Rifampicin-Associated Secondary Minimal Change Disease Presenting with Nephrotic Syndrome in a Pulmonary Tuberculosis Patient

Sathi, Satyanand; Garg, Anil Kumar; Singh, Manoj Kumar; Saini, Virendra Singh; Vohra, Devinder Kumar

doi:10.1155/2021/5546942

Cited by 6 publications

(4 citation statements)

References 8 publications

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“…Moreover, mycobacterium tuberculosis can directly cause AKI [18,23], which can clinically present as NS. Adverse reactions to TB medication can also lead to NS [17]. Therefore, the complex pathogenesis and poor prognosis of NS with TB necessitate further research to inform treatment strategies.…”

Section: Discussionmentioning

confidence: 99%

Association between nephrotic syndrome and tuberculosis in ICU patients: A cross-sectional study of the MIMIC-IV database

Du,

Su,

et al. 2024

Preprint

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Background This study investigated hospital mortality rates among patients with nephrotic syndrome (NS) and tuberculosis (TB) using data from the Medical Information Mart for Intensive Care IV version 2.2 (MIMIC-IV v2.2) database. The aim was to assess the impact of TB infection on in-hospital mortality risk in NS patients. Methods A total of 2167 NS patients were enrolled, among whom 1079 were co-infected with TB. Potential confounding factors included demographics, vital signs, laboratory values, acute physiology score, clinical treatments, and comorbidities. Univariate logistic regression was conduted to identify in-hospital mortality risk factors and multivariable multifactorial logistic regression was performed to explore the TB’s impact on in-hospital mortality. A restricted cubic spline regression analysis was carried out to investigate the linear relationship between hemoglobin, albumin, and in-hospital mortality. Stratified analyses were conducted for age, gender, sepsis, and acute kidney injury(AKI) stage to determine their effect on mortality of NS co-infected with TB. Results The prevalence of NS co-infected with TB was 49.8%, with a 14.6% in-hospital mortality rate, representing a 44% increased risk (P=0.005). The adjusted multivariable analysis revealed a mortality risk exceeding 20%. Among patients with sepsis, the incidence was 48.3% in those without TB and 46.7% in those co-infected with TB, with a 63% incidence of AKI within 7 days. Sepsis was associated with a 2.54-fold increase in mortality risk, and AKI stage 3 had an odds ratio (OR) of 9.03. Subgroup analyses suggested that both sepsis and AKI were independent risk factors for mortality. Hemoglobin and albumin exhibitedL-shaped linear relationships with in-hospital mortality, acting as protective factors below the inflection point. Only 1.8% received steroid treatments (NS 2.6%, NS and TB 0.9%), and 10.1% underwent continuous renal replacement therapy. Conclusions Our study results revealed significantly increased in-hospital mortality risk among NS patients with concurrent TB infection, alongside numerous complications. Sepsis and AKI independently increase mortality risk in NS patients co-infected with TB. These findings inform disease severity assessment and prognosis determination in adult NS patients with TB co-infection.

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Section: Discussionmentioning

confidence: 99%

Association between nephrotic syndrome and tuberculosis in ICU patients: A cross-sectional study of the MIMIC-IV database

Du,

Su,

et al. 2024

Preprint

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“…Rifampicin, a common anti-tuberculosis medication, has been blamed quite rarely for minimal-change disease since 1983. Five case reports with biopsy-proven rifampicin-associated MCD were found in the literature from 1983 to 2021 [ 57 , 58 , 59 , 60 , 61 ]. All 5 cases had been on rifampicin for 20 days to 1 month before nephrotic syndrome development and achieved complete remission 4–8 weeks post discontinuation of the drug.…”

Section: Discussionmentioning

confidence: 99%

“…There is not consensus over the pathogenesis of the MCD, probably due to the small number of cases. Whether toxicity is direct or immune-mediated is still unclear [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

Drug-Induced Podocytopathies: Report of Four Cases and Review of the Literature

Athanasopoulou

Lionaki

Skalioti

et al. 2023

Life

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Kidney injury due to medications is a well-known clinical entity. Although drug-induced tubulointerstitial disease is commonly encountered, there are few reports in the literature associated with glomerular injury due to medications. The recognition of this type of kidney injury is crucial, as rapid discontinuation of the offending agent is critical to maximizing the likelihood of quick and effective renal function recovery. In this article, we present four cases that presented with nephrotic syndrome and were diagnosed with biopsy-proven podocytopathies, associated with exposure to a certain medication. All of them experienced complete resolution of nephrotic syndrome within days or weeks after discontinuation of the offending drug. We also present the data, which were found in a Medline search from the year 1963 until the present, regarding cases with podocytopathies associated with penicillamine, tamoxifen and the combination of pembrolizumab-axitinib, including only adult cases from the English literature. The Medline search revealed nineteen cases of penicillamine-induced minimal-change disease (MCD), one case of tamoxifen-induced MCD, and none associated with pembrolizumab-axitinib therapy. We also searched for the largest studies and meta-analyses regarding drug-induced podocytopathies after a Medline search from 1967 to the present of the English literature.

