Kidney Week

Abstract: FR-PO1293

Chemotherapy-Induced Nephrotic-Range Proteinuria in Thin Basement Membrane Nephropathy

Session Information

• Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Onconephrology

• 1600 Onconephrology

Authors

• Marquez Flores, Sully Mariel, The University of Alabama at Birmingham, Birmingham, Alabama, United States

Sully Mariel Marquez Flores, MD

• Charkviani, Mariam, The University of Alabama at Birmingham, Birmingham, Alabama, United States

Mariam Charkviani, MD, FASN

• Seay, Norman Winn, The University of Alabama at Birmingham, Birmingham, Alabama, United States

Norman Winn Seay, MD

• Fatima, Huma, The University of Alabama at Birmingham, Birmingham, Alabama, United States

Huma Fatima, MD

Introduction

Thin basement membrane nephropathy (TBMN) is classically associated with isolated microscopic hematuria and preserved kidney function. Although nephrotic-range proteinuria can occur, it is uncommon and usually reflects superimposed glomerular pathology such as focal segmental glomerulosclerosis (FSGS). Whether diffuse glomerular basement membrane (GBM) thinning increases susceptibility to secondary glomerular insults remains unclear. We describe a patient with biopsy-proven TBMN who developed severe but reversible nephrotic-range proteinuria temporally associated with carboplatin/paclitaxel therapy.

Case Description

75-year-old woman without prior CKD presented with progressive renal dysfunction, intermittent gross hematuria, and flank pain. Imaging showed bilateral moderate hydroureteronephrosis. Bladder biopsy showed Müllerian carcinoma involving the bladder and retroperitoneum. Bilateral ureteral stents improved creatinine. She began carboplatin, then carboplatin/paclitaxel. Before chemotherapy, creatinine was 1.8 mg/dL, UACR 89 mg/g, and UPCR 250 mg/g. Three months after starting chemotherapy, UPCR rose to 9.6 g/g. Bevacizumab was withheld due to nephrotic-range proteinuria; carboplatin/paclitaxel continued.

Serologies were negative. Kidney biopsy showed diffuse GBM thinning (mean 178 nm, >50% loops), focal foot process effacement, no immune deposits, and no FSGS. Alport testing was negative.

After cytoreductive surgery she completed nine cycles. Creatinine remained 1.1 mg/dL. Proteinuria improved but fluctuated, then resolved two months post-therapy (UPCR 95 mg/g, UACR 7 mg/g).

Discussion

Nephrotic-range proteinuria with carboplatin/paclitaxel in TBMN has not been described. The case suggests that patients with TBMN may have a lower threshold for developing clinically significant proteinuria from secondary insults. The temporal association, fluctuation during therapy, and resolution after cessation support reversible chemotherapy-associated glomerular injury superimposed on TBMN. Platinum agents and taxanes have been associated with endothelial and podocyte toxicity, but nephrotic-range proteinuria remains uncommon. In this patient, diffuse GBM thinning may have increased susceptibility to overt proteinuria fafter otherwise subclinical filtration barrier injury.