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Nocardiosis in glomerular disease patients with immunosuppressive therapy



Glomerular disease patients have a high risk of infection, which contributes to the progression of disease per se and mortality, especially in those with long-term use of glucocorticoids and (or) immunosuppressive agents. Cases of sporadic nocardiosis have been reported in glomerular disease patients, and this observation was conducted to comprehensively understand the manifestations of and treatments for nocardiosis, which is commonly misdiagnosed as pneumonia or tuberculosis or even as lung cancer or metastatic tumors in glomerular disease patients.


We reviewed the demographic characteristics, laboratory abnormalities, radiological features, and treatments of 7 patients with nocardiosis and glomerular disease receiving steroids and immunosuppression therapy at the nephrology department of the Second Xiangya Hospital between 2012 and 2019.


It was found that all 7 patients had been receiving methylprednisolone for renal disease at a median dose of 20 mg per day and a median duration of 4 months before developing nocardiosis. There were 4 males and 3 females, and the median age was 52.14 years. All 7 patients had hypoalbuminemia at the time of admission. In addition, various cystic abscesses in the subcutaneous tissue, with or without lung and brain involvement, were observed in these patients. Encouragingly, body temperatures returned to normal, and subcutaneous abscesses diminished or disappeared with compound sulfamethoxazole treatment alone or in combination with linezolid, imipenem and mezlocillin/sulbactam.


It was shown that multisite abscesses, including subcutaneous, pulmonary and cerebral abscesses, were the common manifestations of nocardiosis in glomerular disease patients. Sulfonamide was the first-line antibiotic therapy for nocardiosis, and combinations of other antibiotics were also needed in some serious cases.

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Glomerular diseases are still common causes of end-stage renal disease (ESRD), a global health epidemic affecting more than 2 million people worldwide [1,2,3,4]. Many glomerular diseases are immunologically mediated disorders [1, 5,6,7,8], and immunosuppressive medications put glomerular disease patients at a high risk of various infections, such as pneumonia, Mycobacterium tuberculosis and hepatitis B virus reactivation, which contribute to the progression of disease per se and mortality [9,10,11,12,13,14]. In recent years, accumulating data have shown an increased rate of opportunistic infections in glomerular disease patients with long-term use of glucocorticoids and (or) immunosuppressive agents, especially in nephrotic syndrome, IgA nephropathy, lupus nephritis and vasculitis patients [14,15,16,17,18,19,20].

Nocardia spp. are gram-positive bacteria belonging to aerobic actinomycetes, which are ubiquitous in soil [21]. Nocardia are rare in healthy individuals but are isolated with increasing frequency from the clinical materials of immunocompromised patients, which can cause a disseminated infection and eventually lead to life-threatening outcomes [22,23,24]. Recently, Nocardia infection, also called nocardiosis, received increasing attention from clinical nephrologists. Sporadic case reports have shown that nocardiosis manifests as fever and various tissue nodules, mainly pulmonary and subcutaneous lesions [25]. Serious cases of nocardiosis can lead to disseminated infections and even the emergence of brain abscesses [26,27,28,29]. Unfortunately, nocardiosis is quite complex and rare, and it is difficult to differentiate it from other fever-related diseases, lung cancers and metastatic tumors [29,30,31]. Misdiagnosis and delayed treatment of nocardiosis are common in glomerular disease patients, which has brought a challenge for the comprehensive understanding of nocardiosis.

The value of clinical guidance from previous sporadic cases may be limited by the small number of patients; thus, we reviewed 7 glomerular disease patients with nocardiosis who received steroids and (or) immunosuppressive agents. We focused on the typical manifestations, antibiotic selection, changes in inflammatory biomarker levels and imaging of nocardiosis after treatment.


