Skip to main content
Download PDF

Glomerulonephritis during Mycobacterium tuberculosis infection: scoping review

BMC Nephrology volume 25, Article number: 285 (2024) Cite this article

Abstract

Introduction

People with Tuberculosis (TB) infection may present with glomerulonephritis (GN). The range of presentations, renal pathologies, and clinical outcomes are uncertain. Whether clinical features that establish if GN etiology is medication or TB related, and possible benefits of immunosuppression remain uncertain.

Methods

A scoping review was completed, searching MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Web of Science and Conference Abstracts from Inception to December, 2023. The study population included patients with TB infection who developed GN and underwent renal biopsy. All data regarding presentation, patient characteristics, renal pathology, management of TB and GN, and outcomes were summarized.

Results

There were 62 studies identified, with 130 patients. These cases included a spectrum of presentations including acute kidney injury, nephrotic syndrome and hypertension, and a range of 10 different renal pathology diagnoses. Cases that included immunosuppression and outcomes ranged from complete remission to long-term dialysis dependence. The presence of granulomas (4/4, 100%), anti-glomerular basement membrane disease (3/3, 100%), amyloidosis (75/76, 98.7%), and focal segmental glomerulosclerosis (2/2, 100%) were specific for GN being TB-infection related. On the other hand, minimal change disease was specific for anti-TB therapy related (7/7, 100%). While patients with more aggressive forms of GN commonly were prescribed immunosuppression, this study was unable to confirm efficacy. Only rifampin or isoniazid were implicated in drug-associated GN.

Discussion

This study provides a clear rationale for renal biopsy in patients with TB and GN, and outlines predictors for the GN etiology. Thus, this study establishes key criteria to optimize diagnosis and management of patients with TB and GN.

Peer Review reports

Introduction

Annually, Mycobacterium tuberculosis (TB) infections infect over 10 million people [1], and represent the 13th leading cause of death worldwide [2]. Urogenital TB commonly involves the urinary collecting system, but renal parenchymal involvement has been reported, including interstitial nephritis and glomerulonephritis (GN) [3]. Optimal management of GN during TB infection remains unclear. Identifying whether GN is primary or secondary, and the role of immunosuppression, is uncertain [4, 5]. It is not always possible to identify whether TB infection or anti-tuberculous therapy (ATT) is the precipitant of GN [6,7,8,9,10]. Tuberculosis often coexists with other comorbidities that can precipitate GN, such as human immunodeficiency virus (HIV) [11] or sickle cell disease; [12] and how to isolate the relative contributions of each comorbid condition is unclear.

There is a wide range of glomerular presentations described in TB infection, including IgA nephropathy [13], membranous nephropathy [14], amyloidosis [15], minimal change [16] and membranoproliferative disease [8]. However, there remains a lack of consensus on how to manage these cases. Improved management in cases of glomerular disease in patients with TB may enhance renal and TB-related outcomes.

This scoping review had four objectives. First, we describe the presentation of glomerulonephritis in patients with TB infection. Secondly, we describe the range of renal pathology diagnoses in patients with TB infection and GN. Thirdly, we evaluate which renal pathology features are predictive of whether the GN is from TB versus medication-related. Finally, we evaluate the impact of immunosuppression on clinical outcomes.

Methods

Our protocol was developed using the recommended methodology for scoping reviews from the Joanna Briggs Institute [17].

Search strategy and study selection criteria

A scoping review was performed using Cochrane, Embase, Medline and Web of Science databases, with no date or language restriction. Search terms included “Glomerulonephritis,” “Glomerulopathy,” “Glomerular disease,” “Nephrotic syndrome,” “Nephritic syndrome,” “Tuberculosis,” “Mycobacterium tuberculosis,” and “Mycobacteria.” Searches were completed using [“Glomerulonephritis” OR “Glomerulopathy” OR “Glomerular disease” OR “Nephrotic syndrome” OR “Nephritic syndrome”] AND [“Mycobacterium tuberculosis” OR “Tuberculosis” OR “Mycobacteria.”].

Studies were included if they described a case of glomerular disease in a patient with TB infection. Renal biopsy matched to the clinical description was mandatory. Adult patients (age 18 or over) were included. All study types were included. References from review articles were screened to assure all cases were identified. Pediatric cases were excluded. Cases in which a renal biopsy was either not performed, or was not matched to the clinical conditions (quantitation of proteinuria, presence of edema or hypertension or acute kidney injury (AKI), etc.) were excluded.

Two authors (BT, AF) screened all titles and abstracts, and completed full text review, using Covidence systematic review software (Veritas Health Innovation, Melbourne, Australia). Conflicts were resolved by discussion and consensus between both authors (BT, AF).

Data extraction

Results

Search of databases yielded 891 references (Fig. 1). After duplicates were removed (n = 204), study titles and abstracts were screened, leaving full text studies for review (n = 184). Additional studies were excluded (n = 125), and 3 studies were added as a result of review of references from review papers. This left 62 studies for final inclusion, which included 130 patients.

Fig. 1
figure 1

PRISMA chart for study inclusion

Full size image

Study characteristics

Most included studies were case reports (55/62, 90.3%) but case series represented a higher proportion (74/130, 56.9%) of patients (Table 1). Most included patients were reported between 2000 and 2019 (103/130, 78.5%), with few studies published before 1990 (10/62, 16.1%). Although most studies were published in high income countries (34/62, 54.8%), the majority of patient cases were from low and middle income countries (96/130, 73.8%), with India as the country with the most studies (14/62, 22.6%) and patients (81/130, 62.3%).

Table 1 Study characteristics
Full size table

Presentation of glomerular disease in tuberculosis

Patient characteristics

Reporting was incomplete for patient age (77.9%) and sex (97.7%). Mean age was 42.3 years and females were a minority of reported cases (27.3%) (Table 2).

Table 2 Patient characteristics and clinical presentation
Full size table

Clinical presentation of glomerulonephritis in patients with tuberculosis

GN presented after TB symptoms in most reported cases (90.7%), and rarely beyond 24 weeks from onset of TB symptoms (7.0%) (Table 2). GN presented after TB diagnosis in most (88.9%) cases, and rarely after 24 weeks from TB diagnosis (5.7%).

