  CAS  PubMed  Google Scholar 

  55. Ye X, Shafi S, Negrete A, Davis WN, Sarac E, Negrete AM, et al. Home blood pressure monitor use in patients with chronic Kidney Disease. Blood Press. 2016;25(5):280–5.

    Article  CAS  PubMed  Google Scholar 

  56. Staplin N, de la Sierra A, Ruilope LM, Emberson JR, Vinyoles E, Gorostidi M, et al. Relationship between clinic and ambulatory blood pressure and mortality: an observational cohort study in 59 124 patients. Lancet Lond Engl. 2023;401(10393):2041–50.

    Article  Google Scholar 

  57. Borrelli S, Garofalo C, Gabbai FB, Chiodini P, Signoriello S, Paoletti E, et al. Dipping Status, ambulatory blood pressure control, Cardiovascular Disease, and Kidney Disease progression: a Multicenter Cohort Study of CKD. Am J Kidney Dis off J Natl Kidney Found. 2023;81(1):15-24e1.

    Article  Google Scholar 

  58. Mansoor GA, White WB. Ambulatory blood pressure monitoring is a useful clinical tool in nephrology. Am J Kidney Dis off J Natl Kidney Found. 1997;30(5):591–605.

    Article  CAS  Google Scholar 

  59. Amar J, Vernier I, Rossignol E, Bongard V, Arnaud C, Conte JJ, et al. Nocturnal blood pressure and 24-hour pulse pressure are potent indicators of mortality in hemodialysis patients. Kidney Int. 2000;57(6):2485–91.

    Article  CAS  PubMed  Google Scholar 

  60. Tripepi G, Fagugli RM, Dattolo P, Parlongo G, Mallamaci F, Buoncristiani U, et al. Prognostic value of 24-hour ambulatory blood pressure monitoring and of night/day ratio in nondiabetic, cardiovascular events-free hemodialysis patients. Kidney Int. 2005;68(3):1294–302.

    Article  PubMed  Google Scholar 

  61. Ekart R, Kanič V, Pečovnik Balon B, Bevc S, Hojs R. Prognostic value of 48-hour ambulatory blood pressure measurement and cardiovascular mortality in hemodialysis patients. Kidney Blood Press Res. 2012;35(5):326–31.

    Article  CAS  PubMed  Google Scholar 

  62. Alborzi P, Patel N, Agarwal R. Home blood pressures are of greater prognostic value than hemodialysis unit recordings. Clin J Am Soc Nephrol CJASN. 2007;2(6):1228–34.

    Article  PubMed  Google Scholar 

  63. Cheung AK, Rahman M, Reboussin DM, Craven TE, Greene T, Kimmel PL, et al. Effects of intensive BP Control in CKD. J Am Soc Nephrol JASN. 2017;28(9):2812–23.

    Article  PubMed  Google Scholar 

  64. Ku E, Lee BJ, Wei J, Weir MR. Hypertension in CKD: Core Curriculum 2019. Am J Kidney Dis off J Natl Kidney Found. 2019;74(1):120–31.

    Article  Google Scholar 

  65. Ari E, Fici F, Robles NR. Hypertension in kidney transplant recipients: where are we today? Curr Hypertens Rep. 2021;23(4):21.

    Article  CAS  PubMed  Google Scholar 

  66. Glicklich D, Lamba R, Pawar R. Hypertension in the kidney transplant recipient: overview of Pathogenesis, Clinical Assessment, and treatment. Cardiol Rev. 2017;25(3):102–9.

    Article  PubMed  Google Scholar 

  67. ESH/ESC Task Force for the Management of Arterial Hypertension. 2013 practice guidelines for the management of arterial Hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the management of arterial Hypertension. J Hypertens. 2013;31(10):1925–38.

    Article  Google Scholar 

  68. Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH et al. /ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018;138(17):e426–83.

  69. Chronic kidney disease: assessment and management. London, National Institute for Health and Care Excellence (NICE). : ; 2021 . (National Institute for Health and Care Excellence: Guidelines). Available from: http://www.ncbi.nlm.nih.gov/books/NBK574714/. Cited 2023 Apr 15.

