Kidney Week

Abstract: FR-PO0474

De Novo Sarcoidosis After Liver Transplantation Presenting as Acute Tubular Necrosis: A Case Report

Session Information

• AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Mekki, Ossama, University of Utah Health, Salt Lake City, Utah, United States

Ossama Mekki, MD

• Awadallah, Mina, University of Utah Health, Salt Lake City, Utah, United States

Mina Awadallah, MD

• Ibrahim, Abdelrahman, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Abdelrahman Ibrahim, MD, MBChB

• Abuelsamen, Tamer, University of Utah Health, Salt Lake City, Utah, United States

Tamer Abuelsamen, MD

• Sameh, Ahmed, University of Utah Health, Salt Lake City, Utah, United States

Ahmed Sameh, MD, MBChB

• Khalil, Menatallah Y., Alexandria University, Alexandria, Alexandria Governorate, Egypt

Menatallah Y. Khalil, MD, MBChB

• Hinckley, Mckinnon, University of Utah Health, Salt Lake City, Utah, United States

Mckinnon Hinckley

Introduction

De novo sarcoidosis following liver transplantation is rare, and its renal involvement is classically described as granulomatous interstitial nephritis (GIN). We report a distinct and underrecognized renal phenotype: severe acute kidney injury (AKI) driven by hypercalcemia-induced acute tubular necrosis (ATN) with no granulomas identified on kidney biopsy in a liver transplant recipient with de novo sarcoidosis.

Case Description

A 41-year-old woman developed progressive AKI (creatinine 1.91→5.29 mg/dL) four months after liver transplantation for alcohol-related cirrhosis. She presented with hypercalcemia (Ca 10.7–11.9 mg/dL), suppressed PTH (7 pg/mL), elevated 1,25-OH-D (89 pg/mL), polyarthralgia, and malaise. Urinalysis was bland. PET imaging demonstrated hypermetabolic mediastinal, hilar, and retroperitoneal lymphadenopathy initially concerning for PTLD. Endobronchial ultrasound-guided lymph node biopsy revealed non-necrotizing granulomatous inflammation without malignancy or infection; ACE was 106–113 U/L. Extensive infectious workup — including BK, CMV, EBV, fungal, AFB cultures, and zoonotic serologies — was negative. Renal biopsy showed marked ATN with tubular and interstitial calcium phosphate deposits and pigmented casts (iron/myoglobin-negative), without granulomas or immune deposits by immunofluorescence or electron microscopy. AKI improved with corticosteroids, supportive care and hypercalcemia management.

Discussion

In sarcoidosis, activated granuloma macrophages drive autonomous 1-alpha-hydroxylation of vitamin D, producing excess 1,25-OH-D independent of PTH — the biochemical signature confirmed in this case. Sustained hypercalcemia causes AKI through tubular calcium deposition, renal vasoconstriction, and impaired urinary concentrating ability, producing ATN without glomerular or interstitial inflammation. This explains the characteristic bland urinalysis despite severe AKI. Granulomas need not infiltrate the kidney itself to cause significant renal injury; the systemic metabolic consequence of extrarenal granulomatous disease is sufficient. This non-GIN phenotype of sarcoidosis-associated nephropathy is likely underrecognized, particularly in the post-transplant setting where PTLD and CNI toxicity dominate the differential.