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Abstract: PO2451

Cytomegalovirus-Associated Collapsing Glomerulopathy in a Renal Transplant Recipient

Session Information

Category: Trainee Case Report

  • 1902 Transplantation: Clinical

Authors

  • Lavani, Chirag, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Gallan, Alexander James, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

Group or Team Name

  • Division of Nephrology
Introduction

Collapsing focal segmental glomerulosclerosis also known as collapsing glomerulopathy (CG) is a glomerular disease presenting with nephrotic syndrome and acute kidney injury (AKI), and showing collapse and sclerosis of glomerular capillaries with hypertrophic and injured podocytes on kidney biopsy. CG is most often seen in association with HIV infection and APOL1 nephropathy; however, CG can be associated with non-HIV viral infections. We describe a case of CMV-associated CG in a renal transplant patient.

Case Description

A 73 year old Caucasian male with history of ESRD due to biopsy-proven arterionephrosclerosis, status post deceased donor kidney transplantation (African-American donor) with baseline serum creatinine of 1.6 – 2 mg/dl presented with one day of explosive diarrhea. Lab revealed AKI with serum creatinine of 6.12 mg/dl. The patient was treated with IV fluids for AKI presumably due to volume depletion; however, serum creatinine and renal function failed to improve. Urinalysis was positive for blood and protein, and urine protein/creatinine ratio was 25 g/g cr with serum albumin of 1.6 g/dL. Testing for complements, serum and urine protein electrophoresis, serum free light chains, hepatitis panel, HIV and polyomavirus virus was negative. Serum cytomegalovirus NAAT was positive and the patient was started on IV Valganciclovir (vGCV). Renal allograft biopsy showed CG, including retraction/collapse of the glomerular tuft and podocyte hypertrophy with accumulation of protein reabsorption droplets. CMV immunostain showed positive staining of few glomerular endothelial cells in glomeruli with collapsing features. Electron microscopy demonstrated extensive foot process effacement without immune complex deposition. Immunosuppression was reduced. Patient was treated with cVGC for 10 weeks and a low dose lisinopril; serum creatinine and UPC improved to 1.69 mg/dl and 0.9 g/ g cr respectively without requiring renal replacement therapy. APOL1 genotyping demonstrated that the allograft kidney was heterozygous for the G1[GA1] risk allele, but homozygosity or compound heterozygosity was not present.

Discussion

Collapsing glomerulopathy can occur with non-HIV infection, such as CMV in renal transplant recipients. Allograft function may be preserved with appropriate therapy.