  70. Cheung AK, Chang TI, Cushman WC, Furth SL, Hou FF, Ix JH, et al. Executive summary of the KDIGO 2021 Clinical Practice Guideline for the management of blood pressure in chronic Kidney Disease. Kidney Int. 2021;99(3):559–69.

    Article  PubMed  Google Scholar 

  71. SPRINT Research Group, Wright JT, Williamson JD, Whelton PK, Snyder JK, Sink KM, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103–16.

    Article  Google Scholar 

  72. Guerrot D, Humalda JK. Blood pressure targets in chronic Kidney Disease: an update on the evidence. Curr Opin Nephrol Hypertens. 2020;29(3):327–32.

    Article  PubMed  Google Scholar 

  73. ACCORD Study Group, Buse JB, Bigger JT, Byington RP, Cooper LS, Cushman WC, et al. Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial: design and methods. Am J Cardiol. 2007;99(12A):21i–33i.

    Google Scholar 

  74. Tsai WC, Wu HY, Peng YS, Yang JY, Chen HY, Chiu YL, et al. Association of Intensive Blood Pressure Control and Kidney Disease progression in nondiabetic patients with chronic Kidney Disease: a systematic review and Meta-analysis. JAMA Intern Med. 2017;177(6):792–9.

    Article  PubMed  PubMed Central  Google Scholar 

  75. Malhotra R, Nguyen HA, Benavente O, Mete M, Howard BV, Mant J, et al. Association between more intensive vs less intensive blood pressure lowering and risk of mortality in chronic Kidney Disease stages 3 to 5: a systematic review and Meta-analysis. JAMA Intern Med. 2017;177(10):1498–505.

    Article  PubMed  PubMed Central  Google Scholar 

  76. Bangalore S, Toklu B, Gianos E, Schwartzbard A, Weintraub H, Ogedegbe G, et al. Optimal systolic blood pressure target after SPRINT: insights from a Network Meta-Analysis of Randomized trials. Am J Med. 2017;130(6):707-719e8.

    Article  PubMed  Google Scholar 

  77. Dasgupta I, Zoccali C. Is the KDIGO systolic blood pressure target < 120 mm hg for chronic Kidney Disease Appropriate in Routine Clinical Practice? Hypertens Dallas Tex 1979. 2022;79(1):4–11.

    CAS  Google Scholar 

  78. Coca A, Aranda P, Bertomeu V, Bonet A, Esmatjes E, Guillén F, et al. [Strategies for effective control of arterial Hypertension in Spain. Consensus document]. Rev Clin Esp. 2006;206(10):510–4.

    Article  CAS  PubMed  Google Scholar 

  79. Gansevoort RT, Correa-Rotter R, Hemmelgarn BR, Jafar TH, Heerspink HJL, Mann JF, et al. Chronic Kidney Disease and cardiovascular risk: epidemiology, mechanisms, and prevention. Lancet Lond Engl. 2013;382(9889):339–52.

    Article  Google Scholar 

  80. Li H, Xue J, Dai W, Chen Y, Zhou Q, Chen W. Visit-to-visit blood pressure variability and risk of chronic Kidney Disease: a systematic review and meta-analyses. PLoS ONE. 2020;15(5): e0233233.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  81. Blood Pressure Lowering Treatment Trialists’ Collaboration, Ninomiya T, Perkovic V, Turnbull F, Neal B, Barzi F, et al. Blood pressure lowering and major cardiovascular events in people with and without chronic Kidney Disease: meta-analysis of randomised controlled trials. BMJ. 2013;347: f5680.

    Article  PubMed Central  Google Scholar 

  82. Sinha AD, Agarwal R. Clinical pharmacology of antihypertensive therapy for the treatment of Hypertension in CKD. Clin J Am Soc Nephrol CJASN. 2019;14(5):757–64.

    Article  CAS  PubMed  Google Scholar 

  83. Strippoli GFM, Bonifati C, Craig M, Navaneethan SD, Craig JC. Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic Kidney Disease. Cochrane Database Syst Rev. 2006;2006(4):CD006257.

