Collapsing Glomerulopathy- A Troublemaker for the Renal Allograft: Lessons Learnt.

Collapsing glomerulopathy (CG) is a well-recognized distinct morphological pattern of proliferative parenchymal injury leading to rapid graft failure. We conducted a single-center retrospective study to evaluate the prevalence, clinicopathological features, and prognosis of CG in renal transplant recepient. We analyzed 2518 renal allograft biopsies performed from 2007 to 2015 and correlated their clinicopathological features. The prevalence of CG was 0.83% (21 out of 2518) of allograft biopsies with a higher prevalence of 1.4% during the period from 2012 to 2015. Out of 21 patients, 18 (85.71%) patients had undergone live donor and 3 (14.28%) patients had undergone deceased donor renal transplant. Hypertension was observed in 3 (14.28%) patients. The mean duration of diagnosis for CG was 1.85 ± 1.91 years. Urinalysis revealed microhematuria in 5 (23.8%) patients. The mean 24 h urinary protein excretion was 4.77 ± 5.3 g and serum creatinine was 2.12 ± 1.5 mg/dl. The predominant native kidney diseases in recipients were chronic glomerulonephritis of unknown etiology in 12 (57.14%) patients and hypertensive nephropathy in 3 (14.28%) patients. CG was associated with rejection in 9 (42.85%), calcineurin-inhibitor toxicity in 2 (9.5%), and BK virus nephropathy in 1 patient. All patients received standard triple immunosuppression. Eleven (52.38%) patients developed graft failure over a mean period of 2.2 ± 1.7 years and 6 (28.57%) patients recovered with stable graft function. CG can coexist with viral infection, drug toxicity, rejection, microvascular injury, etc. CG usually presents with moderate to severe proteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients.

Crescentic Glomerulonephritis Associated with Pulmonary Tuberculosis.

Tuberculosis of kidney and urinary tract is caused by members of the Mycobacterium tuberculosis complex. Kidney is usually infected by haematogenous spread of bacilli from focus of infection in the lungs. Glomerular involvement in tuberculosis presenting as a rapidly progressive glomerulonephritis is a rare entity. We report a rare case of crescentic glomerulonephritis associated with pulmonary tuberculosis in a 26-year-old man. Patient was treated with corticosteroids, haemodialysis, intravenous immunoglobulin and four cycles of plasmapheresis. He did not respond to 4-drug anti-tuberculosis treatment for renal pathology and was switched over to maintenance haemodialysis. However, he responded to pulmonary TB.

Histological and Clinicopathological Evaluation of Liver Allograft Biopsy: An Initial Experience of Fifty Six Biopsies.

INTRODUCTION: Liver biopsy is gold standard for diagnosis of allograft dysfunction. AIM: The aim of study was to evaluate liver allograft biopsies performed for graft dysfunction, study the pattern of injury and intensity, and timeline of occurrence of graft dysfunction. MATERIALS AND METHODS: Retrospective study was carried out of 56 liver allograft biopsies and their histological findings with clinical presentation were correlated. Totally 56 needle liver allograft biopsies from January 1210 to July 2014, obtained from 35 patients were studied for histological and clinicopathological evaluation. RESULTS: The mean age was 53.2±5.48 years. The most common original disease was alcoholic cirrhosis. The most common histological lesion was acute cellular rejection (ACR) in 31 (55.36%) biopsies followed by preservation-reperfusion injury (PRI) in 10 (17.86%) biopsies and drug toxicity in 8 (14.29%) biopsies. Chronic rejection was reported in 2 (3.57%) and recurrence of HCV in 3 (5.36%). Ischemic coagulative necrosis and acute cholangitis were seen in 1 (1.79 %) case each. CONCLUSION: Alcoholic cirrhosis was the most common etiology for end stage liver disease. ACR and PRI were the major complications in liver allograft biopsies at our centre.

C1q nephropathy in India: a single-center study.

C1q nephropathy (C1qN) is defined by conspicuous C1q deposits in the glomerular mesangial regions of patients who do not have any evidence of systemic lupus erythematosus (SLE). We present our experience with C1qN over the last three years. In total, 1775 native renal biopsies were reviewed and dominant/co-dominant C1q mesangial deposits in patients with absence of clinical and/or serological evidence of SLE were considered as C1qN. Their clinical profile and renal function status were studied and correlated. C1qN was observed in 11 patients (0.61%), and included eight males and three females; the mean age was 36.6 years. The most common presentation was nephrotic syndrome. Hematuria was noted in eight patients (72%). The mean serum creatinine was 2.78 mg/dL. Hypertension was seen in two patients (18%). Mesangial proliferative glomerulonephritis (MePGN) was the most common histological pattern, followed by focal and segmental glomerulosclerosis and other lesions. The common codeposits along with C1q were IgM, followed by C3 and others. MePGN had better prognosis than others. To conclude, C1qN was noted in 0.61% of all renal biopsies with bimodal age distribution and may present as podocytopathy or non-podocytopathy. The prognosis depends on the morphological pattern and C1q deposits per se are not prognostic indicators.