“Reporting of proteinuria quantitation was incomplete, but mean 24 hour proteinuria was highest for amyloidosis (10.4 g/day, n = 7 reported), FSGS (8.4 g/day, n = 2 reported) and minimal change disease (7.9 g/day, n = 7 reported) (Fig. 2A). Nephrotic syndrome was common (60.0%, 78/130 total reported), and was most common in FSGS (100%, n = 2 reported), Immunotactoid GN (100%, n = 1 reported) and minimal change disease (85.7%, n = 7 reported) (Fig. 2B).

Hypertension was common (42.1%), and was found in all cases of FSGS (100%, n = 2 reported), Immunotactoid GN (100%, n = 1 reported), MPGN (100%, n = 3 reported), and mixed pathology (100%, n = 1 reported) (Fig. 2C).

Acute kidney injury was common (69.8%), and was identified in all cases of Ant-GBM disease (100%, n = 3 reported), pauci-immune GN (100%, n = 10 reported), FSGS (100%, n = 2 reported), MPGN (100%, n = 5 reported) and mixed pathology (100%, n = 3 reported) (Fig. 2D).”

The initial site of organ involvement of TB was incompletely reported (43.5%, 57/130). The most common site of reported TB organ involvement was lung (78.9%), with lymphadenopathy (8.8%) and renal-limited (7.0%) next most common. Only 1 case explicitly described disseminated TB, but there was insufficient description to rule this out in other cases.

Fig. 2
figure 2

A 24 h protein excretion versus Type of Glomerulonephritis B Percent cases with Nephrotic syndrome versus Type of Glomerulonephritis C Percent cases with Hypertension versus Type of Glomerulonephritis D Percent cases with Acute kidney injury versus Type of Glomerulonephritis LEGEND: AMY = amyloidosis; GBM = Anti-GBM antibody disease; ANCA = pauci-immune GN, FSGS = focal segmental glomerulosclerosis; IgA = IgA nephropathy; IT = immunotactoid GN; MPGN = membranoproliferative glomerulonephritis; MEM = membranous nephropathy; MCD = minimal change disease; MIX = mixed pathology

Full size image

Renal biopsy: general features

Whether crescents were present on renal biopsy could be determined in 59 of 62 studies, and each of these 59 studies included 1 case each. Crescents were commonly identified (20/59, 33.9%) (Appendix 1). In addition to being found in all cases of crescentic (pauci-immune) GN (10/10), crescents were also identified in Anti-GBM disease (3/3), IgA nephropathy (3/13, with 2/3 Henoch Schoenlein purpura (HSP) cases), Membranoproliferative glomerulonephritis (MPGN) (3/5), and mixed pathology with features of IgA/MPGN/Membranous nephropathy (1/3). Patients with crescents on renal biopsy had GN attributed to medications in 4 cases (4/20, 20.0%); this included crescentic pauci-immune GN (3/10) and MPGN (1/5) (Table 3, Appendix 1).

Table 3 Renal pathology and attribution to medication
Full size table

Granulomas were rarely reported (Appendix 1) (4/59, 6.8%), in IgA nephropathy (1/13), and membranous nephropathy (3/13). Patients with granulomas on renal biopsy had GN attributed to TB in all cases (4/4).

AIN was common (Appendix 1) (15/59, 25.4%), in crescentic (pauci-immune) GN (5/10), IgA nephropathy (1/13 cases), membranous nephropathy (6/10) and minimal change disease (3/7). Patient with AIN on renal biopsy had GN attributed to medication exposure in 6 cases (6/15, 40.0%); this included minimal change disease (3/7), Crescentic pauci-immune GN (2/10), and membranous nephropathy (1/10).

Cases with urogenital tuberculosis as primary site

There were four cases in which urogenital system was considered the primary site of infection of tuberculosis. The cases included membranous nephropathy (3/4) and IgA nephropathy (1/4).

The three cases of membranous nephropathy presented with nephrotic syndrome (3/3), and also had AIN (3/3) and granulomas (2/3) on renal biopsy. The case of IgA nephropathy presented with AKI, hematuria and subnephrotic-range albuminuria. There was no AIN, crescents or granulomas on renal biopsy.

All four cases were attributed to tuberculosis infection, with GN improving with ATT.

Attribution of glomerulonephritis to medication

Attribution of GN to Anti-Tuberculosis medication was most common in minimal change disease (100%, 7/7 reported), but also was found in crescentic pauci-immune GN (30%, 3/10 reported), MPGN (20%, 2/10 reported) and membranous nephropathy (20%, 2/10 reported) (Fig. 3).

Reporting of medications used in ATT was complete (Appendix 2) in 13/15 (86.7%) and partially complete in 1 (6.7%) cases. The most commonly prescribed ATT medications were rifampin (13/13) and isoniazid (13/13), followed by pyrazinamide (11/13), ethambutol (8/13), levofloxacin (1/13), streptomycin (1/13) and clarithromycin (1/13).

When GN was medication-associated (Appendix 2), rifampin (10/15), isoniazid (1/15), either isoniazid or rifampin (3/15) or unknown (1/15) was implicated. No drug other than isoniazid or rifampin was implicated in medication-associated GN in patients with TB.

Fig. 3
figure 3

Percent cases attributed to Anti-Tuberculosis Therapy versus Type of Glomerulonephritis LEGEND: AMY = amyloidosis; GBM = Anti-GBM antibody disease; ANCA = pauci-immune GN, FSGS = focal segmental glomerulosclerosis; IgA = IgA nephropathy; IT = immunotactoid GN; MPGN = membranoproliferative glomerulonephritis; MEM = membranous nephropathy; MCD = minimal change disease; MIX = mixed pathology

Full size image

Use of immunosuppression

Combined use of corticosteroids with cyclophosphamide and plasmapheresis was reserved for cases (Appendix 2) of Anti-GBM (3/3) and pauci-immune crescentic GN (1/10). Corticosteroids alone were used in pauci-immune crescentic GN (4/10), Focal segmental glomerulosclerosis (FSGS) (2/2), IgA nephropathy (3/13), Membranous nephropathy (3/10), MPGN (1/5) and minimal change disease (3/7).