    PubMed  PubMed Central  Google Scholar 

  84. Bakris GL, Sarafidis PA, Weir MR, Dahlöf B, Pitt B, Jamerson K, et al. Renal outcomes with different fixed-dose combination therapies in patients with Hypertension at high risk for cardiovascular events (ACCOMPLISH): a prespecified secondary analysis of a randomised controlled trial. Lancet Lond Engl. 2010;375(9721):1173–81.

    Article  CAS  Google Scholar 

  85. Fu EL, Clase CM, Evans M, Lindholm B, Rotmans JI, Dekker FW, et al. Comparative effectiveness of Renin-Angiotensin System Inhibitors and Calcium Channel Blockers in individuals with Advanced CKD: a Nationwide Observational Cohort Study. Am J Kidney Dis off J Natl Kidney Found. 2021;77(5):719-729e1.

    Article  CAS  Google Scholar 

  86. Lin YC, Lin JW, Wu MS, Chen KC, Peng CC, Kang YN. Effects of calcium channel blockers comparing to angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients with Hypertension and chronic Kidney Disease stage 3 to 5 and dialysis: a systematic review and meta-analysis. PLoS ONE. 2017;12(12): e0188975.

    Article  PubMed  PubMed Central  Google Scholar 

  87. Zhao HJ, Li Y, Liu SM, Sun XG, Li M, Hao Y, et al. Effect of calcium channels blockers and inhibitors of the renin-angiotensin system on renal outcomes and mortality in patients suffering from chronic Kidney Disease: systematic review and meta-analysis. Ren Fail. 2016;38(6):849–56.

    Article  CAS  PubMed  Google Scholar 

  88. Ghamami N, Chiang SHY, Dormuth C, Wright JM. Time course for blood pressure lowering of dihydropyridine calcium channel blockers. Cochrane Database Syst Rev. 2014;(8):CD010052.

  89. Zhu J, Chen N, Zhou M, Guo J, Zhu C, Zhou J, et al. Calcium channel blockers versus other classes of Drugs for Hypertension. Cochrane Database Syst Rev. 2021;2021(10):CD003654.

    PubMed Central  Google Scholar 

  90. Heerspink HJL, Kröpelin TF, Hoekman J, de Zeeuw D. Reducing Albuminuria as Surrogate Endpoint (REASSURE) Consortium. Drug-Induced reduction in Albuminuria is Associated with subsequent renoprotection: a Meta-analysis. J Am Soc Nephrol JASN. 2015;26(8):2055–64.

    Article  CAS  PubMed  Google Scholar 

  91. Abraham G, Almeida A, Gaurav K, Khan MY, Patted UR, Kumaresan M. Reno protective role of amlodipine in patients with hypertensive chronic Kidney Disease. World J Nephrol. 2022;11(3):86–95.

    Article  PubMed  PubMed Central  Google Scholar 

  92. Tamargo J. [New calcium channel blockers for the treatment of Hypertension]. Hipertens Riesgo Vasc. 2017;34(Suppl 2):5–8.

    Article  PubMed  Google Scholar 

  93. Neal B, Perkovic V, Mahaffey KW, de Zeeuw D, Fulcher G, Erondu N, et al. Canagliflozin and Cardiovascular and renal events in type 2 Diabetes. N Engl J Med. 2017;377(7):644–57.

    Article  CAS  PubMed  Google Scholar 

  94. Zinman B, Lachin JM, Inzucchi SE. Empagliflozin, Cardiovascular outcomes, and mortality in type 2 Diabetes. N Engl J Med. 2016;374(11):1094.

    PubMed  Google Scholar 

  95. Perkovic V, Jardine MJ, Neal B, Bompoint S, Heerspink HJL, Charytan DM, et al. Canagliflozin and renal outcomes in type 2 Diabetes and Nephropathy. N Engl J Med. 2019;380(24):2295–306.

