Kidney Week

Abstract: PUB016

Biopsy-Proven Osmotic Tubulopathy Presenting as AKI Within Hours of Low-Osmolar Contrast Exposure: A Case Report

Session Information

• Publication Only

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Randhawa, Aaronbir Singh, Weill Cornell Medicine, New York, New York, United States

Aaronbir Singh Randhawa, MBBS

• Yehounatan, Matania, Weill Cornell Medicine, New York, New York, United States

Matania Yehounatan, MD

• Yang, Yihe, Weill Cornell Medicine, New York, New York, United States

Yihe Yang, MD, MS

• Choi, Mary E., Weill Cornell Medicine, New York, New York, United States

Mary E. Choi, MD

Introduction

Contrast associated AKI remains a common hospital complication, traditionally defined by a creatinine rise within 24-48 hours of iodinated contrast exposure via vasoconstriction, medullary hypoxia and tubular toxicity. Osmotic tubulopathy proximal tubular vacuolization from osmotically active substances has been documented primarily with high osmolality agents. Its occurrence with low osmolar contrast and potential for earlier onset remain poorly characterized.

Case Description

A 33 year old woman with type 2 diabetes, CKD stage 3a, and nephrotic range proteinuria developed AKI shortly after receiving iohexol (Omnipaque ~672 mOsm/kg) for diagnostic imaging. Serum creatinine rose from 1.37 mg/dL to 1.85 mg/dL within hours of contrast exposure, peaking at 4.7 mg/dL by day six. Serologic workup for immune mediated and paraprotein related etiologies along with other diagnostic tests were negative. Kidney biopsy performed demonstrated advanced diabetic nephropathy with extensive proximal tubular vacuolization consistent with osmotic tubulopathy. Prior reports of osmotic nephrosis have predominantly involved agents of significantly higher osmolality; this case demonstrates biopsy proven osmotic tubular injury with low osmolar contrast media. The patient was managed supportively with diuresis and albumin infusions, with creatinine improving to 2.3 mg/dL at follow-up.

Discussion

This case highlights two important considerations: first, that contrast associated osmotic tubulopathy may present much earlier than the traditionally described 24-48 hour window and second, that even low osmolar contrast agents can induce biopsy proven osmotic tubular injury in susceptible patients supporting management decisions.

A-C: Light microscopy
D: Tubular vacuolization (EM)
E-F: IgG, kappa, lambda (IF)