This observation was conducted to review the clinical records of 7 glomerular disease patients affected by nocardiosis at the nephrology department of the Second Xiangya Hospital of Central South University (a tertiary hospital with 3500 beds) between 2012 and 2019. The data are from the department depository, and 9292 glomerular disease patients were followed during this period. The involvement of 2 noncontiguous organs is defined as disseminated nocardiosis. The inclusion criteria were as follows: glomerular disease patients with immunosuppressive therapy; cough or expectoration, unexplained renal deterioration, and subcutaneous, pulmonary or cerebral abscess suggesting nocardiosis; and confirmed nocardiosis through a positive Nocardia culture, acquired from the puncturing of abscesses.

We collected demographic characteristics, including sex and age, as well as renal diseases, laboratory abnormalities, radiological features, and treatments in 7 culture-proven cases. To analyze the therapeutic effect, we analyzed inflammatory biomarkers (N%, percentage of neutrophils; CRP, C- reactive protein; PCT, procalcitonin) and indicators of renal function before and after treatment. For biochemical data, serum albumin was detected by bromocresol green colorimetry, and serum creatinine was measured by the sarcosine oxidase method. For imaging evaluation, B-mode ultrasonography, computed tomography (CT) and magnetic resonance imaging (MRI) were used. For microbiological tests, gram staining and modified acid-fast staining were used for direct bacterioscopy; the streak plate method was used for Nocardia isolation; and blood-containing medium and Lowenstein-Jensen medium were used for culture. Considering the risk factors and antibiotic selections for nocardiosis, we were particularly concerned with the categories, doses, and courses of immunosuppressive agents and antibiotics, respectively.

All statistical analyses were completed using SPSS 20.0, IBM, Chicago, IL, USA. Continuous variables were expressed as the means with standard deviations (SDs), while discrete variables were expressed as the medians with interquartile ranges (IQRs). Paired t-tests were used to compare the inflammatory biomarker levels of patients before and after antibiotic treatment.


Basic characteristics of patients infected with Nocardia

Seven glomerular disease patients suffering from nocardiosis were enrolled: 5 had nephrotic syndrome (71.4%), 1 had lupus nephritis, and 1 had IgA nephropathy. Renal histology showed that 3 of 7 patients had membranous nephropathy. The median time between kidney disease diagnosis and nocardiosis was 6 months (IQR, 6–10.5 months). There were 4 males and 3 females, and the median age was 52.14 years (IQR, 50–61 years). Four patients had concomitant diabetes, including 3 glucocorticoid-dependent patients. One patient was even diagnosed with pneumonia 2 months prior, and the other patients had no history of respiratory system diseases (Table 1).

Table 1 The basic characteristics of 7 patients affected by Nocardia

Immunosuppressive treatment before and after Nocardia infection

All 7 patients had been receiving methylprednisolone for renal disease at a median dosage of 20 mg (IQR, 16–32 mg) per day and a median duration of 4 months (IQR, 4–6 months) before developing nocardiosis. Furthermore, 3 patients had been taking a combination of methylprednisolone and an immunosuppressor, including 2 with tacrolimus (n = 2) and 1 with cyclophosphamide (Table 1). Six patients developed nocardiosis within 4 months after the initiation of immunosuppressive treatment. The baseline lymphocyte count in 4 patients decreased (Table 1). After Nocardia infection, 3 patients, including the two with disseminated nocardiosis, decreased the dose of immunosuppressive treatment; 1 patient stopped immunosuppressive treatment; and 3 patients did not receive modifications.