    Article  CAS  PubMed  Google Scholar 

  96. Li N, Zhou G, Zheng Y, Lv D, Zhu X, Wei P, et al. Effects of SGLT2 inhibitors on cardiovascular outcomes in patients with stage 3/4 CKD: a meta-analysis. PLoS ONE. 2022;17(1): e0261986.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  97. Dahlöf B, Sever PS, Poulter NR, Wedel H, Beevers DG, Caulfield M, et al. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac outcomes Trial-Blood pressure lowering arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet Lond Engl. 2005;366(9489):895–906.

    Article  Google Scholar 

  98. Bhandari S, Mehta S, Khwaja A, Cleland JGF, Ives N, Brettell E, et al. Renin-angiotensin system inhibition in Advanced chronic Kidney Disease. N Engl J Med. 2022;387(22):2021–32.

    Article  CAS  PubMed  Google Scholar 

  99. Yoshimura M, Kawai M. Synergistic inhibitory effect of angiotensin II receptor blocker and thiazide diuretic on the tissue renin-angiotensin-aldosterone system. J Renin-Angiotensin-Aldosterone Syst JRAAS. 2010;11(2):124–6.

    Article  CAS  PubMed  Google Scholar 

  100. National High Blood Pressure Education Program. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda (MD): National Heart, Lung, and Blood Institute (US); 2004 . Available from: http://www.ncbi.nlm.nih.gov/books/NBK9630/. Cited 2023 Apr 16.

  101. Hung SC, Kuo KL, Peng CH, Wu CH, Lien YC, Wang YC, et al. Volume overload correlates with cardiovascular risk factors in patients with chronic Kidney Disease. Kidney Int. 2014;85(3):703–9.

    Article  CAS  PubMed  Google Scholar 

  102. Ecder T, Edelstein CL, Fick-Brosnahan GM, Johnson AM, Chapman AB, Gabow PA, et al. Diuretics versus angiotensin-converting enzyme inhibitors in autosomal dominant polycystic Kidney Disease. Am J Nephrol. 2001;21(2):98–103.

    Article  CAS  PubMed  Google Scholar 

  103. Agarwal R, Kolkhof P, Bakris G, Bauersachs J, Haller H, Wada T, et al. Steroidal and non-steroidal mineralocorticoid receptor antagonists in cardiorenal medicine. Eur Heart J. 2021;42(2):152–61.

    Article  CAS  PubMed  Google Scholar 

  104. Patel V, Joharapurkar A, Jain M. Role of mineralocorticoid receptor antagonists in kidney Diseases. Drug Dev Res. 2021;82(3):341–63.

    Article  CAS  PubMed  Google Scholar 

  105. Williams B, MacDonald TM, Morant S, Webb DJ, Sever P, McInnes G, et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug-resistant Hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet Lond Engl. 2015;386(10008):2059–68.

    Article  CAS  Google Scholar 

  106. Bakris GL, Agarwal R, Anker SD, Pitt B, Ruilope LM, Rossing P, et al. Effect of Finerenone on chronic Kidney Disease outcomes in type 2 Diabetes. N Engl J Med. 2020;383(23):2219–29.

    Article  CAS  PubMed  Google Scholar 

  107. Kolkhof P, Delbeck M, Kretschmer A, Steinke W, Hartmann E, Bärfacker L, et al. Finerenone, a novel selective nonsteroidal mineralocorticoid receptor antagonist protects from rat cardiorenal injury. J Cardiovasc Pharmacol. 2014;64(1):69–78.

    Article  CAS  PubMed  Google Scholar 

  108. Palmer BF, Clegg DJ. Diagnosis and treatment of hyperkalemia. Cleve Clin J Med. 2017;84(12):934–42.

    Article  PubMed  Google Scholar 

  109. Kovesdy CP. Management of hyperkalaemia in chronic Kidney Disease. Nat Rev Nephrol. 2014;10(11):653–62.

    Article  CAS  PubMed  Google Scholar 

  110. Weir MR, Bakris GL, Bushinsky DA, Mayo MR, Garza D, Stasiv Y, et al. Patiromer in patients with Kidney Disease and hyperkalemia receiving RAAS inhibitors. N Engl J Med. 2015;372(3):211–21.