When AIN was present on renal biopsy, immunosuppression was commonly prescribed (Appendix 2) (7/15, 46.7%). Improvement in renal outcomes (proteinuria or eGFR) was incompletely reported (14/15), but improvement was comparable in cases in which immunosuppression was used (5/7 vs. 7/7). Each of the two patients with AIN on renal biopsy who failed to improve with immunosuppression had crescentic pauci-immune GN.

When crescents were present on renal biopsy, immunosuppression was commonly prescribed (Appendix 2) (15/19, 78.9%). Renal outcomes (improvement in proteinuria or GFR) were incompletely reported but similarly improved in cases in which immunosuppression was used compared with those where immunosuppression was withheld (12/15 vs. 4/4). The three patients with crescents on renal biopsy who failed to improve with immunosuppression included two patients with anti-GBM disease and one patient with crescentic pauci-immune GN; all three of these patients remained persistently dialysis-dependent, despite immunosuppression with corticosteroids and plasmapheresis in all three cases, and additionally cyclophosphamide in the two cases of anti-GBM disease.

When granulomas were present on renal biopsy, immunosuppression was used in only one case (Appendix 2) (1/4, 25.0%). In this case of membranous nephropathy with AIN and granulomas [19], corticosteroids were added after initial improvement in proteinuria (from 7.6 g/day) was noted with anti-tuberculous therapy. Whether immunosuppression impacted renal outcomes in this case is thus uncertain.

Specific types of glomerulonephritis

Cases of Glomerular disease in Tuberculosis were categorized by diagnosis based on renal pathology (Appendices 1 and 2).

Amyloidosis

This study is not designed to predict accurately the incidence of different types of glomerulonephritis in tuberculosis infection. Most of the cases (69/76) of amyloidosis in tuberculosis infection came from 2 cohort studies [20, 21]. Amyloidosis presented with AKI (54/74, 73.0%), nephrotic-range proteinuria (49/76, 64.5%), and hypertension (20/47, 42.6%) [15, 20,21,22,23,24,25,26]. Most cases of amyloidosis in this scoping review did not report whether AIN, crescents or granulomas were present; however, in those cases in which this information was reported, they were consistently absent (0/5). Amyloidosis was attributed to TB in most cases (75/76, 98.7%). Only one case used immunosuppression; in this case, a 25 year old man developed nephrotic syndrome, hypertension and AKI necessitating hemodialysis, simultaneous to the presentation of pulmonary TB. Initiation of monthly tocilizumab and anti-tuberculous therapy (ATT) led to improvement in renal function and dialysis independence. The subtype of amyloidosis (AA versus AL) was not consistently reported; tuberculosis infection was implicated in 90% of cases of AA amyloidosis in one case series from India [21], but in 51–65% of cases of other historic cohorts [27,28,29].

Anti-glomerular basement membrane disease glomerulonephritis

Cases of Anti-GBM GN presented with AKI (3/3, 100.0%) with 2 patients starting hemodialysis [30,31,32]. Nephrotic range proteinuria with clinical features of nephrotic syndrome was reported in 2 cases. Renal pathology revealed crescents (3/3), but granulomas and AIN were absent. All cases were attributed to TB. Immunosuppression was used in all cases, with cyclophosphamide + corticosteroids + plasmapheresis in all cases. Improvement in renal function was noted in one patient, but both patients who started hemodialysis remained dialysis dependent.

Crescentic (pauci-immune) glomerulonephritis

Cases of crescentic (pauci-immune) GN presented with AKI (10/10, 100.0%), hypertension (4/7 reported, 57.1%), and nephrotic syndrome (3/10, 30.0%) [4, 9, 32,33,34,35,36,37,38,39]. Most (7/10, 70.0%) cases were ANCA-negative, with the remainder Anti-Proteinase-3 (2/10) or Anti-Myeloperoxidase (1/10) positive. Two patients required initiation of dialysis at the time of diagnosis of crescentic GN; neither patient recovered renal function, despite cure of TB with ATT, and immunosuppression in both cases. Renal pathology revealed crescents (10/10, 100.0%), AIN (5/10, 50.0%) but no granulomas. Cases were most often attributed to TB (6/10, 60.0%), then to ATT (3/10, 30.0%). When attribution was to ATT, rifampin was the culprit medication in each case. Immunosuppression was used in most cases (8/10, 80.0%). In cases where immunosuppression was not used (2/10), one patient fully recovered renal function by stopping rifampin, while another patient fully recovered by curing TB with ATT. In total, full (4/10) or partial (2/10) recovery of renal function, persistent need for dialysis (2/10) and unknown long-term renal outcomes (2/10) were seen.

Focal segmental glomerulosclerosis

There were 2 cases of FSGS, both of which presented with nephrotic syndrome, hypertension, and AKI [11, 40]. Renal pathology did not reveal crescents, AIN or granulomas. Both cases were attributed to TB, but corticosteroids were prescribed in both cases. Improvement in renal function and proteinuria was noted in both cases, with timing coinciding better with corticosteroid therapy than with ATT in one case.

IgA nephropathy

IgA nephropathy presented with nephrotic syndrome (6/13, 46.2%) and AKI (6/13, 46.2%) [6, 12, 13, 34, 41,42,43,44,45,46,47,48,49]. Blood pressure was uncommonly reported (7/13), but hypertension was present in only a minority of reported cases (1/7, 14.3%). HSP-IgA nephritis was reported (3/13, 23.1%); in these cases, patients presented with AKI (2/3, 66.7%) and nephrotic syndrome (1/3, 33.3%). Renal pathology revealed AIN (1/13), crescents (2/13) and granulomas (1/13). Cases of HSP presented with AIN (1/3), crescents (2/3) and granulomas (1/3). IgA nephropathy was attributed to TB in most cases (11/13, 84.6%) although it often was unclear (2/13). Renal function and proteinuria improved in most cases (11/13) with ATT. In cases with corticosteroid use (3/13), initiation of corticosteroids coincided with improvement in renal outcomes in 2 cases.

Immunotactoid glomerulonephritis

In the only case of immunotactoid GN, a 37 year old man presented 9 weeks after TB diagnosis with nephrotic syndrome and anasarca, AKI and hypertension [50]. Renal pathology revealed no crescents, AIN or granulomas, and immunotactoid GN was attributed to TB. Proteinuria improved but did not completely resolve, with ATT (without immunosuppression).

