Co-existence of anti-glomerular basement membrane (GBM) nephritis and membranous nephropathy (MN) is exceedingly rare. MN can occur simultaneously or sequentially to anti-GBM nephritis. Here, we report a patient with gout having severe renal dysfunction. Light microscopy revealed crescentic glomerulonephritis. Linear and granular positivity in the capillary wall was noted for immunoglobulin G. Serum and immunohistochemistry for PLA2R were negative. He developed end-stage renal disease and is hemodialysis dependent. Careful evaluation of immunofluorescence helps in clinching the diagnosis. The factors which predict renal outcome include serum creatinine at presentation; hence, earlier detection may lead to the reversal of renal function.
This article examines the widening gap between the growing burden of end-stage kidney disease (ESKD) and limited access to kidney transplantation in India. It outlines key structural, financial, and sociocultural barriers while highlighting regional disparities and gender imbalances. It presents practical, policy-oriented recommendations to strengthen deceased and living donor programs, enhance referral pathways, and improve transplant infrastructure. With a focus on equity, sustainability, and systemic reform, the article emphasizes the need for coordinated national efforts to ensure timely, ethical, and accessible kidney transplantation for all patients, particularly those in underserved and economically disadvantaged communities.
Background: Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, with variable clinical presentations and outcomes. Treatment approaches remain heterogeneous due to the lack of uniform risk stratification and inconsistent response to immunosuppression. This study aimed to evaluate the clinical and histopathological spectrum of IgAN and analyze outcomes in relation to different treatment regimens. Materials and Methods: A retrospective observational study was conducted on 86 patients with biopsy-proven primary IgAN at a tertiary care center in south India (2005–2021). Patients were categorized into four syndromic presentations and four treatment groups: supportive care, glucocorticoids alone, glucocorticoids with cyclophosphamide/azathioprine, and mycophenolate-based regimens. Outcomes were defined as complete remission (CR), partial remission, stable renal function (non progressors) and progressive kidney disease. Histopathology was graded using the Oxford MEST-C score. Statistical analyses were performed using SPSS 22.0. Results: Mean age at presentation was 32.56 ± 12.39 years, 69.8% were males. The most common clinical presentation was nephritic syndrome (52.3%). Segmental sclerosis (64%) and tubular atrophy (T1/T2: 57%) were common histopathological findings. Fifty percent of patients achieved CR, 34.9% progressed to end-stage renal disease, and 15% had partial or stable outcomes. There was no statistically significant difference in outcomes between the treatment groups (P = 0.254). Adverse events were significantly higher in immunosuppressive groups compared to supportive care (P = 0.031). Conclusion: IgAN exhibits significant clinical and histopathological heterogeneity. Immunosuppressive therapy did not confer a statistically significant benefit over supportive care in our study but was associated with higher adverse events. Risk stratification based on clinical syndrome and histology may help guide personalized treatment decisions.
Introduction: Posttransplant diabetes mellitus (PTDM) is a major determinant of renal allograft dysfunction, posttransplant infections, and increased risk of cardiovascular morbidity and mortality, and can significantly affect the clinical outcome of the transplant recipients. We aimed to determine the incidence, risk factors, and underlying mechanisms of PTDM in kidney transplant recipients. Methods: In a single-center, prospective, observational cohort study of 80 nondiabetic kidney transplant recipients (2023–2024), the clinical, metabolic, immunosuppressive, and infectious parameters were recorded. Pretransplant fasting plasma glucose, glycosylated hemoglobin (HbA1C), lipid profile, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Homeostatic Model Assessment of β-cell Function (HOMA-β), and tacrolimus trough levels at 1.5 and 3 months posttransplant were analyzed. Logistic regression and receiver operating characteristic curves defined predictors. Results: PTDM developed in 23.8% (n = 19). Significant risk factors included family history of diabetes and hypertension, smoking, higher pretransplant Body Mass Index, waist circumference, fasting blood glucose, HbA1c, lipid abnormalities, and high net immunosuppression. Independent predictors of PTDM were pretransplant triglycerides >134.5 mg/dL (odds ratio [OR] 1.05, 95% confidence interval [CI] 1.01–1.10) and trough tacrolimus level ≥7.5 ng/mL at 1.5 months (OR– 2.1, 95% CI 1.06–4.14). HOMA-β was significantly lower than HOMA IR in the PTDM group (P < 0.001), suggesting beta-cell dysfunction as the predominant pathophysiologic mechanism. Conclusion: PTDM occurred in 23.8% of kidney transplant recipients in our cohort, with the majority developing PTDM within the 1st-year posttransplantation. Pretransplant hypertriglyceridemia and high early tacrolimus exposure were independently associated with the development of PTDM. Beta-cell dysfunction appears to be the main contributor. Early metabolic screening and individualized immunosuppression may mitigate PTDM risk.