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“…Among the greatest problems related to their utilization, bacterial resistance development is particularly severe, especially in the case of injudicious use; but another very serious concern related to antibacterial use is their potential to induce adverse effects, as their action in the patient's body is not limited to the pathogenic microbial agent. Even though these drugs are regularly bio-transformed in the human body and eliminated, and their toxicity is generally selective, they often induce serious adverse effects or significant toxicity (nephrotoxicity, hepatotoxicity, cardiotoxicity) [1].…”

Section: Introductionmentioning

confidence: 99%

Differential Protective Effect of Zinc and Magnesium for the Hepatic and Renal Toxicity Induced by Acetaminophen and Potentiated with Ciprofloxacin in Rats

Ciocan (Moraru),

Ciubotariu,

Ghiciuc

et al. 2024

Medicina

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Background and Objectives: The purpose of this study was to investigate the influence induced by magnesium chloride (MgCl2) and zinc gluconate (ZnG) supplementation on liver and kidney injuries experimentally induced with acetaminophen (AAPh) and potentiated by a ciprofloxacin addition in rats. Material and Methods: The experiment was performed on five animal groups: group 1—control, treated for 6 weeks with normal saline, 1 mL/kg; group 2—AAPh, treated for 6 weeks with AAPh, 100 mg/kg/day; group 3—AAPh + C, treated for 6 weeks with AAPh 100 mg/kg/day and ciprofloxacin 50 mg/kg/day, only in the last 14 days of the experiment; group 4—AAPh + C + Mg, with the same treatment as group 3, but in the last 14 days, MgCl2 10 mg/ kg/day was added; and group 5—AAPh + C + Zn, with the same treatment as group 3, but in the last 14 days, zinc gluconate (ZnG), 10 mg/kg/day was added. All administrations were performed by oral gavage. At the end of the experiment, the animals were sacrificed and blood samples were collected for biochemistry examinations. Results: Treatment with AAPh for 6 weeks determined an alteration of the liver function (increases in alanine aminotransferase, aspartate aminotransferase, lactic dehydrogenase, and gamma-glutamyl transferase) and of renal function (increases in serum urea and creatinine) (p < 0.001 group 2 vs. group 1 for all mentioned parameters). Furthermore, the antioxidant defense capacity was impaired in group 2 vs. group 1 (superoxide dismutase and glutathione peroxidase activity decreased in group 2 vs. group 1, at 0.001 < p < 0.01 and 0.01 < p < 0.05, respectively). The addition of ciprofloxacin, 50 mg/kg/day during the last 14 days, resulted in further increases in alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, urea, and creatinine (0.01 < p < 0.05, group 3 vs. group 2). MgCl2 provided a slight protection against the increase in liver enzymes, and a more pronounced protection against the increase in serum urea and creatinine (0.001 < p < 0.01 group 4 vs. group 3). MgCl2 provided a slight protection against the decrease in superoxide dismutase (0.01 < p < 0.05 group 4 vs. group 3), but not against decrease of glutathione peroxidase. The improvement of mentioned parameters could also be seen in the case of ZnG, to a higher extent, especially in the case of alanine aminotransferase and lactic dehydrogenase (0.01 < p < 0.05 group 5 vs. group 4). Conclusions: This study presents further proof for the beneficial effect of magnesium and zinc salts against toxicity induced by different agents, including antibacterials added to the analgesic and antipyretic acetaminophen; the protection is proven on the liver and kidney’s function, and the antioxidant profile improvement has a key role, especially in the case of zinc gluconate.

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Rifampicin-Associated Secondary Minimal Change Disease Presenting with Nephrotic Syndrome in a Pulmonary Tuberculosis Patient

Cited by 6 publications

References 8 publications

Association between nephrotic syndrome and tuberculosis in ICU patients: A cross-sectional study of the MIMIC-IV database

Association between nephrotic syndrome and tuberculosis in ICU patients: A cross-sectional study of the MIMIC-IV database

Drug-Induced Podocytopathies: Report of Four Cases and Review of the Literature

Differential Protective Effect of Zinc and Magnesium for the Hepatic and Renal Toxicity Induced by Acetaminophen and Potentiated with Ciprofloxacin in Rats

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