Renal and extrarenal manifestations

Before nocardiosis, all 7 patients had already presented with hypoalbuminemia; 6 patients had proteinuria; 4 patients had hematuria; 3 patients exhibited a decreased eGFR; and only 2 patients achieved nephrotic syndrome remission after immunosuppressive treatment, with the disappearance of edema (Table 1). After nocardiosis, all 7 patients exhibited hypoalbuminemia and elevated 24-h urinary protein concentrations at the time of admission, 2 patients exhibited increased serum creatinine, and 1 patient had acute kidney injury (AKI) with a serum creatinine level of 267.5 μmol/L (Table 2). In addition, only 3 patients had fever. Six patients showed respiratory system involvement: 4 with cough, 3 with expectoration, 2 with pleural effusion, 1 with chest distress and 1 with dyspnea (Table 3). Notably, B-mode ultrasonography showed various cystic abscesses in the subcutaneous tissue in all 7 patients, which was accompanied with or without lung and brain involvement on CT or MRI (Fig. 1). All patients underwent head MRI, and 2 patients showed brain abscesses; both of them had no central nervous system symptoms. One patient taking 40 mg qd methylprednisolone for 4 months and the other patient taking a combination of methylprednisolone and tacrolimus presented with serious disseminated disease, characterized by multisite nodules, including subcutaneous nodules, concomitant with pulmonary or cerebral abscess. And abscess was the source of bacteriological diagnosis.

Table 2 Comparison of partial inflammatory biomarkers of 7 patients before and after antibiotic treatment
Table 3 The clinical manifestations of 7 patients affected by Nocardia
Fig. 1

Lung CT and head MRI images of No.7 patient

Response to the treatment of antibacterial therapy

All 7 patients accepted antibiotic treatment once they were diagnosed. One patient received a single regimen with compound sulfamethoxazole, and 5 patients were treated with a double-regimen antibiotic treatment in which compound sulfamethoxazole was prescribed with a combination of linezolid, imipenem and mezlocillin/sulbactam for 2 patients, 2 patients and 1 patient, respectively (Table 4). Meanwhile, 1 serious disseminated Nocardiosis patient was performed intracranial medication as well as subcutaneous abscess puncture drainage and three kinds of antibiotics; and other 6 patients did not undergo abscess puncture drainage. Encouragingly, after antibiotic treatment and abscess drainage, abscess diminished or disappeared ranging from 3 days to 80 days. By CT and MRI, it was shown that pulmonary and cerebral abscess also diminished as well. Moreover, inflammatory biomarkers, including neutrophilia count, CRP and PCT significantly declined (p<0.05) compared to that of before treatment; proteinuria excretion slightly ameliorated (Table 2). When abscess disappeared and inflammatory indicators improved, antibiotic treatment was stopped. The duration of antibiotic treatment and follow-up for these patients ranging from 3 months to 6 months (Table 5).

Table 4 The category and course of antibiotics treatment in 7 patients
Table 5 The time interval of mass begins reducing after antibiotics treatment and length of follow-up among 7 patients


Nocardiosis is an uncommon infection and is constantly neglected in the clinic in glomerular disease patients. Eleven sporadic glomerular disease cases with nocardiosis have ever been reported in the literature. All these eleven patients accepted immunosuppressive agents for kidney disease; pulmonary infection was the most common; 45% of patients accepted trimethoprim-sulfamethoxazole treatment; and only two patients died [31,32,33,34]. Here, we comprehensively reviewed the manifestations of and treatments for nocardiosis in 7 glomerular disease patients who received glucocorticoids alone or combined with immunosuppressive agents. It was delineated that in addition to fever, subcutaneous and pulmonary nodules were major extrarenal manifestations, while renal involvement was nonspecific. Serious nocardiosis cases manifested as dissemination of multisite subcutaneous abscesses concomitant with pulmonary or cerebral abscesses. Compound sulfamethoxazole was effective for nocardiosis in glomerular disease patients and even for disseminated nocardiosis, which was characterized by diminished subcutaneous and pulmonary abscesses as a therapeutic response.

It has been suggested that nocardiosis mainly occurs in patients suffering from autoimmune diseases, chronic renal disease, hematological diseases and HIV infection, especially in those who receive glucocorticoids or other immunosuppressive treatments [29, 35,36,37,38]. Here, we observed that all 7 patients with nocardiosis had been receiving glucocorticoids alone or combined with immunosuppressive agents, which is consistent with the previous literature. The diagnosis of nocardiosis mainly includes gram stains, microbial cultures and gene sequencing of pus or serum [39, 40]. The 7 cases of nocardiosis in our center were confirmed through abscess puncture and pus microbial culture. In addition, supplementary examinations showed elevated levels of inflammatory biomarkers, and subcutaneous, pulmonary and cerebral abscesses were detected by CT/MRI.

