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Alabdul Razzak I, El Naamani H, Dimitrov D, Morin R, Jaber BL. Bile cast nephropathy: A systematic review of case reports and case series. World J Hepatol 2025; 17:105120. [PMID: 40308820 PMCID: PMC12038420 DOI: 10.4254/wjh.v17.i4.105120] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/13/2025] [Revised: 02/27/2025] [Accepted: 03/25/2025] [Indexed: 04/25/2025] Open
Abstract
BACKGROUND Bile cast nephropathy (BCN) is suspected in the setting of liver disease and hyperbilirubinemia and is characterized by the formation of tubular bile casts and acute tubular injury. While postmortem studies reveal a high prevalence of BCN, little is known about this orphan acute kidney injury syndrome. AIM To address this knowledge gap, we performed a systematic review of case reports and case series of BCN, focusing on risk factors, diagnostic criteria, clinical presentation, kidney biopsy findings, severity, treatment approaches, and outcomes. METHODS Electronic databases were searched to identify eligible studies of patients with possible, probable, or definite BCN, using pre-established criteria. Relevant variables were extracted and analyzed. We explored the impact of serum total bilirubin levels and alcoholic liver disease on BCN severity and outcomes by stratifying cases into total bilirubin tertiles and alcoholic vs non-alcoholic liver disease. Univariate and multivariable logistic regression analyses were used to examine factors associated with the composite outcome of dialysis requirement or death. RESULTS Sixty-seven case reports and six case series (involving 2 patients each) met the inclusion criteria, totaling 79 cases of BCN. The mean age was 48.3 years, and 83.5% were men. The most common cause of liver disease was drug-induced injury (30.4%), followed by infection (18.9%) and alcoholism (12.7%). BCN diagnosis was deemed definite, probable, and possible in 65.8%, 32.9%, and 1.3% of cases, respectively. Levels of serum creatinine, dialysis requirement, and renal recovery did not differ among the total bilirubin tertile groups. However, both initial and peak serum creatinine were significantly higher in the alcoholic liver disease group compared to the non-alcoholic group (P = 0.011 and P = 0.012, respectively). There was also a non-significant trend toward a higher incidence of dialysis requirement or death in the alcoholic liver disease group (80% vs 52%, P = 0.098). Finally, higher initial serum creatinine (per 1 mg/dL increase) was independently associated with dialysis requirement or death (adjusted odds ratio 1.291, 95% confidence interval: 1.032-1.615, P = 0.025). CONCLUSION BCN is a common and potentially serious cause of acute kidney injury in patients with liver disease. The degree of hyperbilirubinemia does not appear to correlate with BCN severity or outcomes. However, in alcoholic liver disease, BCN is associated with a greater rise in serum creatinine and a trend toward worse outcomes compared to non-alcoholic liver disease. Serum creatinine may be a valuable predictor of BCN prognosis. Further studies are needed to develop non-invasive diagnostic tools and establish effective treatments for BCN.
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Affiliation(s)
- Iyiad Alabdul Razzak
- Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, United States.
| | - Hind El Naamani
- Department of Medicine, St. Elizabeth's Medical Center, Boston, MA 02135, United States
| | - Dimo Dimitrov
- Department of Medicine, St. Elizabeth's Medical Center, Boston, MA 02135, United States
| | - Rebecca Morin
- Department of Research and Instruction, Tufts University, Boston, MA 02111, United States
| | - Bertrand L Jaber
- Department of Medicine, St. Elizabeth's Medical Center, Boston, MA 02135, United States
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Somagutta MR, Jain MS, Pormento MKL, Pendyala SK, Bathula NR, Jarapala N, Mahadevaiah A, Sasidharan N, Gad MA, Mahmutaj G, Hange N. Bile Cast Nephropathy: A Comprehensive Review. Cureus 2022; 14:e23606. [PMID: 35505725 PMCID: PMC9053373 DOI: 10.7759/cureus.23606] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/19/2022] [Accepted: 03/29/2022] [Indexed: 11/14/2022] Open
Abstract
Bile cast nephropathy (BCN) or cholemic nephropathy (CN) is an acute renal dysfunction, including acute kidney injury (AKI) in the setting of liver injury. It is a common phenomenon in patients with liver disease and is associated with significant morbidity and mortality. CN is characterized by hemodynamic changes in the liver, kidney, systemic circulation, intratubular cast formation, and tubular epithelial cell injury. CN has been overlooked as a differential diagnosis in chronic liver disease patients due to more importance to hepatic injury. However, frequent and considerable reporting of case reports recently has further investigated this topic in the last two decades. This review determines the evidence behind the potential role of bile acids and bilirubin in acute renal dysfunction in liver injury, summarizing the implied pathophysiology risk factors, and incorporating the therapeutic mechanisms and outcomes.