Background: Urinary beta 2 microglobulin levels (UB2) are indicative of tubular proteinuria and suggest tubular inflammation. This exploratory study was done to determine UB2 levels after ingestion of Nonsteroidal anti-inflammatory drugs (NSAIDs) and to explore their association with reduced glomerular filtration rate (GFR) that could indicate asymptomatic acute tubulointerstitial nephritis. Methods: Urine samples were collected for a routine examination and UB2 levels from one to five days after the NSAID dose ingestion, which was given in the appropriate dose in a Pediatric outpatient department and demographic, dose data were collected. If the UB2 level was elevated (more than 300 ng/mL), the child underwent a blood test to measure the serum creatinine, and the estimated GFR (eGFR) was calculated based on the modified Schwartz formula. Results: Of 50 children in the study (22 girls and 28 boys), 33 children had received Ibuprofen, and 17 children had received mefenamic acid in appropriate doses from 1 to 6 times. Thirty-four children had received NSAIDs for fever, 14 children for pain, and 2 for fever and pain. In 20 children, UB2 was elevated (14/33 children ibuprofen, 6/17 children mefenamic acid). Of these, 12 showed a reduced eGFR, and 5/12 children showed a severely reduced eGFR (<60 mL/min). One child underwent a kidney biopsy that showed Acute tubulointerstitial nephritis (TIN). In the other children, eGFR improved without intervention. Conclusion: In this study, we demonstrated that UB2 levels were elevated after ingestion of NSAIDs in a significant proportion of children. Reduced GFR was seen in 60% of these children. Larger studies are required to conclusively prove the association of NSAIDs with elevated UB levels.
Introduction: Serum osmolality may predict the development of acute kidney injury (AKI) at an earlier stage, even before changes in biochemical parameters, such as serum creatinine become evident and may help prevent AKI in intensive care unit (ICU) settings. The present study was conducted to investigate the association between serum osmolality and AKI in critically ill patients. Methods: This observational study was conducted between April 2022 and June 2023 in the ICU of a tertiary care hospital. A total of 1,300 ICU patients aged 18 years or older were included. The primary and secondary objectives were to determine the incidence of abnormal serum osmolality at admission and to find an association of serum osmolality with AKI and mortality in critically ill patients. Results: Serum osmolality was <280 mmol/L in 547 patients (42.1%), between 280 and 295 mmol/L in 692 patients (53.2%), and >295 mmol/L in 61 patients (4.7%). AKI developed in 346 patients (26.6%), and 75 patients (5.8%) succumbed. Age, presence of diabetes mellitus, serum osmolality <280 mmol/L and >295 mmol/L, and the median duration of ICU stay were significantly associated with the development of AKI. AKI Stage 3 and serum osmolality >295 mmol/L were significantly associated with inhospital mortality. Multivariate analysis revealed that a hospital stay >10 days and serum osmolality <280 mmol/L or >295 mmol/L at the time of admission were significantly associated with AKI. Conclusions: High or low serum osmolality at the time of admission were significantly associated with an increased risk of developing AKI in critically ill patients.
Penile tuberculosis (TB) is a rare entity, and the detection of it close to the end of antitubercular drug therapy has been seldom seen. We report a 50-year-old male with human immunodeficiency virus, who was diagnosed to have renal TB and was started on appropriate antitubercular treatment. Towards the end of his therapy, he underwent circumcision, and the prepucial skin biopsy showed the presence of a tubercular granuloma.