It has been found that approximately 80% of nocardiosis patients have hypoimmunity through CD4 + Th/Ts counting detection, and glucocorticoids are the crucial risk factor for nocardiosis development [41]. We observed that the median dosage of methylprednisolone was 20 mg per day, and the median use time was 4 months before nocardiosis diagnosis. Six patients received methylprednisolone for or more than 4 months, and 4 patients had low lymphocyte counts, which revealed that long-term steroid treatment might increase the risk of Nocardia infection.

The clinical manifestations are very complicated and difficult to distinguish promptly in the clinic. Hematuria, proteinuria, serum albumin levels and serum creatinine levels did not show significant differences before or after nocardiosis, which indicates that the inflammation associated with nocardiosis did not worsen the glomerular disease in our 7 patients. It was observed that extrarenal presentations included fever, cough, and multisite abscesses. Only 3 out of 7 patients had fever, so fever is not always present in nocardiosis patients. Multisite abscesses includes subcutaneous, pulmonary and cerebral abscesses [42, 43], which are commonly misdiagnosed as pneumonia or tuberculosis or even as lung cancer or metastatic tumors. Considering that direct extrinsic contact and inhalation are the main routes of Nocardia infection, subcutaneous and lung tissues are the most frequently affected sites of nocardiosis [44, 45]. Here, it was observed that all 7 nocardiosis patients presented with subcutaneous abscesses, and 4 of them presented with concomitant pulmonary abscesses, suggesting that subcutaneous and pulmonary abscesses are important signs of nocardiosis in glomerular disease patients who receive glucocorticoids alone or combined with immunosuppressive therapy. In addition, disseminated nocardiosis is delineated to spread to the brain with or without central nervous system (CNS) manifestations [24]. We also found that 2 nocardiosis patients with cerebral abscesses exhibited no CNS symptoms, indicating that CT/MRI is indispensable for nocardiosis patients, especially in patients with disseminated nocardiosis.

Nocardia spp. are susceptible to various antibiotics, including sulfonamide, linezolid, imipenem and amikacin. Among these, sulfonamide is recommended as the optimal therapy [46,47,48]. In addition, 94.6% of Nocardia isolates are susceptible to trimethoprim-sulfamethoxazole [49]. Therefore, the 7 nocardiosis patients in our center were treated with sulfonamide alone or in combination with other antibiotics for 3 months to 6 months, and no relapse was found during the follow-up. Moreover, previous literature has suggested that long-term antibiotic treatment for more than 3 months, even 6–12 months, might be beneficial for low nocardiosis relapse rates [50, 51]. Thus, the appropriate duration of sulfonamide for nocardiosis in glomerular disease needs to be further clarified. In our center, cerebral abscesses in 2 disseminated nocardiosis patients obviously decreased in size after combination treatment with sulfonamide and linezolid or imipenem. For some nocardiosis patients with cerebral abscesses, surgery is necessary in addition to antibiotic therapy [52].


In summary, multisite abscesses, including subcutaneous, pulmonary and cerebral abscesses, with or without fever, are the common manifestations of nocardiosis in glomerular disease patients with glucocorticoid and immunosuppressive therapy. Sulfonamide was the first-line antibiotic treatment for nocardiosis, and combinations of other antibiotics are also needed in some serious cases.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.



End-stage renal disease


C-reactive protein




Computed tomography


Magnetic resonance imaging


Estimated glomerular filtration rate


Acute kidney injury


Human immunodeficiency virus


Central nervous system


  1. 1.

    Floege J, Barbour SJ, Cattran DC, Hogan JJ, Nachman PH, Tang SCW, Wetzels JFM, Cheung M, Wheeler DC, Winkelmayer WC, et al. Management and treatment of glomerular diseases (part 1): conclusions from a kidney disease: improving global outcomes (KDIGO) controversies conference. Kidney Int. 2019;95(2):268–80.