    Article  PubMed  Google Scholar 

  111. Peacock WF, Rafique Z, Vishnevskiy K, Michelson E, Vishneva E, Zvereva T, et al. Emergency potassium normalization treatment including Sodium Zirconium Cyclosilicate: a phase II, Randomized, Double-blind, placebo-controlled study (ENERGIZE). Acad Emerg Med off J Soc Acad Emerg Med. 2020;27(6):475–86.

    Article  Google Scholar 

Download references

Acknowledgements

We want to thank “Armstrong Laboratorios de México” for covering the fee to publish this work.

Mexican Group of Experts on Arterial Hypertension

Silvia Palomo-Piñón MD PhD 1,2,3, José Manuel Enciso-Muñoz MD 1, Eduardo Meaney MD PhD 1,4, Ernesto Díaz-Domínguez MD 1,5, David Cardona-Muller PhD 1,6, Fabiola Pazos Pérez MD MsC 1,7, Emilia Cantoral-Farfán MD 1,8, Juan Carlos Anda-Garay MD MsC 1,7, Janet Mijangos-Chavez MD 1,9, Neftali Eduardo Antonio-Villa MD PhD 1,10, Luis Alcocer MD MsC 1,11, Humberto Álvarez-López MD MsC 1,12, Ernesto G. Cardona-Muñoz MD 1,13, Adolfo Chávez-Mendoza MD MsC 1,14, Enrique Díaz-Díaz 1,14, Héctor Galván-Oseguera MD 1,14, Martin Rosas-Peralta MD PhD 1,15 & Vidal José González Coronado MD.1

Affiliations:

1. Grupo de Expertos en Hipertensión Arterial México (GREHTA), Ciudad de México, México.

2. Colaborador Externo, Unidad de Investigación Médica en Enfermedades Nefrológicas Siglo XXI (UIMENSXII), UMAE Hospital de Especialidades "Dr. Bernardo Sepúlveda G" Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México.

3. Grupo Colaborativo en Hipertensión Arterial (GCHTA), Ciudad de México, México.

4. Escuela Superior de Medicina, Instituto Politecnico Nacional, Ciudad de México, México.

5. UMAE Hospital de Cardiología, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México.

6. Universidad de Guadalajara, Guadalajara, Jalisco.

7. UMAE Hospital de Especialidades "Dr. Bernardo Sepúlveda G" Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México.

8. Jefatura de Nefrología, Hospital General De Zona Médico Familiar No. 8 Gilberto Flores Izquierdo, Instituto Mexicano del Seguro Social, Ciudad de México.

9. Jefatura de Cardiología, UMAE Dr. Antonio Fraga Mouret, Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social, Ciudad de México.

10. Departamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, México.

11. Hospital Ángeles del Pedregal, Ciudad de México, México.

12. Hospital Puerta de Hierro Andares, Jalisco, México.

13. Universidad de Guadalajara, (CUCS), Jalisco, México.

14. UMAE Hospital de Cardiologia Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.

15. Titular Academia Nacional de Medicina, Ciudad de México, México.

Funding

This work was funded by “Armstrong Laboratorios SA de CV”. The funder provided support in the form of publication fee support. The sponsor did not have any additional role in the study design, writing of the study, decision to publish, or manuscript preparation.

Author information

Authors and Affiliations

  1. Grupo de Expertos en Hipertensión Arterial México (GREHTA), Ciudad de México, México

    Silvia Palomo-Piñón, José Manuel Enciso-Muñoz, Eduardo Meaney, Ernesto Díaz-Domínguez, David Cardona-Muller, Fabiola Pazos Pérez, Emilia Cantoral-Farfán, Juan Carlos Anda-Garay, Janet Mijangos-Chavez & Neftali Eduardo Antonio-Villa

  2. Colaborador Externo, Unidad de Investigación Médica en Enfermedades Nefrológicas Siglo XXI (UIMENSXII), UMAE Hospital de Especialidades “Dr. Bernardo Sepúlveda G” Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México