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Bile acid nephropathy induced by anabolic steroids: A case report and review of the literature. Clin Nephrol Case Stud 2021; 9:123-129. [PMID: 34790517 PMCID: PMC8594315 DOI: 10.5414/cncs110711] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2021] [Accepted: 08/24/2021] [Indexed: 01/13/2023] Open
Abstract
Bile acid nephropathy also known as cholemic nephropathy is a rare and overlooked form of acute kidney injury that occurs in the setting of severe hyperbilirubinemia. The exact etiology remains unknown, and there is a lack of treatment guidelines for this clinical condition. Anabolic steroids are known to cause hepatoxicity occasionally leading to acute kidney injury. We report the case of a 27-year-old male patient who developed bile acid nephropathy as a result of severe hyperbilirubinemia secondary to anabolic steroids-induced liver injury. He was conservatively managed. We review the current literature touching on the etiology, pathophysiology, diagnosis, and management of bile acid nephropathy in an attempt to shed light on this clinical condition, which may present as a diagnostic and therapeutic challenge.
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Zhao X, Huang R, Wong P, Fiset PO, Deschênes M. Renal tubular injury in hyperbilirubinemia: Bile cast nephropathy. CANADIAN LIVER JOURNAL 2021; 4:332-337. [PMID: 35992254 PMCID: PMC9202769 DOI: 10.3138/canlivj-2020-0031] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/17/2020] [Accepted: 12/26/2020] [Indexed: 04/25/2025]
Abstract
The toxic renal accumulation of bile pigment sparked clinical intrigue almost a century ago. More recently, however, the identification of bile casts within renal tubules in patients with liver dysfunction has been largely overlooked. We have reviewed the literature, including natural history, pathophysiology, and potential treatment of bile cast nephropathy (BCN). We report two cases of acute kidney injury (AKI) associated with acute-on-chronic liver failure in which prolonged hyperbilirubinemia and bile cast identification on renal biopsy evoked the diagnosis of BCN.
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Affiliation(s)
- Xun Zhao
- Department of Hepatology, Royal Victoria Hospital, McGill University Health Centre, Montréal, Québec, Canada
| | - Ruiyao Huang
- Department of Hepatology, Royal Victoria Hospital, McGill University Health Centre, Montréal, Québec, Canada
| | - Philip Wong
- Department of Hepatology, Royal Victoria Hospital, McGill University Health Centre, Montréal, Québec, Canada
| | - Pierre-Oliver Fiset
- Department of Pathology, Royal Victoria Hospital, McGill University Health Centre, Montréal, Québec, Canada
| | - Marc Deschênes
- Department of Hepatology, Royal Victoria Hospital, McGill University Health Centre, Montréal, Québec, Canada
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Wu YH, Wu CY, Cheng CY, Tsai SF. Severe hyperbilirubinemia is associated with higher risk of contrast-related acute kidney injury following contrast-enhanced computed tomography. PLoS One 2020; 15:e0231264. [PMID: 32294106 PMCID: PMC7159198 DOI: 10.1371/journal.pone.0231264] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2019] [Accepted: 03/19/2020] [Indexed: 12/20/2022] Open
Abstract
INTRODUCTION Contrast-induced acute kidney injury (CI-AKI) is associated with high risks of morbidity and mortality. Hyperbilirubinemia might have some renal protection but with no clear cutoff value for protection. Related studies are typically on limited numbers of patients and only in conditions of vascular intervention. METHODS We performed this study to elucidate CI-AKI in patients after contrast-enhanced computed tomography (CCT). The outcomes were CI-AKI, dialysis and mortality. Patients were divided to three groups based on their serum levels of total bilirubin: ≤1.2 mg/dl, 1.3-2.0 mg/dl, and >2.0 mg/dl. RESULTS We enrolled a total of 9,496 patients who had received CCT. Patients with serum total bilirubin >2.0 mg/dl were associated with CI-AKI. Those undergoing dialysis had the highest incidence of PC-AKI (p<0.001). No difference was found between the two groups of total bilirubin ≤1.2 and 1.3-2.0 