Primary renal carcinoid tumor.

Primary renal carcinoid tumor is extremely rare and, therefore, its pathogenesis and prognosis is not well known. We report a primary renal carcinoid in a 26-year-old man treated by radical nephrectomy.

Incidentally detected lymphatic filariasis in a renal allograft recipient.

Post-transplntation lymphocele is a well known complication, and lymphatic filariasis (LF) has occasionally been found to present as post-transplantation lymphocele. However, incidentally detected LF during transplantation surgery has not been reported. We present an incidentally detected LF presenting as enlarged lymph node in the right iliac fossa of a recipient during transplantation of donor kidney. He was subsequently treated after transplantation and had stable graft function without any complications after 8 months of follow-up.

Operational tolerance in living-related renal transplantation: a single-center experience.

INTRODUCTION: Various methods have been tried to induce operational tolerance in organ transplantation. We present a single-center experience using 6 tolerance induction protocols (TIP) in living-related renal transplantation. METHODS: We evaluated 6 TIP protocols: (1) peripheral blood stem cells employed (n = 38); (2) midified the protocol by portal infusion (n = 292); (3) the second protocol plus TIP+DST+BM+intrathymic and intramarrow infusion plus low-dose, nonmyeloablative conditioning employed (n = 174), (4) the third protocol of TIP plus cultured hematopoietic stem cells (HSC) with target-specific irradiation (n = 290); (5) TIP 4 plus thymus, intramarrow infusion, and target-specific irradiation converted to total lymphoid irradiation (TLI) (n = 366); and (6) TIP 5 plus bortzomib-TLI (n = 165). Patient/donor demographics were comparable. RESULTS: We evaluated patient and graft survival, rejection episodes, recurrence, drug toxicity, and chimerism revealed; groups 4 and 5 showed better survival, graft function, chimerism, and decreased rejection episodes compared with previous protocols. Serum creatinine (mg/dL) at 1 year was 1.5, 1.39, 1.5, 1.51, 1.46, and 1.41, and at 5 years, 1.69, 1.72, 1.82 and 1.59, in groups 1-6, respectively. Chronic rejection episodes were 10.5%, 14.1%, 10.4%, 9.3%, 3.5%, 1.7%, and 1.8% respectively. Patient survival of groups 1, 2, and 3 at 1, 5, and 10 years was 86.5%, 56.8%, and 40.1%; 89.4%, 69.1%, and 56.4%; and 89.6%, 67.7%, and 64.6%, respectively; of group 4 for 1 and 5 years was 92.4% and 81.8%; for groups 5 and 6 for 1 year was 94% and 96.3%, respectively. The death-censored graft survival of groups 1, 2, and 3 at 1, 5, and 10 years was 91.9%, 70.3%, and 64.7%; 89%, 66%, and 57.6%; and 86.7%, 67%, and 42.5%, respectively. In group 4 for 1 and 5 years was 87.9% and 74.7%; and for groups 5 and 6 for 1 year was 94% and 96.5%, respectively. CONCLUSION: TIP results showed improved graft/patient survivals, minimum immunosuppression, and fewer rejection episodes and recurrence.

Immunoglobulin M nephropathy nephropathy in adults and adolescents in India: a single-center study of natural history.

BACKGROUND: Immunoglobulin M nephropathy (IgMN) is an idiopathic glomerulonephritis (GN) usually presenting clinically as steroid resistant/dependent nephrotic syndrome (NS) with pathology of mesangial proliferative GN or focal and segmental glomerulosclerosis with diffuse predominant mesangial IgM deposits. Not much information is available about its natural history. This is the first Indian study to our knowledge on IgMN in adults and adolescents. MATERIALS AND METHODS: We evaluated renal biopsies performed at our center between January,'04 to September,'09. Biopsies of all adolescents and adults were evaluated for IgMN and we studied their age, gender distribution, blood pressure (BP), disease duration, steroid/immunosuppressive management and serial serum creatinine (SCr), urinary proteins, and BP values. Patients with other systemic diseases/infections and children were excluded. RESULTS: IgMN constituted 4.3% of 2702 adult renal biopsies. No significant gender predilection was noted. Males presented at average age of 23.1 years, females at 30 years. Steroid-dependent NS was the commonest presentation noted in 75% followed by steroid-resistant NS. Hypertension was noted in 10% patients. Mesangial proliferative GN (MePGN) was commonest histopathological finding noted in 74.4%, followed by focal segmental glomerulosclerosis (FSGS) in 16.2%, and minimal change disease (MCD) in 9.4% biopsies. Sole IgM deposits were noted in 88.5%. All MCD, 35.6% MePGN reached remission, FSGS progressed to renal failure by 1 year. Hypertension, proteinuria, interstitial fibrosis, and FSGS were bad prognosticators. CONCLUSIONS: This is the first Indian study of IgMN in adults and adolescents carried out over a period of 5.8 years, which has shown that hypertension, proteinuria, and interstitial fibrosis at presentation have bad prognosis.