Kidney Week

Abstract: TH-PO0365

Collapsing Glomerulopathy Associated with Diffuse Large B-Cell Lymphoma Causing Nephrotic Syndrome and AKI

Session Information

• Glomerular Diseases: Genetics to Therapeutics
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

• Shahid, Shahzad, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Shahzad Shahid, MD, MBBS

• Khan, Inam Ullah, Bahria University, Karachi, Sindh, Pakistan

Inam Ullah Khan, MBBS

• Khan, Maida, Services Hospital Lahore, Lahore, Punjab, Pakistan

Maida Khan, MBBS

• Velagapudi, Ramya Krishna, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Ramya Krishna Velagapudi, MD, FASN

• Arwani, Suneel, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Suneel Arwani, MD, MBBS

• Yunas, Samia, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Samia Yunas, MD

• Abro, Sheeraz G., The University of Mississippi Medical Center, Jackson, Mississippi, United States

Sheeraz G. Abro, MD

Introduction

Collapsing glomerulopathy is an aggressive podocytopathy causing rapid kidney function decline and severe nephrotic syndrome. It is commonly linked to viral infections, autoimmune disease, medications, and APOL1 risk variants, while malignancy-associated cases are rare.

Case Description

An 84-year-old woman with CKD stage 3A, hypertension, and paroxysmal atrial fibrillation presented with dyspnea, poor intake, and syncope requiring cardioversion for atrial fibrillation with rapid ventricular response. Hospitalization was complicated by rapidly progressive acute kidney injury and nephrotic syndrome, with serum creatinine rising from 0.9–1.0 to 7.48 mg/dL and urine protein-creatinine ratio increasing from 1.35 to 64 g/g. Laboratory evaluation showed hypoalbuminemia, hypertriglyceridemia, hematuria, pyuria, granular casts, and dysmorphic red blood cells. Autoimmune, infectious, and paraprotein serologic workup was negative.

Kidney biopsy demonstrated acute tubular injury with collapsing focal segmental glomerulosclerosis, negative immunofluorescence, and diffuse podocyte foot process effacement on electron microscopy, consistent with collapsing glomerulopathy. Genetic testing identified a heterozygous APOL1 G2 allele, sickle cell trait, and likely pathogenic CASR variant.

Further evaluation revealed gastric diffuse large B-cell lymphoma with stage IV-E disease. Suspected paraneoplastic collapsing glomerulopathy prompted deferral of immunosuppression and initiation of mini R-CHOP chemotherapy. Renal function improved markedly without dialysis, with creatinine returning near baseline and proteinuria decreasing to 2.52 g/g after treatment.

Discussion

Collapsing glomerulopathy is a severe podocytopathy with poor renal outcomes and frequent progression to kidney failure. In this case, rapid nephrotic syndrome onset, negative serologies, biopsy findings, and improvement after lymphoma therapy supported a paraneoplastic mechanism and the need to evaluate for occult malignancy.

Collapsing glomerulopathy,foot process effacement