Membranoproliferative glomerulonephritis

Cases of MPGN typically presented with AKI (5/5, 100.0%), hypertension (3/5, 60.0%) and nephrotic syndrome (3/5, 60.0%) [8, 51,52,53,54]. One case presented with anuric AKI, necessitating renal replacement therapy. Renal pathology revealed crescents in multiple (3/5, 60.0%) cases, but AIN and granulomas were not reported. MPGN was attributed to ATT in 1/5 cases which improved after holding rifampin and giving corticosteroids; however, MPGN was attributed to TB in all other cases (4/5, 80.0%). MPGN improved in all reported cases, 2 of which combined anti-tuberculous therapy with immunosuppression (Corticosteroids +/- mycophenolate mofetil).

Membranous nephropathy

Cases of membranous nephropathy presented with nephrotic syndrome (7/10, 70.0%), AKI (3/10, 30.0%) and hypertension (2/10, 20.0%) [7, 10, 14, 19, 55,56,57,58,59,60]. Renal pathology revealed AIN (6/10, 60.0%), and granulomas (3/10, 30.0%) but no crescents. Cases were attributed to TB (6/10), medication (2/10) or unclear (2/10). All cases with granulomas were attributed to TB. Anti-phospholipase-2-receptor (PLA2R) testing was reported in 2 cases, with one case being positive. In the case of anti-PLA2R positive membranous nephropathy, the GN was attributed to ATT, with full resolution of the nephrotic syndrome (5.3 g/day proteinuria) within 2 weeks of stopping Rifampin. Corticosteroids were used in three cases, and in 2 of these the GN was attributed to ATT. In all three cases, proteinuria improvement coincided with ATT, with uncertain impact of corticosteroid therapy.

Minimal change disease

Cases of minimal change disease typically presented with nephrotic syndrome (6/7, 85.7%), and AKI was common (4/7, 57.1%) [16, 61,62,63,64,65,66]. Hypertension was not reported in any case (0/7, 0.0%). Renal pathology revealed concurrent AIN in 3 cases (42.9%) but crescents and granulomas were not described. Minimal change disease was attributed to anti-tuberculous therapy in all cases, with rifampin or isoniazid identified as the culprit medication in all cases. Proteinuria improved in most cases by stopping the offending medication (6/7), and in two of three cases with corticosteroid use.

Mixed pathology

Three cases of mixed IgA/Membranous/MPGN pathology were identified, in which patients presented with AKI (3/3), hypertension (1/3), but without nephrotic syndrome (0/3) [67,68,69]. Renal pathology did not reveal AIN or granulomas. One case was attributed to rifampin, with resolution of GN within 1 month of stopping rifampin. In the other two cases, GN was attributed to TB, but renal outcomes with ATT were not noted in one case. Crescents were identified in one GN case attributed to TB; corticosteroids and cyclophosphamide were administered simultaneous with ATT with GN resolution later noted.

Discussion

This review explores the presentation, diagnosis, management and outcomes of glomerular disease in Mycobacterium tuberculosis infections. The reported case reports and case series make up 62 studies, representing 130 patients. These cases included a spectrum of presentations that included AKI, nephrotic syndrome or hypertension, a range of 10 unique renal pathologies, cases that used immunosuppression, and a variety of outcomes ranging from complete remission to long-term dialysis dependence. This study thus represents the most comprehensive study of glomerular disease in TB infections.

When caring for a patient with TB and GN, a clinician must consider the utility of performing a renal biopsy. Unfortunately, patient presentation with nephrotic syndrome, hypertension or AKI was not specific to any of the 10 renal pathologies. However, there were specific features on renal pathology that were highly predictive of whether the GN was attributed to TB infection or anti-tuberculous therapy. When identified, granulomas (4/4), anti-GBM disease (3/3), amyloidosis (75/76), and FSGS (2/2) were highly specific for the etiology of GN being from TB infection. On the other hand, every case of minimal change disease (7/7) was attributed to ATT.

When ATT is implicated as the precipitant of GN, a change in therapy should be considered. In addition, depending on the renal pathology, such as patients with crescentic pauci-immune GN (n = 12), the addition of immunosuppression may also be considered. While this study is underpowered to establish the efficacy of immunosuppression in patients with TB, it is generally agreed that immunosuppression in such instances should be considered [70]. There are significant risks of immunosuppression, especially in patients with active TB infection; exposure of patients to this risk should only be considered if renal biopsy features suggest possible benefit.

When a patient has GN attributed to TB infection, clinicians may continue to use the most effective ATT, and to minimize patient exposure to second line therapies that may have increased toxicity, cost, and monitoring [71]. On the other hand, only isoniazid or rifampin were implicated when GN was determined to be secondary to anti-TB medications. Since both of these medications are considered the backbone of TB treatment and commonly prescribed as part of the standard first-line treatment regimen for TB, a high threshold must be met before modifying standard ATT.

Given the volume of cases identified in this study, coincidental primary GN cannot be ruled out, despite the timing of presentation suggesting a link with TB infection or ATT. The serum Anti-PLA2R antibody was checked in three cases of membranous nephropathy. In the only case in which Anti-PLA2R antibody was positive [60], the GN was attributed to the ATT, and indeed resolved upon ATT completion. Cases of Anti-PLA2R antibody positive secondary membranous nephropathy are well described [72], and production of pathogenic autoantibodies is increased by TB infection by persistent stimulation of the antibody-mediated immune response [73]. Therefore, the clinical utility of Anti-PLA2R antibodies to differentiate between primary and secondary infections may be reduced in patients with active TB infection.

TB modifies humoral mediated immunity by several mechanisms, predisposing to immune complex deposition and glomerulonephritis. Patients with TB may produce IgA antibodies against A-60 mycobacterial antigen, which activates lectin and alternative complement pathways [37]. Similarly, hypersensitivity reactions to TB wall antigens lead to immune complex deposition in the perivascular, peritubular, vascular and glomerular spaces. This ultimately leads to vasculitis, with the renal pathology determined in part by the mycobacterial cell wall antigen initiating the cascade [74]. Chronic infections including TB cause chronic stimulation of innate and adaptive immune responses through Interferon and Th1-immune response [73].