    Article  Google Scholar 

  2. 2.

    O'Shaughnessy MM, Hogan SL, Poulton CJ, Falk RJ, Singh HK, Nickeleit V, Jennette JC. Temporal and demographic trends in glomerular disease epidemiology in the southeastern United States, 1986-2015. Clin J Am Soc Nephrol. 2017;12(4):614–23.

    PubMed  PubMed Central  Article  Google Scholar 

  3. 3.

    Robinson BM, Akizawa T, Jager KJ, Kerr PG, Saran R, Pisoni RL. Factors affecting outcomes in patients reaching end-stage kidney disease worldwide: differences in access to renal replacement therapy, modality use, and haemodialysis practices. Lancet. 2016;388(10041):294–306.

    PubMed  PubMed Central  Article  Google Scholar 

  4. 4.

    Chen TK, Knicely DH, Grams ME. Chronic kidney disease diagnosis and management: a review. Jama. 2019;322(13):1294–304.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  5. 5.

    Natale P, Palmer SC, Ruospo M, Saglimbene VM, Craig JC, Vecchio M, Samuels JA, Molony DA, Schena FP, Strippoli GF. Immunosuppressive agents for treating IgA nephropathy. Cochrane Database Syst Rev. 2020;3(3):Cd003965.

    PubMed  Google Scholar 

  6. 6.

    Pani A. Standard immunosuppressive therapy of immune-mediated glomerular diseases. Autoimmun Rev. 2013;12(8):848–53.

    CAS  PubMed  Article  Google Scholar 

  7. 7.

    Christian K, Ulf P, Hans-Joachim A, Rees AJ. The immune system and kidney disease: basic concepts and clinical implications. Nat Rev Immunol. 2013;13(10):738–53.

    Article  CAS  Google Scholar 

  8. 8.

    Ponticelli C, Locatelli F. Glucocorticoids in the treatment of glomerular diseases: pitfalls and pearls. Clin J Am Soc Nephrol. 2018;13(5):815–22.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  9. 9.

    Fardet L, Petersen I, Nazareth I. Common infections in patients prescribed systemic glucocorticoids in primary care: a population-based cohort study. PLoS Med. 2016;13(5):e1002024.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  10. 10.

    Jefferson JA. Complications of immunosuppression in glomerular disease. Clin J Am Soc Nephrol. 2018;13(8):1264–75.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  11. 11.

    Cholongitas E, Haidich AB, Apostolidou-Kiouti F, Chalevas P, Papatheodoridis GV. Hepatitis B virus reactivation in HBsAg-negative, anti-HBc-positive patients receiving immunosuppressive therapy: a systematic review. Ann Gastroenterol. 2018;31(4):480–90.

    PubMed  PubMed Central  Google Scholar 

  12. 12.

    Lim CC, Tung YT, Tan BH, Lee PH, Mok I, Oon L, Chan KP, Choo JC. Epidemiology and risk factors for cytomegalovirus infection in glomerular diseases treated with immunosuppressive therapy. Nephrology (Carlton). 2018;23(7):676–81.

    CAS  Article  Google Scholar 

  13. 13.

    Hassan HIC, Tang M, Djurdjev O, Langsford D, Sood MM, Levin A. Infection in advanced chronic kidney disease leadsto increased risk of cardiovascular events, end-stage kidney disease and mortality. Kidney Int. 2016;90(4):897–904.

    Article  Google Scholar 

  14. 14.

    Yin X, Ge H, Miao R. A case report of ocular tuberculosis in a patient with membranous nephropathy. Medicine (Baltimore). 2019;98(1):e13892.

    Article  Google Scholar 

  15. 15.

    Buttgereit F, Burmester GR, Lipworth BJ. Optimised glucocorticoid therapy: the sharpening of an old spear. Lancet. 2005;365(9461):801–3.

    CAS  PubMed  Article  Google Scholar 

  16. 16.