mg/dl. Patients with total bilirubin >2mg/dl were associated with CI-AKI (OR = 1.89, 1.53-2.33 of 95% CI), dialysis (OR = 1.40, 1.01-1.95 of 95% CI) and mortality (OR = 1.63, 1.38-1.93 of 95% CI) after adjusting for laboratory data and all comorbidities (i.e., cerebrovascular disease, coronary artery disease, peripheral arterial disease, and acute myocardial infarction, diabetes mellitus, hypertension, gastrointestinal bleeding, cirrhosis, peritonitis, ascites, hepatoma, shock lung and colon cancer). We concluded that total bilirubin level >2 mg/dl is an independent risk factor for CI-AKI, dialysis and mortality after CCT. These patients also had high risks for cirrhosis or hepatoma. CONCLUSION This is the first study providing evidence that hyperbilirubinemia (total bilirubin >2.0 mg/dl) being an independent risk factor for CI-AKI, dialysis and mortality after receiving CCT. Most patients with total bilirubin >2.0mg/dl had cirrhosis or hepatoma.
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Affiliation(s)
- Yu-Hsien Wu
- School of Medicine, China Medical University, Taichung, Taiwan
| | - Chun-Yi Wu
- Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
| | - Ching-Yao Cheng
- Department of Pharmacy, Taichung Veterans General Hospital, Taichung, Taiwan
- Department of Pharmacy, China Medical University, Taichung, Taiwan
| | - Shang-Feng Tsai
- Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
- Department of Life Science, Tunghai University, Taichung, Taiwan
- School of Medicine, National Yang-Ming University, Taipei, Taiwan
- * E-mail:
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Torrealba J, Sweed NT, Burguete D, Hendricks AR. Bile Cast Nephropathy: A Pathologic Finding with Manifold Causes Displayed in an Adult with Alcoholic Steatohepatitis and in a Child with Wilson's Disease. Case Rep Nephrol Dial 2018; 8:207-215. [PMID: 30397601 PMCID: PMC6206956 DOI: 10.1159/000493231] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2017] [Accepted: 08/21/2018] [Indexed: 01/12/2023] Open
Abstract
Bile cast nephropathy (BCN) is seen in patients who have acute kidney injury and severe hyperbilirubinemia due to a wide range of hepatobiliary system diseases. Findings seen by renal biopsy include acute tubular injury with necrotic and sloughed epithelial cells, yellow-green pigment within tubular epithelial cells, and pigmented granular casts. Hall's special stain for bile turns these casts green. In recent years, BCN has been described in a small number of case reports and clinical studies primarily in the setting of severe liver dysfunction. We present 2 diverse cases of BCN. The first involves an adult with hepatorenal syndrome secondary to alcoholic steatohepatitis and early cirrhosis. Second, we describe the first reported case of BCN in a child with fulminant hepatic failure due to Wilson's disease. Our cases expand the spectrum of causative diseases, and they provide further evidence that BCN is a distinct pathologic entity which may be found in both adult and pediatric patients with a variety of severe liver diseases.
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Affiliation(s)
- Jose Torrealba
- Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
| | - Nathan T Sweed
- Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
| | - Daniel Burguete
- University of Texas Southwestern Medical School, Dallas, Texas, USA
| | - Allen R Hendricks
- Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
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Sood V, Lal BB, Lata S, Rastogi A, Alam S. Cholemic or Bile Cast Nephropathy in a Child with Liver Failure. J Clin Exp Hepatol 2017; 7:373-375. [PMID: 29234203 PMCID: PMC5715444 DOI: 10.1016/j.jceh.2017.05.006] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/27/2016] [Accepted: 05/02/2017] [Indexed: 12/12/2022] Open
Abstract
Cholemic or bile cast nephropathy is an under-reported entity characterized by acute renal dysfunction in patients with hepatic insult. Limited literature is available regarding its clinical presentation, pathogenesis and prognosis. We hereby present a pediatric case who presented with acute on chronic liver failure with renal dysfunction secondary to cholemic nephropathy.