Rifampin and isoniazid-induced GN in patients with TB may arise from a variety of mechanisms. First, anti-rifampin antibodies have been described in patients with crescentic GN, and it is postulated that antibody specificity relates to renal pathology [75]. Intermittent gaps, then re-initiation in ATT may be followed by an intense immune reaction [76]. Secondly, medication may have direct toxin effects on glomeruli [77]. Thirdly, both cell-mediated and humoral immune responses secondary to rifampin have been described [16, 61]. While isoniazid has been described to precipitate a systemic necrotizing vasculitis [78], whether autoantibodies to isoniazid or a direct toxin effect on glomeruli precipitates GN remains uncertain [63].

This study has several strengths and weaknesses. To date, this is the most comprehensive review of GN cases in patients with TB. However, most studies were published in high income countries with correspondingly low TB rates. Therefore, cases from high TB prevalence regions, and cases of drug-resistant TB, are underrepresented. Attribution of GN to ATT versus TB is based on clinical judgment, and thus may be inaccurate in some cases. There was likely to have been reporting bias, with published cases more likely reflecting treatment successes than failures. Case reports and case series are subject to information bias including recall bias, and thus may be less representative and associated with limited or incomplete qualitative data. However, this study explored the link between renal pathology features (crescents, granulomas, AIN) and clinical presentation and outcomes. This study has reported renal pathologic features that may predict whether GN is related to anti-TB therapy versus TB infection, which has important treatment implications for clinicians. Important trends and predictive factors were identified despite the study limitations.

Patient demographics collected included patient age and sex. Clinical presentation data included timing of GN from TB symptoms and diagnosis, GN presentation symptoms, quantification of proteinuria, and presence of nephrotic syndrome, hypertension, or AKI.

Renal biopsy data included the pathologic diagnosis, whether the renal biopsy contained acute interstitial nephritis (AIN), granulomas or crescents, and whether the GN was attributed to TB or medications.

The attribution of GN to either TB or anti-TB medications was deferred to the included studies’ determination. When included studies did not attribute the GN to either TB or anti-TB medications, this was also recorded.

Management data collected included whether immunosuppression was prescribed (with regimen and duration if used), and modifications in anti-TB medications. Outcomes of the TB and renal disease were also collected.

Ethics

This study is consistent with the principles outlined by the Committee on Publication Ethics. Health Sciences Research Ethics Board approval was not required, since all information used in this manuscript was already freely available in the public domain, and the dataset analyzed was properly anonymized with informed consent obtained at the time of original data collection.

Registration

This trial was not registered since PROSPERO does not permit registration of scoping reviews.

Data availability

Database of studies is summarized in Appendices 1 and 2. However, raw data is available on request to the corresponding author.

Abbreviations

AKI:

Acute kidney injury

AIN:

Acute interstitial nephritis

ANCA:

Anti-neutrophil cytoplasmic antibody

ATT:

Anti-tuberculous Therapy

eGFR:

Estimated glomerular filtration rate

FSGS:

Focal segmental glomerulosclerosis

GBM:

Glomerular basement membrane

GN:

Glomerulonephritis

HSP:

Henoch-Schonlein purpura

HIV:

Human Immunodeficiency Virus

LMIC:

Low or Middle Income Country

MPGN:

Membranoproliferative glomerulonephritis

PLA2R:

Phospholipase-A2 receptor

TB:

Tuberculosis

References

  1. Global Tuberculosis report. World Health Organization. 2023. pp. 1–39.

  2. Organization WH. Tuberculosis. Newsroom fact sheets. World Health Organization; 2023.

  3. Chapagain A, Dobbie H, Sheaff M, Yaqoob MM. Presentation, diagnosis, and treatment outcome of tuberculous-mediated tubulointerstitial nephritis. Kidney Int. 2011;79(6):671–77.

    Article  CAS  PubMed  Google Scholar 

  4. Oxley Oxland J, Ensor J, Freercks R. Tuberculosis and pauci-immune crescentic glomerulonephritis. BMJ Case Rep. 2018;2018.

  5. Griffin SOB, McLaughlin B, Keane AM. J. ANCA associated glomerulonephritis in tuberculosis: a paradoxical reaction. BMJ Case Rep. 2021;14(6).

  6. Kitamura H, Shimizu K, Takeda H, Tai H, Ito Y, Fukunaga M. A case of henoch-schonlein purpura nephritis in pulmonary tuberculosis. Am J Med Sci. 2007;333(2):117–21.

    Article  PubMed  Google Scholar 

  7. Yuan Q, Sun L, Feng J, Liu N, Jiang Y, Ma J, et al. Lumbar tuberculosis associated with membranous nephropathy and interstitial nephritis. J Clin Microbiol. 2010;48(6):2303–6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Samuel G, Storey D, Singh D, Zhou XJ. Membranoproliferative glomerulonephritis secondary to disseminated tuberculosis after Withdrawal of Adalimumab. Am J Respir Crit Care Med. 2017;195.

  9. Iijima Y, Kobayashi Y, Uchida Y, Tsutsui T, Kakizaki Y, Naganuma T, et al. A case report of granulomatous polyangiitis complicated by tuberculous lymphadenitis. Med (Baltim). 2018;97(43):e12430.

    Article  Google Scholar 

  10. Morimoto N, Nagahama K, Tsuura Y, Terai A, Tanabe M, Otani M, et al. Membranous nephropathy in a patient with pulmonary tuberculosis infection and lung adenocarcinoma: a case report. CEN Case Rep. 2022;11(1):126–33.

    Article  PubMed  Google Scholar 

  11. Rodrigues CE, Sette LH, Torritani J, Malheiros DM, Titan SM, Barros RT, et al. Tuberculosis-associated collapsing glomerulopathy: remission after treatment. Ren Fail. 2010;32(1):143–6.

    Article  PubMed  Google Scholar 

  12. Bowman SJ. Pulmonary tuberculosis precipitating the nephrotic syndrome in a patient with sickle cell disease. Nephron. 1991;57(2):236.

    Article  CAS  PubMed  Google Scholar 

  13. Cohen AJ, Rosenstein ED. IgA nephropathy associated with disseminated tuberculosis. Arch Intern Med. 1985;145(3):554–6.

    Article  CAS  PubMed  Google Scholar 

  14. Rodriguez-Garcia JL, Fraile G, Mampaso F, Teruel JL. Pulmonary tuberculosis associated with membranous nephropathy. Nephron. 1990;55(2):218–9.