    Thomas R, Frank E, Christina F, Claudia S, Martin Z, Britta O, Ulf P, Harm P, Urs B, Mertens PR. Intensive supportive care plus immunosuppression in IgA nephropathy. N Engl J Med. 2015;373(23):2225–36.

    Article  CAS  Google Scholar 

  17. 17.

    Narayanan M. The many faces of infection in CKD: evolving paradigms, insights, and novel therapies. Adv Chronic Kidney Dis. 2019;26(1):5–7.

    PubMed  Article  Google Scholar 

  18. 18.

    Li J, Zhang Q, Su B. Clinical characteristics and risk factors of severe infections in hospitalized adult patients with primary nephrotic syndrome. J Int Med Res. 2017;45(6):2139–45.

    PubMed  PubMed Central  Article  Google Scholar 

  19. 19.

    Liu P, Tan HZ, Li H, Lim CC, Choo JCJ. Infections in hospitalized lupus nephritis patients: characteristics, risk factors, and outcomes. Lupus. 2018;27(7):1150–8.

    CAS  PubMed  Article  Google Scholar 

  20. 20.

    Thomas K, Vassilopoulos D. Infections and vasculitis. Curr Opin Rheumatol. 2017;29(1):17–23.

    CAS  PubMed  Article  Google Scholar 

  21. 21.

    Beaman BL, Beaman L. Nocardia species: host-parasite relationships. Clin Microbiol Rev. 1994;7(2):213.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  22. 22.

    Mcneil MM, Brown JM. The medically important aerobic actinomycetes: epidemiology and microbiology. Clin Microbiol Rev. 1994;7(3):357.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  23. 23.

    Ambrosioni J, Lew D, Garbino J. Nocardiosis: updated clinical review and experience at a tertiary center. Infection. 2010;38(2):89–97.

    CAS  PubMed  Article  Google Scholar 

  24. 24.

    Steinbrink J, Leavens J, Kauffman CA, Miceli MH. Manifestations and outcomes of nocardia infections: comparison of immunocompromised and nonimmunocompromised adult patients. Medicine (Baltimore). 2018;97(40):e12436.

    Article  Google Scholar 

  25. 25.

    Castellana G, Grimaldi A, Castellana M, Farina C, Castellana G. Pulmonary nocardiosis in chronic obstructive pulmonary disease: a new clinical challenge. Respir Med Case Rep. 2016;18:14–21.

    PubMed  PubMed Central  Google Scholar 

  26. 26.

    Wang HK, Sheng WH, Hung CC, Chen YC, Lee MH, Lin WS, Hsueh PR, Chang SC. Clinical characteristics, microbiology, and outcomes for patients with lung and disseminated nocardiosis in a tertiary hospital. J Formos Med Assoc. 2015;114(8):742–9.

    PubMed  Article  Google Scholar 

  27. 27.

    Galacho-Harriero A, Delgado-López PD, Ortega-Lafont MP, Martín-Alonso J, Castilla-Díez JM, Sánchez-Borge B. Nocardia farcinica brain abscess: report of 3 cases. World Neurosurgery. 2017;106:1053.e1015.

    Article  Google Scholar 

  28. 28.

    Coussement J, Lebeaux D, Rouzaud C, Lortholary O. Nocardia infections in solid organ and hematopoietic stem cell transplant recipients. Curr Opin Infect Dis. 2017;30(6):545.

    PubMed  Article  Google Scholar 

  29. 29.

    Mahajan KR. Disseminated nocardiosis with cerebral and subcutaneous lesions on low-dose prednisone. Pract Neurol. 2019;19(1):62–3.

    PubMed  Article  Google Scholar 

  30. 30.

    Conville PS, Brown-Elliott BA, Smith T, Zelazny AM. The complexities of nocardia taxonomy and identification. J Clin Microbiol. 2018;56(1):01419–17.

  31. 31.

    Wang T, Jia Y, Chu B, Liu H, Dong X, Zhang Y. Nocardiosis in kidney disease patients under immunosuppressive therapy: case report and literature review. Int J Med Sci. 2019;16(6):838–44.