Opportunistic infections frequently manifest in patients undergoing immunosuppressive therapy. This case series outlines three cases of atypical/unique infections in individuals with renal diseases undergoing immunosuppression. The first patient, who was receiving immunosuppression for a renal transplant, was diagnosed with extrapulmonary tuberculosis (TB), specifically TB of the spine and a cold abscess in the right thigh, which was addressed through cold abscess drainage and the initiation of modified anti-TB therapy. The second patient was diagnosed with disseminated strongyloides infection in the background of immunosuppression for immunoglobin A (IgA) nephropathy, experiencing complications such as pneumonia, subacute intestinal obstruction and Gram-negative meningitis, all appropriately managed. The third case, presenting with pulmonary symptoms and renal transplant graft dysfunction, was diagnosed with pulmonary histoplasmosis through histopathological examination of an endobronchial biopsy specimen. Treatment involved anti-fungal medications and a reduction in immunosuppression. This case series highlights the importance of considering atypical infections in immunocompromised patients with renal disease. Vigilant monitoring for signs of unusual or opportunistic infections is vital, given the intricate nature of diagnosis and treatment in individuals with compromised immune systems.
Peripheral arterial thrombosis in the early posttransplant period is rare and may prove to be organ or limb-threatening. We report the case of a 28-year-old renal transplant recipient who developed acute unprovoked brachial, radial, and ulnar artery thrombosis during early postoperative hospitalization after transplant. The initial presentation was sudden onset arteriovenous fistula dysfunction associated with the symptoms of limb ischemia. A multidisciplinary approach involving interventional radiology (IR) and cardiovascular thoracic surgery led to prompt diagnosis and treatment. Under IR guidance, catheter-directed thrombolysis with minimal-dose alteplase (2.5 mg) and thrombosuction was successfully performed, salvaging the ischemic limb. The patient was transitioned to apixaban and discharged in stable condition. This case highlights the need for early suspicion and tailored thrombolytic strategies in posttransplant patients presenting with subtle vascular signs and the importance of a multidisciplinary team approach.
Sarcoidosis is a multisystem inflammatory disorder that most often affects the lungs and lymph nodes. Renal involvement is uncommon and may be related to disordered calcium metabolism or granulomatous interstitial nephritis (GIN), the latter reported in about 1% of native biopsies. We describe a young woman who developed sarcoidosis-related GIN, presenting unusually as dialysis-dependent acute kidney injury in the absence of marked hypercalcemia or pulmonary disease.
Heart failure (HF) and chronic kidney disease (CKD) frequently coexist, each exacerbating the other through complex hemodynamic, neurohormonal, and inflammatory mechanisms collectively referred to as the cardiorenal syndrome. Both conditions share overlapping risk factors such as hypertension, diabetes, and atherosclerosis, and their coexistence significantly worsens patient outcomes. Although both conditions manifest with fluid overload, the anatomical distribution and prognostic implications differ between cardiac and renal causes, making accurate differentiation important but challenging. Symptoms, signs, and radiological findings frequently overlap, especially in advanced stages. While elevated biomarker levels in CKD do not necessarily indicate HF, they are associated with greater cardiac morbidity and mortality. Dialysis-dependent patients have unique challenges related to volume fluctuations. Conventional diagnostic algorithms developed for non-CKD populations tend to overdiagnose HF in CKD patients, as biomarker and imaging abnormalities may be innate to CKD, even in the absence of HF. In this review, we discuss the challenges of diagnosing HF in CKD using a common clinical scenario.
Background: Diabetic kidney disease (DKD) is a major microvascular complication of type 2 diabetes mellitus. Although the renometabolic benefits of sodium-glucose co-transporter 2 (SGLT2) inhibitors are well established, their effects on bone mineral metabolism in DKD remain underexplored. This study prospectively evaluated changes in key bone-related biomarkers among DKD patients receiving SGLT2 inhibitors. Materials and Methods: In this prospective, open-label, hospital-based case–control study, 50 patients with type 2 diabetes and DKD (estimated glomerular filtration rate [eGFR] >30 mL/min/1.73 m2) were enrolled. Forty patients received SGLT2 inhibitors (empagliflozin or dapagliflozin), and ten continued standard therapy. Baseline and 3-month assessments included glycemic indices, renal function, and bone mineral parameters – serum calcium, phosphorus, 25-hydroxy Vitamin D [25(OH) D], intact parathyroid hormone (iPTH), fibroblast growth factor 23 (FGF23), and bone mineral density (BMD). Results: SGLT2 inhibitor therapy significantly reduced body weight, body mass index, urinary albumin-to-creatinine ratio, and eGFR. It was associated with significant increases in iPTH and FGF23, without significant changes in serum calcium, 25(OH) D, or BMD. Dapagliflozin produced a greater reduction in serum uric acid than empagliflozin (P = 0.04). Conclusion: SGLT2 inhibitor therapy in DKD was associated with favorable metabolic and renal effects along with hormonal alterations involving iPTH and FGF23, suggesting possible modulation of phosphate handling. These short-term findings likely reflect adaptive biochemical changes, but long-term studies are needed to determine their clinical relevance and implications for skeletal health and monitoring strategies during therapy.