    Article  CAS  PubMed  Google Scholar 

  15. Rhodes KM. Amyloidosis in Vanuatu. Trans R Soc Trop Med Hyg. 1987;81(2):297–8.

    Article  CAS  PubMed  Google Scholar 

  16. Tada T, Ohara A, Nagai Y, Otani M, Ger YC, Kawamura S. A case report of nephrotic syndrome associated with rifampicin therapy. Nihon Jinzo Gakkai Shi. 1995;37(2):145–50.

    CAS  PubMed  Google Scholar 

  17. Peters M, Godfrey C, McInerney P, Munn Z, Tricco A, Khalil H. Chapter 11: scoping review. In: Aromataris E, editor Manual for evidence synthesis. JBI.

  18. World Bank Country and Lending Groups. In. Bank TW, editor Working for a World Free of Poverty2023.

  19. Pal M, Sengupta M, Basu K, Roychowdhury A. Membranous nephropathy associated with Tuberculosis- a case report. Asian Pac J Trop Med. 2022;15(4):183–85.

    Article  Google Scholar 

  20. Dixit R, Gupta R, Dave L, Prasad N, Sharma S. Clinical profile of patients having pulmonary tuberculosis and renal amyloidosis. Lung India. 2009;26(2):41–5.

    Article  PubMed  PubMed Central  Google Scholar 

  21. Engineer DP, Kute VB, Patel HV, Shah PR. Clinical and laboratory profile of renal amyloidosis: a single-center experience. Saudi J Kidney Dis Transpl. 2018 Sep-Oct;29(5):1065–72.

  22. El-Hennawy AS, Goldstein M, Nicastri A. Renal amyloidosis secondary to tuberculosis of cecum. Nephron. 2002;92(3):708–10.

    Article  CAS  PubMed  Google Scholar 

  23. Magro-Checa C, Casado ANP, Borrego-Garcia E, Raya-Alvarez E, Rosales-Alexander JL, Salvatierra J, et al. Successful use of Tocilzumab in a patient with nephritic syndrome due to a rapidly progressing AA amlyoidosis secondary to latent tuberculosis. Amyloid- J Protein Fold Disorders. 2011;18:235–39.

    Article  CAS  Google Scholar 

  24. Monsel G, Martinez V, Izzedine H, Mory B, Bricaire F, Caumes E. Anal tuberculosis complicated by secondary amyloidosis. Med Mal Infect. 2011;41(5):264–6.

    Article  CAS  PubMed  Google Scholar 

  25. Mandal SK, Sil K, Ganguly J, Chatterjee K, Chatterjee S, Mandal SS. Two cases of nephrotic syndrome with different etiologies. Annals Trop Med Public Health. 2013;6(1):105–08.

    Article  Google Scholar 

  26. Akram A. Tuberculosis-Induced Bronchiectasis complicated by recurrent respiratory tract infections and renal amyloidosis: a Classic Revisited. Cureus. 2020;12(11):e11638.

    PubMed  PubMed Central  Google Scholar 

  27. Chugh KS, Datta BN, Singhal PC, Jain SK, Sakhuja V, Dash SC. Pattern of renal amyloidosis in Indian patients. Postgrad Med J. 1981;57(663):31–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Mehta HJ, Talwalkar NC, Merchant MR, Mittal BV, Suratkal LH, Almeida AF, et al. Pattern of renal amyloidosis in western India. A study of 104 cases. J Assoc Physicians India. 1990;38(6):407–10.

    CAS  PubMed  Google Scholar 

  29. Shah VB, Phatak AM, Shah BS, Kandalkar BM, Haldankar AR, Ranganathan S. Renal amyloidosis–a clinicopathologic study. Indian J Pathol Microbiol. 1996;39(3):179–85.

    CAS  PubMed  Google Scholar 

  30. Hsieh YP, Wen YK. Anti-glomerular basement membrane glomerulonephritis with subsequent pulmonary hemorrhage in the course of pulmonary tuberculosis. Ren Fail. 2012;34(9):1177–80.

    Article  CAS  PubMed  Google Scholar 

  31. Kashif W, Yaqub S, Mahmood SF, Patel J. Double-positive goodpasture’s syndrome with concomitant active pulmonary tuberculosis. Saudi J Kidney Dis Transpl. 2013;24(4):783–8.

    Article  PubMed  Google Scholar 

  32. Wen YK, Wen KI. Pulmonary hemorrhage complicating Goodpasture’s disease in the course of pulmonary tuberculosis. Int Urol Nephrol. 2013;45(6):1773–7.

    Article  PubMed  Google Scholar 

  33. Murray AN, Cassidy MJ, Templecamp C. Rapidly progressive glomerulonephritis associated with rifampicin therapy for pulmonary tuberculosis. Nephron. 1987;46(4):373–6.

    Article  CAS  PubMed  Google Scholar 

  34. O’Brien AA, Kelly P, Gaffney EF, Clancy L, Keogh JA. Immune complex glomerulonephritis secondary to tuberculosis. Ir J Med Sci. 1990;159(6):187.

    Article  PubMed  Google Scholar 

  35. Muthukumar T, Jayakumar M, Fernando EM, Muthusethupathi MA. Acute renal failure due to rifampicin: a study of 25 patients. Am J Kidney Dis. 2002;40(4):690–6.

    Article  CAS  PubMed  Google Scholar 

  36. Yoshioka K, Satake N, Kasamatsu Y, Nakamura Y, Shikata N. Rapidly progressive glomerulonephritis due to rifampicin therapy. Nephron. 2002;90(1):116–8.

    Article  PubMed  Google Scholar 

  37. Solak Y, Gaipov A, Anil M, Atalay H, Ozbek O, Turkmen K, et al. Glomerulonephritis associated with tuberculosis: a case report and literature review. Kaohsiung J Med Sci. 2013;29(6):337–42.

    Article  PubMed  Google Scholar 

  38. Kanodia KV, Vanikar AV, Patel RD, Suthar KS, Trivedi HL. Crescentic Glomerulonephritis Associated with Pulmonary Tuberculosis. J Clin Diagn Res. 2016;10(1):ED01–2.