    Silvia Palomo-Piñón

  3. Grupo Colaborativo en Hipertensión Arterial (GCHTA), Ciudad de México, México

    Silvia Palomo-Piñón

  4. Grupo de Expertos en Hipertensión Arterial México (GREHTA), Calle Retorno del Escorial #13, Col. El Dorado, Tlanepantla de Baz, Estado de México, 54020, México

    Silvia Palomo-Piñón

  5. Asociación Mexicana para la Prevención de la Aterosclerosis y sus Complicaciones A.C, Ciudad de México, México

    José Manuel Enciso-Muñoz

  6. Escuela Superior de Medicina, Instituto Politecnico Nacional, Ciudad de México, México

    Eduardo Meaney

  7. UMAE Hospital de Cardiología, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México

    Ernesto Díaz-Domínguez

  8. Universidad de Guadalajara, Guadalajara, Jalisco, México

    David Cardona-Muller

  9. UMAE Hospital de Especialidades “Dr. Bernardo Sepúlveda G” Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México

    Fabiola Pazos Pérez & Juan Carlos Anda-Garay

  10. Jefatura de Nefrología, Hospital General De Zona Médico Familiar No. 8 Gilberto Flores Izquierdo, Instituto Mexicano del Seguro Social, Ciudad de México, México

    Emilia Cantoral-Farfán

  11. Jefatura de Cardiología, UMAE Dr. Antonio Fraga Mouret, Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social, Ciudad de México, México

    Janet Mijangos-Chavez

  12. Departamento de Endocrinologia, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, México

    Neftali Eduardo Antonio-Villa

Authors
  1. Silvia Palomo-Piñón
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. José Manuel Enciso-Muñoz
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Eduardo Meaney
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Ernesto Díaz-Domínguez
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. David Cardona-Muller
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Fabiola Pazos Pérez
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Emilia Cantoral-Farfán
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Juan Carlos Anda-Garay
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Janet Mijangos-Chavez
    View author publications

    You can also search for this author in PubMed Google Scholar

  10. Neftali Eduardo Antonio-Villa
    View author publications

    You can also search for this author in PubMed Google Scholar

Consortia

on behalf of the Mexican Group of Experts on Arterial Hypertension

  • Silvia Palomo-Piñón
  • , José Manuel Enciso-Muñoz
  • , Eduardo Meaney
  • , Ernesto Díaz-Domínguez
  • , David Cardona-Muller
  • , Fabiola Pazos Pérez
  • , Emilia Cantoral-Farfán
  • , Juan Carlos Anda-Garay
  • , Janet Mijangos-Chavez
  • , Neftali Eduardo Antonio-Villa
  • , Luis Alcocer
  • , Humberto Álvarez-López
  • , Ernesto G. Cardona-Muñoz
  • , Adolfo Chávez-Mendoza
  • , Enrique Díaz-Díaz
  • , Héctor Galván-Oseguera
  • , Martin Rosas-Peralta
  •  & Vidal José González Coronado

Contributions

Research idea: SPP, JMEM; Analysis/interpretation: SPP, JMEM; Manuscript drafting: SPP, JMEM, EM, EDD, DCM, FPP, ECF, JCAG, JMC; Manuscript editing: NEAV; Figure drafting: NEAV; Supervision or mentorship: SPP.

Corresponding author

Correspondence to Silvia Palomo-Piñón.

Ethics declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

All authors approved the final version of this manuscript. Each author contributed important intellectual content during manuscript drafting or revision and accepted accountability for the overall work by ensuring that questions about the accuracy or integrity of any part of the work were appropriately investigated and resolved.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Palomo-Piñón, S., Enciso-Muñoz, J.M., Meaney, E. et al. Strategies to prevent, diagnose and treat kidney disease related to systemic arterial hypertension: a narrative review from the Mexican Group of Experts on Arterial Hypertension. BMC Nephrol 25, 24 (2024). https://doi.org/10.1186/s12882-023-03450-5

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12882-023-03450-5

Keywords

BMC Nephrology

ISSN: 1471-2369

Contact us