Hematopoietic stem cell transplantation (HSCT) is a curative modality for various hematological malignancies. Renal complications are increasingly recognized after transplant, with chronic kidney disease (CKD) developing in 15%–20% of patients. Transplant-associated thrombotic microangiopathy (TMA) is a potential but often underdiagnosed etiology. We report a case of CKD with biopsy-proven chronic TMA following allogeneic HSCT, most likely secondary to chronic graft-versus-host disease (GVHD), in the absence of systemic GVHD or other typical TMA triggers. Although electron microscopy was not performed, histological features supported chronic TMA. Immunosuppression with corticosteroids led to stabilization of renal function. This case emphasizes the need to consider renal-limited GVHD in the differential diagnosis of post-HSCT renal dysfunction, even when extrarenal manifestations are absent.
Background: Glomerular diseases (GDs) are the third most common cause of chronic kidney disease if not detected and treated at an early stage. It is crucial to be aware of variations in the histological pattern of GD within a specific region, as the disease varies based on geographical location, ethnicity, age, and specific histological characteristics. This study was conducted to analyze Clinical and histopathologic profile of glomerulopathies in the Himalayan Belt of North India. Materials and Methods: The medical records of 169 cases from the Department of Nephrology in Super Speciality Hospital, Government Medical College, Jammu, were retrospectively analyzed over 4 years to review all diagnosed cases of glomerulopathies through histopathology, documenting basic demographic profiles, clinical presentations, relevant investigations, and histopathological classifications of GD for each patient. Results: In our research, males constituted 52.7% and females 47.3%, with a male-to-female ratio of 1.1:1. The average age was 36.17 ± 14.43 years. Systolic blood pressure was 144.22 ± 16.76 mmHg, and diastolic blood pressure was 88.01 ± 7.49 mmHg. Twenty-four-hour Urine protein level was 4.47 ± 2.87 g/day, and serum albumin measured 2.68 ± 0.64 g/dL. Out of 169 biopsies studied, 95 had nephrotic syndrome, 19 had nephritic syndrome, and 55 had nephrotic-nephritic presentation. We found that 79.9% had primary glomerulopathy and 20.1% had secondary glomerulopathy, with membranous glomerulopathy at 31.9%, focal segmental glomerulosclerosis at 26.7%, and minimal change disease (MCD) at 20.7%. The pattern of glomerulopathy was significantly associated with age (P < 0.05); MCD was higher in those aged up to 30 years, whereas membrane glomerulonephritis was more prevalent in the 31–60 age group. A significant observation was a higher prevalence of membranous nephropathy right from the 2nd decade of life, with a peak in the 3rd and 4th decades. Renal amyloidosis was more common in those over 60 years. Conclusion: The primary GDs, mainly membranous glomerulopathy, accounted for about 80% of cases in the Himalayan region of Northern India. A notable occurrence of membranous nephropathy in younger age groups was documented, which raises an important question about the presence of a novel antigen in the Himalayan belt for which further studies might be needed.
