Abstract: FR-PO1255
Chromogranin Tubulopathy: A Case Series of Paraneoplastic Proximal Tubular Injury Associated with High Chromogranin A in Patients with a Neuroendocrine Tumor (NET)
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
- Wazir, Maha, The Ohio State University, Columbus, Ohio, United States
- Ullah, Farhan, Ochsner Medical Center, New Orleans, Louisiana, United States
- Kimbrough, Denise M., The Ohio State University, Columbus, Ohio, United States
- Brodsky, Sergey V., The Ohio State University, Columbus, Ohio, United States
- Madhavan, Sethu M., The Ohio State University, Columbus, Ohio, United States
Group or Team Name
- OSU Nephrology
Introduction
Chromogranin A (CgA), an established NET tumor marker, undergoes glomerular filtration and megalin-mediated proximal tubular reabsorption; its nephrotoxic potential is undescribed. We present the first case series of chromogranin tubulopathy (CgA positivity within proximal tubular epithelial cells) as a novel paraneoplastic nephropathy in NET patients with unexplained AKI.
Case Description
Case 1: A 64-year-old male with G1 functional duodenal NET, hepatic metastases, and carcinoid syndrome (CgA 36,090→50,280 ng/mL) developed AKI (creatinine 1.6→3 mg/dL) and tubular proteinuria (UPCR 6.3 g/g). Biopsy confirmed chromogranin (Cg) positive proximal tubular epithelial cells; serologic workup was unrevealing. CgA declined to 17,430 ng/mL with octreotide and CAPTEM. Concurrent IgA vasculitis represented a second paraneoplastic manifestation. He progressed to HD and is on comfort care.
Case 2: A 53-year-old female with G2 pancreatic NET (Ki-67 18%, CgA 311,800 ng/mL), treated with CAPTEM, Y90, and lenvatinib, developed KDIGO stage 3 AKI (creatinine 2.5→6 mg/dL). A 2023 biopsy was normal; repeat biopsy in 2024 demonstrated Cg tubulopathy with acute tubular injury, positive Cg in the tubular epithelial cells, and moderate-to-severe fibrosis. CgA declined to 68,810 ng/mL with lenvatinib held, but renal recovery was absent. She died dialysis-dependent.
Case 3: A 66-year-old female with G1 functional sphenoorbital NET on octreotide (CgA 515 ng/mL) developed progressive CKD (creatinine 1.4→2.1 mg/dL). Biopsy revealed 25–30% fibrosis with Cg staining in proximal tubular epithelial cells. She required HD and died of disease progression.
Discussion
These cases suggest that markedly elevated CgA causes direct proximal tubular toxicity, representing an underrecognized mechanism of AKI and CKD progression in NET patients. Chromogranin immunostaining on kidney biopsy is essential to distinguish this entity from other tubulointerstitial processes. All three patients progressed to dialysis dependence & two died, underscoring the grave prognosis of this nephropathy. Notably, renal recovery was absent despite meaningful CgA reduction, suggesting irreversible fibrosis develops before nephrotoxicity is recognized. Earlier identification through routine CgA monitoring and timely biopsy may allow tumor-directed therapy to preserve renal function before irreversible injury occurs.