    CAS  PubMed  PubMed Central  Google Scholar 

  39. Rostami Z, Cegolon L, Jafari NJ, Gholami N, Mousavi SV, Allahyari F, et al. A rare case of coexistence of Wegener’s granulomatosis and pulmonary tuberculosis with subsequent development of thrombosis of the cerebral veins. BMC Infect Dis. 2021;21(1):948.

    Article  PubMed  PubMed Central  Google Scholar 

  40. Srinivasaprasad ND, Chandramohan G, Praveen V, Fernando ME. Collapsing glomerulopathy associated with pulmonary tuberculosis. Indian J Nephrol. 2016;26(5):373–75.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Shribman JH, Eastwood JB, Uff J. Immune complex nephritis complicating miliary tuberculosis. Br Med J (Clin Res Ed). 1983;287(6405):1593–4.

    Article  CAS  PubMed  Google Scholar 

  42. Han BG, Choi SO, Shin SJ, Kim HY, Jung SH, Lee KH. A case of Henoch-Schonlein purpura in disseminated tuberculosis. Korean J Intern Med. 1995;10(1):54–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. De Siati L, Paroli M, Ferri C, Muda AO, Bruno G, Barnaba V. Immunoglobulin a nephropathy complicating pulmonary tuberculosis. Ann Diagn Pathol. 1999;3(5):300–3.

    Article  PubMed  Google Scholar 

  44. Matsuzawa N, Nakabayashi K, Nagasawa T, Nakamoto Y. Nephrotic IgA nephropathy associated with disseminated tuberculosis. Clin Nephrol. 2002;57(1):63–8.

    Article  CAS  PubMed  Google Scholar 

  45. Keven K, Ulger FA, Oztas E, Ergun I, Ekmekci Y, Ensari A, et al. A case of pulmonary tuberculosis associated with IgA nephropathy. Int J Tuberc Lung Dis. 2004;8(10):1274–5.

    CAS  PubMed  Google Scholar 

  46. Singh P, Khaira A, Sharma A, Dinda AK, Tiwari SC. IgA nephropathy associated with pleuropulmonary tuberculosis. Singap Med J. 2009;50(7):e268–9.

    CAS  Google Scholar 

  47. Bueno Filho R, Cordeiro AP, Almeida FT, Shaletich C, Costa RS, Roselino AM. Rare association of cutaneous vasculitis, IgA nephropathy and antiphospholipid antibody syndrome with tuberculous lymphadenitis. Clin (Sao Paulo). 2012;67(12):1497–500.

    Article  Google Scholar 

  48. Pradeep I, Anupama SH, Koshy P, Kurien A, Rohit A, Mathew M, et al. A rare association of Mycobacterium tuberculosis infection of kidney and urinary tract with immunoglobulin A nephropathy. Indian J Med Microbiol. 2019 Oct-Dec;37(4):587–89.

  49. Audley G, Davidson B, Jones E, Price B, Rayner B, Wearne N, et al. Disseminated Mycobacterium Tuberculosis and IgA Nephropathy. Case Rep Nephrol. 2022;2022:3785713.

    PubMed  PubMed Central  Google Scholar 

  50. Gupta A, Khaira A. Immunotactoid glomerulopathy and tuberculosis: a novel association. Nefrologia. 2011;31(3):369–71.

    CAS  PubMed  Google Scholar 

  51. Meyrier A, Valensi P, Sebaoun J. Mesangio-capillary glomerulonephritis and the nephrotic syndrome in the course of disseminated tuberculosis. Nephron. 1988;49(4):341–2.

    Article  CAS  PubMed  Google Scholar 

  52. Kistler A, Lappin DW, Coward RA. Therapeutic dilemma: crescentic mesangiocapillary glomerulonephritis type 1 in a patient on antituberculous therapy with rifampicin. Nephrol Dial Transpl. 1999;14(1):243–4.

    Article  CAS  Google Scholar 

  53. Ram R, Sandeep P, Sridhar AV, Rukumangadha N, Sivakumar V. Membranoproliferative glomerulonephritis and Pott’s disease. Clin Kidney J. 2014;7(4):391–3.

    Article  PubMed  PubMed Central  Google Scholar 

  54. Helvaci O, Erten Y, Gonul I, Ozet A, Hazneda R. Tuberculosis presenting as proliferative glomerulonephritis with monoclonal immunoglobulin deposits. Revista De Nefrologia Dialisis y Transplante. 2021;41(3):202–06.

    Google Scholar 

  55. Gabow PA, Lacher JW, Neff TA. Tubulointerstitial and glomerular nephritis associated with rifampin. Report of a case. JAMA. 1976;235(23k0):2517–8.

    Article  CAS  PubMed  Google Scholar 

  56. Suzuki Y, Hasegawa H, Ushiyama E, Inomata A, Satoh H, Ogino S, et al. [A case of nephrotic syndrome with membranous nephropathy and renal tuberculous granuloma]. Nihon Naika Gakkai Zasshi. 1989;78(8):1181–6.

    Article  CAS  PubMed  Google Scholar 

  57. Ghosh B, Pande A, Ghosh A, Banerjee A, Saha S. Membranous glomerulonephritis and tuberculous peritonitis: a rare association. J Infect Dev Ctries. 2011;5(7):550–2.

    Article  PubMed  Google Scholar 

  58. Ram R, Swarnalatha G, Desai M, Rakesh Y, Uppin M, Prayaga A, et al. Membranous nephropathy and granulomatous interstitial nephritis due to tuberculosis. Clin Nephrol. 2011;76(6):487–91.

    Article  CAS  PubMed  Google Scholar 

  59. Malhotra KP, Chandra A, Rao N, Shukla S, Gupta A. Tuberculosis as a microbiologically proven etiology of membranous nephropathy and interstitial nephritis. Saudi J Kidney Dis Transpl. 2019 Nov-Dec;30(6):1447–49.

  60. Balwani MR, Pasari AS, Bhawane A, Tolani P. Anti-phospholipase A2 Receptor Antibody-Positive Membranous Glomerulopathy due to Anti-Koch’s Therapy in a Tuberculosis Patient. Saudi J Kidney Dis Transpl. 2021 Nov-Dec;32(6):1800–03.