    PubMed  PubMed Central  Article  Google Scholar 

  32. 32.

    Akasaka E, Ikoma N, Mabuchi T, Tamiya S, Matuyama T, Ozawa A, Saito E, Wakabayashi T, Yamada C, Aoyama K, et al. A novel case of nocardiosis with skin lesion due to Nocardia araoensis. J Dermatol. 2011;38(7):702–6.

    PubMed  Article  Google Scholar 

  33. 33.

    Shimizu T, Furumoto H, Asagami C, Kanaya K, Mikami Y, Muto M. Disseminated subcutaneous Nocardia farcinica abscesses in a nephrotic syndrome patient. J Am Acad Dermatol. 1998;38(5):874–6.

    CAS  PubMed  Article  Google Scholar 

  34. 34.

    Sirijatuphat R, Niltwat S, Tiangtam O, Tungsubutra W. Purulent pericarditis and cardiac Tamponade caused by Nocardia farcinica in a nephrotic syndrome patient. Intern Med. 2013;52(19):2231–5.

    PubMed  Article  Google Scholar 

  35. 35.

    Weber M, Rüddel J, Bruns T, Pletz MW, Stallmach A. Pulmonary co-infection with nocardia species and nontuberculous mycobacteria mimicking miliary tuberculosis in a patient with Crohn's disease under combined immunosuppressive therapy. Z Gastroenterol. 2018;56(06):569–72.

    PubMed  Article  Google Scholar 

  36. 36.

    Wu Y, Yu S, Xie Q. Nocardia infection in an immunosuppressive patient with Dermatomyositis. J Clin Rheumatol. 2020;26(1):e9.

  37. 37.

    Zhu N, Zhu Y, Wang Y, Dong S. Pulmonary and cutaneous infection caused by Nocardia farcinica in a patient with nephrotic syndrome: a case report. Medicine. 2017;96(24):e7211.

    PubMed  PubMed Central  Article  Google Scholar 

  38. 38.

    Sonesson A, Oqvist B, Hagstam P, Bjorkman-Burtscher IM, Miorner H, Petersson AC. An immunosuppressed patient with systemic vasculitis suffering from cerebral abscesses due to Nocardia farcinica identified by 16S rRNA gene universal PCR. Nephrol Dial Transplant. 2004;19(11):2896–900.

    PubMed  Article  Google Scholar 

  39. 39.

    Brown-Elliott BA, Brown JM, Conville PS, Wallace RJ. Clinical and laboratory features of the Nocardia spp. based on current molecular taxonomy. Clin Microbiol Rev. 2006;19(2):259–82.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  40. 40.

    Canouï E, Blanc K, Loubinoux J, Valade S, Hamard C, Lefebvre A, Amorim S, Bébéar C, Rodriguez-Nava V, Lebeaux D. The value of molecular techniques to diagnose Ureaplasma urealyticum and Nocardia farcinica Pleuropneumonia in a Patient with Diffuse large B-Cell Lymphoma. Int J Infect Dis. 2017;64:S1201971217302394.

    Article  Google Scholar 

  41. 41.

    Yang M, Min XU, Wei W, Gao H, Zhang X, Zhao H, Jianhua HU, Dong H, Lichen XU, Lanjuan LI. Clinical findings of 40 patients with nocardiosis: A retrospective analysis in a tertiary hospital. Exp Ther Med. 2014;8(1):25–30.

    PubMed  PubMed Central  Article  Google Scholar 

  42. 42.

    Ono M, Kobayashi Y, Shibata T, Maruyama D, Kim S-W, Watanabe T, Mikami Y, Tobinai K. Nocardiaexalbidabrain abscess in a patient with follicular lymphoma. Int J Hematol. 2008;88(1):95–100.

    PubMed  Article  Google Scholar 

  43. 43.