Introduction: Human leukocyte antigens (HLA) crossmatch (XM) detects preformed donor-specific antibodies (DSA) that can cause antibody-mediated rejection, even at low titers. XM methods have evolved from complement-dependent cytotoxicity XM (CDCXM) to flow cytometry (FCXM) and virtual XM on Luminex platforms, enhancing sensitivity for low-level antibodies undetected by cell-based assays. This study aimed to evaluate XM results and correlate them with solid-phase assays (SPAs), including panel reactive antibody (PRA) screening, percentage, and single antigen bead (SAB) assays for HLA Class I and II. Materials and Methods: All incidental XMs performed between December 2020 and December 2024 were analyzed. Samples with concurrent or recent (within 1 month) PRA or SAB results were included in the study. CDCXM (antihuman globulin-enhanced) included T-cell, B-cell, auto, and allo XM with serial dilutions up to 1:8. Positive auto-XMs were dithiothreitol-treated, and pronase treatment was applied when a history of treatment with intravenous immunoglobulin or rituximab was present. SPAs were performed using One Lambda kits on the Flexmap three-dimensional Luminex platform. XM results were classified as true positive (TP), true negative, false positive (FP), or false negative (FN) after correlation with SPAs. Results: Among 544 patient samples (456 FCXM, 477 CDCXM), 89.1% were negative for both assays. Six cases were TPs (CDCXM + and FCXM + with DSAs). Notably, 57.9% of DSA-positive cases had negative CDCXM and FCXM, representing FNs. One CDCXM+/FCXM + case lacked DSA due to antigen nonrepresentation, and two were FPs from nonspecific antibodies. Conclusion: Cell-based assays alone may miss low-titer DSAs. Combining XM with solid-phase testing ensures accurate immune stratification before transplantation.
Renal cell carcinoma (RCC) and multiple myeloma (MM) represent distinct malignancies with disparate origins and clinical presentations, yet emerging evidence suggests a potential association between them, evidenced by a higher-than-expected co-occurrence rate. Shared genetic predispositions, immune dysregulation, paraneoplastic syndromes, and cytokine-mediated mechanisms, particularly involving interleukin-6 from RCC cells, and treatment-related factors, such as chemotherapy-induced genomic instability, may contribute to MM development or progression. The presence of lytic lesions in a patient with prior RCC may simulate bone metastasis, thus leading to a diagnostic pitfall with potentially adverse clinical implications. Here, we describe two patients, a 52-year-old lady and 66-year-old gentleman who were incidentally found to have RCC-MM coexistence. In our two reported cases, the discovery of the neoplasias was synchronous, which rules out the hypothesis of secondary cancer induced by chemotherapy or radiotherapy. Vigilant monitoring and personalized management strategies are essential, necessitating further research to elucidate molecular mechanisms and inform clinical practice.
Introduction: Chronic kidney disease (CKD) is a growing global health concern, frequently associated with gastrointestinal (GI) symptoms such as dyspepsia, which can significantly impair quality of life. Helicobacter pylori (H. pylori) infection, a well-known cause of gastritis and peptic ulcer disease, is hypothesized to exacerbate GI symptoms and systemic inflammation in CKD patients. This study aimed to determine the prevalence of H. pylori infection in dialysis-naïve CKD patients with upper GI symptoms and compare it with non-CKD symptomatic controls. Materials and Methods: This prospective, comparative, cross-sectional study enrolled 54 CKD Stage 3–5 patients and 53 symptomatic non-CKD controls. Recent Proton pump inhibitor (PPI) (2 weeks) and antibiotic use (4 weeks) were excluded. All participants underwent upper GI endoscopy; a single antral biopsy was obtained for rapid urease test (RUT). Multivariable logistic regression was adjusted for age and sex. Results: H. pylori infection was detected in 32/54 CKD cases (59.3%) and 23/53 controls (43.4%) (χ2 = 2.10, P = 0.147), indicating a nonsignificant trend toward higher prevalence among CKD patients. Antral gastritis was the most frequent endoscopic finding in CKD (68.5%). In multivariable analysis, older age (P = 0.05), lower hemoglobin (P = 0.02), and higher urinary albumin-creatinine ratio (UACR) (P = 0.04) independently predicted H. pylori positivity within CKD patients. Conclusion: Although H. pylori prevalence was numerically higher in CKD patients, the difference was not statistically significant. Associations of H. pylori with age, anemia, and UACR in CKD should be interpreted as exploratory. Given the high burden of GI abnormalities in CKD, targeted evaluation remains justified, but routine screening solely based on CKD status cannot be recommended from this study.