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Affiliation(s)
- Vikrant Sood
- Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi, India
| | - Bikrant B. Lal
- Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi, India
| | - Suman Lata
- Department of Nephrology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi, India
| | - Archana Rastogi
- Department of Pathology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi, India
| | - Seema Alam
- Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi, India,Address for correspondence: Seema Alam, Professor and Head, Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, D-1, Vasant Kunj, New Delhi 110070, India. Tel.: +91 9540951008.Seema Alam, Professor and Head, Department of Pediatric Hepatology, Institute of Liver and Biliary SciencesD-1, Vasant KunjNew Delhi110070India
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Nayak SL, Kumar M, Bihari C, Rastogi A. Bile Cast Nephropathy in Patients with Acute Kidney Injury Due to Hepatorenal Syndrome: A Postmortem Kidney Biopsy Study. J Clin Transl Hepatol 2017; 5:92-100. [PMID: 28660146 PMCID: PMC5472929 DOI: 10.14218/jcth.2016.00063] [Citation(s) in RCA: 25] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/15/2017] [Revised: 03/15/2017] [Accepted: 03/31/2017] [Indexed: 12/19/2022] Open
Abstract
Background and Aims: The role of bile cast nephropathy (BCN) in pathogenesis of hepatorenal syndrome (HRS) in decompensated cirrhosis and acute on chronic liver failure (ACLF) is unknown. This study aimed to determine the frequency of BCN detected on postmortem renal biopsy among patients with decompensated cirrhosis and ACLF who had been admitted with acute kidney injury due to HRS (HRA-AKI) and expired during that hospitalization. Methods: One-hundred-twenty-seven postmortem renal biopsies with adequate size (>1 cm in length) were included for analysis. These were obtained from 84 patients with decompensated cirrhosis and 43 patients with ACLF. Results: BCN was detected in 57 of the total 127 (44.8%) renal biopsy specimens. Patients with BCN had significantly higher levels of serum total bilirubin, total leukocyte count and model for end-stage liver disease score, as compared to those without BCN. BCN was detected in 32/43 (74.4%) of the patients with ACLF, as compared to 25/84 (29.7%) of the patients with decompensated cirrhosis (p < 0.001). On multivariate analysis, direct bilirubin (OR (95% CI): 1.27 (1121-1.698); p < 0.001) and presence of ACLF (OR (95% CI): 2.603 (1.054-7.111); p = 0.041) were found to be significant predictors of BCN on postmortem renal biopsy. Conclusion: BCN was found in 72.1% of patients with ACLF and 27.4% patients with decompensated cirrhosis who had been hospitalized with an admitting diagnosis of HRS-AKI and who expired during that hospitalization and underwent postmortem renal biopsy. Direct serum bilirubin and presence of ACLF were found to be significant predictors of BCN on postmortem renal biopsy.
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Affiliation(s)
- Suman Lata Nayak
- Department of Nephrology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - Manoj Kumar
- Department of Hepatology and Liver Transplatation, Institute of Liver and Biliary Sciences, New Delhi, India
- *Correspondence to: Manoj Kumar, Department of Hepatology, Institute of Liver and Biliary Sciences, D1 Vasant Kunj, New Delhi 110070, India. Tel: +91-11-46300000, Fax: +91-11-46300063, E-mail:
| | - Chhagan Bihari
- Department of Pathology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - Archana Rastogi
- Department of Pathology, Institute of Liver and Biliary Sciences, New Delhi, India
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Patel J, Walayat S, Kalva N, Palmer-Hill S, Dhillon S. Bile cast nephropathy: A case report and review of the literature. World J Gastroenterol 2016; 22:6328-6334. [PMID: 27468221 PMCID: PMC4945990 DOI: 10.3748/wjg.v22.i27.6328] [Citation(s) in RCA: 43] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/30/2015] [Revised: 02/29/2016] [Accepted: 03/18/2016] [Indexed: 02/06/2023] Open
Abstract
Bile cast nephropathy is a condition of renal dysfunction in the setting of hyperbilirubinemia. There are very few cases of this condition reported in the last decade and a lack of established treatment guidelines. While the exact etiology remains unknown, bile cast nephropathy is presumed to be secondary to multiple concurrent insults to the kidney including direct toxicity from bile acids, obstructive physiology from bile casts, and systemic hypoperfusion from vasodilation. Therapy directed at bilirubin reduction may improve renal function, but will likely need dialysis or plasmapheresis as well. We report our case of bile cast nephropathy and the therapeutic measures undertaken in a middle-aged male with chronic renal insufficiency that developed hyperbilirubinemia and drug-induced liver injury secondary to antibiotic use. He developed acute renal injury in the setting of rising bilirubin. He subsequently had a progressive decline in renal and hepatic function, requiring dialysis and plasmapheresis with some improvement, ultimately requiring transplantation.