    Kato K, Noguchi S, Naito K, Ikushima I, Hanaka T, Yamasaki K, Kawanami T, Yatera K. Pulmonary Nocardiosis caused by Nocardia exalbida in a patient with lung cancer and radiation pneumonitis: a case report and literature review. Intern Med. 2019;58(11):1605–11.

    PubMed  PubMed Central  Article  Google Scholar 

  44. 44.

    Mazzaferri F, Cordioli M, Segato E, Adami I, Azzini AM. Nocardia infection over 5 years (2011-2015) in an Italian tertiary care hospital. New Microbiol. 2018;41(2):136–40.

    CAS  PubMed  Google Scholar 

  45. 45.

    Woodworth MH, Saullo JL, Lantos PM, Cox GM, Stout JE. Increasing Nocardia incidence associated with bronchiectasis at a tertiary care center. Ann Am Thorac Soc. 2017;14(3):347.

    PubMed  Article  Google Scholar 

  46. 46.

    Huang L, Chen X, Xu H, Sun L, Li C, Guo W, Xiang L, Luo G, Cui Y, Lu B. Clinical features, identification, antimicrobial resistance patterns of Nocardia species in China: 2009-2017. Diagn Microbiol Infect Dis. 2019;94(2):165–72.

    CAS  PubMed  Article  Google Scholar 

  47. 47.

    Paige EK, Spelman D. Nocardiosis: 7-year experience at an Australian tertiary hospital. Intern Med J. 2019;49(3):373–9.

    CAS  PubMed  Article  Google Scholar 

  48. 48.

    Uttamchandani RB, Daikos GL, Reyes RR, Fischl MA, Dickinson GM, Yamaguchi E, Kramer MR. Nocardiosis in 30 patients with advanced human immunodeficiency virus infection: clinical features and outcome. Clin Infect Dis. 1994;18(3):348–53.

    CAS  PubMed  Article  Google Scholar 

  49. 49.

    Lebeaux D, Bergeron E, Berthet J, Djadi-Prat J, Mouniée D, Boiron P, Lortholary O, Rodriguez-Nava V. Antibiotic susceptibility testing and species identification of Nocardia isolates: a retrospective analysis of data from a French expert laboratory, 2010-2015. Clin Microbiol Infect. 2019;25(4):489–95.

  50. 50.

    Hui CH, Au V, Rowland K. Pulmonary nocardiosis re-visited: experience of 35 patients at diagnosis. Respir Med. 2003;97(6):709–17.

    CAS  PubMed  Article  Google Scholar 

  51. 51.

    Wallace RJ Jr, Septimus EJ, Williams TW Jr, Conklin RH, Satterwhite TK, Bushby MB, Hollowell DC. Use of trimethoprim-sulfamethoxazole for treatment of infections due to Nocardia. Rev Infect Dis. 1982;4(2):315–25.

    CAS  PubMed  Article  Google Scholar 

  52. 52.

    Chung TT, Lin JC, Hsieh CT, Chen GJ, Ju DT. Nocardia farcinica brain abscess in an immunocompetent patient treated with antibiotics and two surgical techniques. J Clin Neurosci. 2009;16(12):1675–7.

    PubMed  Article  Google Scholar 

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The authors thank the members and staff of the Department of Nephrology of the 2nd Xiangya Hospital who contributed to this study. We thank the 18th Asian Pacific Congress of Nephrology for having presented this work as a poster presentation (The online abstract is available at:


This study was funded by National Natural Science Foundation of China (Grant/Award Number: 81570658). The funder had a role in the data collection, analysis and writing the manuscript.

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All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by YH, ZH and HZ, and they contributed equally to this work. The first draft of the manuscript was written by YH, ZH and HZ and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

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Correspondence to Li Xiao.

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Han, Y., Huang, Z., Zhang, H. et al. Nocardiosis in glomerular disease patients with immunosuppressive therapy. BMC Nephrol 21, 516 (2020).

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  • Nocardiosis
  • Glomerular disease
  • Glucocorticoids
  • Sulfanilamide