ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO0721

Enteric Infection-Associated Chronic Active Interstitial Nephritis and Collapsing Glomerulopathy in a Patient with a COL4A3 Variant

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Bhuiyan, Md Refayat, Northwell Health, New Hyde Park, New York, United States
  • Kuruvada, Krishna Mohita, Northwell Health, New Hyde Park, New York, United States
  • Ross, Daniel W., Northwell Health, New Hyde Park, New York, United States
  • Jhaveri, Kenar D., Northwell Health, New Hyde Park, New York, United States
  • Wu, Ming, Northwell Health, New Hyde Park, New York, United States
  • Sajid, Saira, Northwell Health, New Hyde Park, New York, United States
Introduction

Acute interstitial nephritis (AIN) is a common cause of acute kidney injury (AKI), with infections representing the second most common cause of AIN after medications. Collapsing glomerulopathy (CG) is a severe podocytopathy associated with infections, medications, autoimmune disease, and genetic susceptibility. We present a novel case of chronic active interstitial nephritis (CAIN) with concurrent CG occurring in the setting of enteric bacterial infection with Campylobacter jejuni and enteroaggregative Escherichia coli in a patient with a heterozygous COL4A3 variant.

Case Description

A 55-year-old African American man presented with three months of anasarca, dyspnea, foamy urine, and intermittent diarrhea. He was found to have nephrotic syndrome and AKI, with serum creatinine peaking at 6.31 mg/dL (baseline unknown), serum albumin of 1.3 g/dL, and urine protein-to-creatinine ratio (UPCR) of 15.2 g/g, accompanied by microscopic hematuria and pyuria. Autoimmune and infectious serologic evaluations were unrevealing except for stool PCR positive for Campylobacter species and enteroaggregative Escherichia coli (non–Shiga toxin producing). Kidney biopsy demonstrated collapsing glomerulopathy with diffuse interstitial lymphocytic infiltrates and eosinophils consistent with chronic active interstitial nephritis. Immunofluorescence studies were negative, and electron microscopy showed >90% podocyte foot process effacement.
Patient was treated with pulse intravenous methylprednisolone 500mg daily for 3 days followed by prednisone taper over 6 weeks, and one dose of Rituximab 1gm, resulting in marked renal recovery. Serum creatinine improved to 1.36 mg/dL by day 35 after initiation of treatment, with reduction in proteinuria (UPCR 1.35 g/g). Genetic testing later identified a heterozygous COL4A3 variant, while APOL1 testing was negative.

Discussion

This case highlights a previously unreported association between enteric bacterial infection and concurrent CAIN and CG, supporting a potential infection-triggered inflammatory response and podocytopathy in a genetically susceptible host.