  61. Neugarten J, Gallo GR, Baldwin DS. Rifampin-induced nephrotic syndrome and acute interstitial nephritis. Am J Nephrol. 1983 Jan-Feb;3(1):38–42.

  62. Barnes N, Bellamy D, Ireland R, Parsons V, Costello J. Pulmonary tuberculosis complicated by haemophagocytic syndrome and rifampicin-induced tubulointerstitial nephritis. Br J Dis Chest. 1984;78(4):395–403.

    Article  CAS  PubMed  Google Scholar 

  63. Mori S, Matsushita Y, Arizono K. Minimal-change nephrotic syndrome associated with isoniazid in anti-tuberculosis chemoprophylaxis for a patient with rheumatoid arthritis. Intern Med. 2011;50(3):253–7.

    Article  PubMed  Google Scholar 

  64. Park DH, Lee SA, Jeong HJ, Yoo TH, Kang SW, Oh HJ. Rifampicin-induced minimal change disease is improved after cessation of rifampicin without steroid therapy. Yonsei Med J. 2015;56(2):582–5.

    Article  PubMed  PubMed Central  Google Scholar 

  65. Kim JS, Kim KJ, Choi EY. Minimal change disease related to rifampicin presenting with acute renal failure during treatment for latent tuberculosis infection: a case report. Med (Baltim). 2018;97(22):e10556.

    Article  Google Scholar 

  66. Sathi S, Garg AK, Singh MK, Saini VS, Vohra D. Rifampicin-Associated secondary minimal change Disease presenting with nephrotic syndrome in a pulmonary tuberculosis patient. Case Rep Nephrol. 2021;2021:5546942.

    PubMed  PubMed Central  Google Scholar 

  67. Sopena B, Sobrado J, Javier Perez A, Oliver J, Courel M, Palomares L, et al. Rapidly progressive glomerulonephritis and pulmonary tuberculosis. Nephron. 1991;57(2):251–2.

    Article  CAS  PubMed  Google Scholar 

  68. Isotalo PA, Ford JC, Veinot JP. Diffuse glomerulonephritis associated with rifampin treatment for tuberculosis. Pathology. 2002;34(3):295–97.

    Google Scholar 

  69. Yong JL, Killingsworth MC. Diffuse glomerulonephritis associated with rifampicin treatment for tuberculosis. Pathology. 2002;34(3):295–7.

    Article  PubMed  Google Scholar 

  70. Asim M, Akhtar M. Epidemiology, impact, and management strategies of anti-glomerular basement membrane disease. Int J Nephrol Renovasc Dis. 2022;15:129–38.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  71. Nyang’wa BT, Berry C, Kazounis E, Motta I, Parpieva N, Tigay Z, et al. A 24-Week, all-oral regimen for Rifampin-resistant tuberculosis. N Engl J Med. 2022;387(25):2331–43.

    Article  PubMed  Google Scholar 

  72. Dai H, Zhang H, He Y. Diagnostic accuracy of PLA2R autoantibodies and glomerular staining for the differentiation of idiopathic and secondary membranous nephropathy: an updated meta-analysis. Sci Rep. 2015;5:8803.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Smith KD, Alpers CE. Pathogenic mechanisms in membranoproliferative glomerulonephritis. Curr Opin Nephrol Hypertens. 2005;14(4):396–403.

    Article  CAS  PubMed  Google Scholar 

  74. Perez-Noriega FA, Salinas-Lara C, Sanchez-Garibay C, Torres-Ruiz JJ, Maravillas-Montero JL, Castanon-Arreola M et al. Mycobacterium tuberculosis Cell Wall Antigens induce the formation of Immune complexes and the development of Vasculitis in an experimental murine model. Int J Mol Sci. 2023;24(2).

  75. Ogata H, Kubo M, Tamaki K, Hirakata H, Okuda S, Fujishima M. Crescentic glomerulonephritis due to rifampin treatment in a patient with pulmonary atypical mycobacteriosis. Nephron. 1998;78(3):319–22.

    Article  CAS  PubMed  Google Scholar 

  76. Bassi L, Pernal G, Silvestri L. Antibodies against rifampicin in patients with tuberculosis after discontinuation of daily treatment. Am Rev Respir Dis. 1976;114:1189–90.

    Google Scholar 

  77. Glassock RJ. Secondary minimal change disease. Nephrol Dial Transpl. 2003;18(Suppl 6):vi52–8.

    Google Scholar 

  78. Tan CD, Smith A, Rodriguez ER. Systemic necrotizing vasculitis induced by isoniazid. Cardiovasc Pathol 2014 May-Jun;23(3):181–2.

Download references

Acknowledgements

None.

Funding

None.

Author information

Authors and Affiliations

  1. Division of Nephrology, Department of Medicine, Western University, London, ON, Canada

    Adam Forster

  2. Division of Pulmonary Medicine, St. Michael’s Hospital and West Park Healthcare Centre, University of Toronto, Toronto, ON, Canada

    Natasha Sabur

  3. Division of Nephrology, Department of Medicine, McMaster University, Hamilton, ON, Canada

    Ali Iqbal

  4. Division of Infectious Diseases, University of Calgary, Calgary, AB, Canada

    Stephen Vaughan

  5. Bloomberg School of Public Health, Johns Hopkins University, Baltimore Maryland, USA

    Benjamin Thomson

Authors
  1. Adam Forster
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Natasha Sabur
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Ali Iqbal
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Stephen Vaughan
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Benjamin Thomson
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

All authors provided critical input to each draft of the manuscript, including the final manuscript that has been submitted. AF and BT designed the study and completed the scoping review. The design of the study had input from NS, SV and AI.

Corresponding author

Correspondence to Benjamin Thomson.

Ethics declarations

Ethical approval

Health Sciences Research Ethics Board approval was not required, since all information used in this manuscript was already freely available in the public domain, and the dataset analyzed was properly anonymized with informed consent obtained at the time of original data collection.

Consent for publication

Not applicable.

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.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary Material 1

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/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Forster, A., Sabur, N., Iqbal, A. et al. Glomerulonephritis during Mycobacterium tuberculosis infection: scoping review. BMC Nephrol 25, 285 (2024). https://doi.org/10.1186/s12882-024-03716-6

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12882-024-03716-6

Keywords

BMC Nephrology

ISSN: 1471-2369

Contact us