Abstract

Diabetic Nephropathy is the leading cause of End Stage Renal Disease (ESRD) in many countries. 35-45% of both Type-1 and Type-2 diabetic patients develop ESRD in 20-35 years. Some patients present with new onset nephrotic range proteinuria and detriorating renal functions. Renal biopsy showed non-diabetic glomerular leision in 10-12%. The development of collapsing glomerulopathy in the background of diabetic nephropathy is a very rare phenomenon. We present a case series of 6 cases of Collapsing Glomerulopathy superimposed on Diabetic nephropathy. The above case series was done retrospectively where patients with diabetic nephropathy who showed Collapsing Glomerulopathy on Renal biopsy were analysed and presented in a tabular column as depicted below.Tabled 1Patient no.AgeSexDuration of DiabetesHypertensionBaseline s.creatinineBaseline proteinuriaIndication for biopsyS.creatinine at presentation24 hour proteinuriafollow up durationOutcome167 ymale10 ynoNA1+volume overload and ICU care13 mg/dl8 g1 yearDialysis dependent239 ymale10 yyes1.8 mg/dl4+worsening pedal oedema5.7mg/dl6 g1 yearDialysis dependent360 ymale15 yyes3.5 mg/dl2+worsening oedema7.2mg/dl10 g1 yearDialysis dependent459 ymale21 yyes2.4 mg/dlNAworsening oedema6.1 mg/dl9 g2 yearsdialysis dependent544 ymale15 ynoNANAnew onset HTN and oedema2.4mg/dl12 g3 yearsrecently progressed to ESRD676 ymale15 ynoNANAVolume overload and ICU care1.8mg/dl10 g3 yearsrecently progressed to ESRD Open table in a new tab The average age of our patients was 55years. All 6 patients had history of long standing Type -2 Diabetes Mellitus - average of 15 years. Baseline serum creatinine in 3 of them was in the range of 1.8 -3.5 mg/dl. The clinical presentation and indications for renal biopsy were: 2 patients had severe breathlesness due to volume overload requiring ICU care, 3 patients had worsening oedema and uncontrolled blood pressures, 1 patient had new onset hypertension and pedal oedema. All patients had nephrotic range proteinuria. 4 patients had severe renal failure at presentation and were initiated on dialysis. 2 patients had a serum creatinine of 2.4 mg/dl and 1.8mg/dl. Renal biopsy showed collapsing glomerulopathy superimposed on diabetic nephropathy. 1 had class IIb,1 had class III, and 4 had class IV diabetic nephropathy. 3 biopsies had Interstitial fibrosis and Tubular atrophy (IFTA) more than 50%. All biopsies showed arterial hyalinosis. 4 patients who presented with severe renal failure were declared as ESRD and were continued on hemodialysis. 2 patients were in CKD stage 3 at presentation, progressed to ESRD by next 2 years and later underwent renal transplant. Collapsing Glomerulopathy contributes to an increased level or a new onset proteinuria in Diabetic nephropathy. This is usually intractable and rapidly progresses to End Stage Renal Diasease (ESRD). Collapsing Glomerulopathy in Diabetic nephropathyis presumbly due to ischemic podocyte injury and is of prognostic significance.

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