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Mohapatra MK, Behera AK, Karua PC, Bariha PK, Rath A, Aggrawal KC, Nahak SR, Gudaganatti SS. Urinary bile casts in bile cast nephropathy secondary to severe falciparum malaria. Clin Kidney J 2016; 9:644-8. [PMID: 27478612 PMCID: PMC4957722 DOI: 10.1093/ckj/sfw042] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2016] [Accepted: 04/23/2016] [Indexed: 01/27/2023] Open
Abstract
BACKGROUND Severe cholestatic jaundice may complicate with bile cast nephropathy (BCN) causing severe acute kidney injury (AKI). In this study, we investigate BCN in severe falciparum malaria complicated with jaundice and AKI. METHODS This prospective study was conducted in a tertiary health care institution with high prevalence of malaria. A cohort of 110 patients with falciparum malaria complicated with cerebral malaria, jaundice and AKI were enrolled. Species diagnosis was made from peripheral blood smear or rapid diagnostic test. Severe malaria was diagnosed from WHO criteria. BCN was diagnosed with the detection of bile casts in urine or in biopsy. The recovery pattern and outcome with and without BCN was assessed. RESULTS Out of 110 patients, 20 (18.2%) patients had BCN and 15 (13.6%) patients had hepato-renal syndrome. Patients with BCN had high conjugated bilirubin (26.5 ± 4.1 mg/dL), urea (75.9 ± 10.3 mg/dL) and creatinine (7.2 ± 0.8 mg/dL), longer duration of illness (6.4 ± 1.1 days), higher mortality (25.0%) and prolonged recovery time of hepatic (9.6 ± 2.4 days) and renal dysfunction (15.1 ± 6.5 days) compared with patients without BCN. CONCLUSIONS Prolonged duration of illness and increased bilirubin cause BCN among patients with severe falciparum malaria with jaundice and AKI, which is associated with high mortality and morbidity.
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Affiliation(s)
- Manoj Kumar Mohapatra
- Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Ashok Kumar Behera
- Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Purna Chandra Karua
- Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Prafulla Kumar Bariha
- Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Ashutosh Rath
- Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Kailash Chandra Aggrawal
- Department of Pathology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Snigdha Rani Nahak
- Department of Pathology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
| | - Santosh Shankar Gudaganatti
- Department of Pathology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha , India
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Mikhalkova D, Khanna S, Vaidya R, Sethi S, Hogan MC. Epstein-Barr virus-associated nephrotic syndrome. Clin Kidney J 2012; 5:50-52. [PMID: 26069749 PMCID: PMC4400449 DOI: 10.1093/ndtplus/sfr119] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/27/2011] [Accepted: 08/24/2011] [Indexed: 11/26/2022] Open
Abstract
Acute infection with Epstein-Barr virus (EBV) causes fever, fatigue and pharyngitis. Renal involvement in systemic EBV infections typically manifests as acute tubular necrosis or tubulointerstitial nephritis. Rarely, EBV infection causes nephrotic syndrome due to minimal change disease. A 22-year-old male with infectious mononucleosis (IM) presented with nephrotic syndrome. Renal biopsy showed minimal change disease with diffuse foot process effacement of the podocytes. Treatment with methylprednisone led to rapid and complete clinical remission. Minimal change nephropathy is a very rare manifestation of EBV infection and should be considered in patients with IM and proteinuria.
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Affiliation(s)
- Deana Mikhalkova
- Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
| | - Sahil Khanna
- Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
| | - Rakhee Vaidya
- Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
| | - Sanjeev Sethi
- Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA
| | - Marie C. Hogan
- Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
- Division of Nephrology and Hypertension, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
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