Abstract: FR-PO0414
An Unusual Discordance Between Cystatin C and Serum Creatinine in a Patient with Postrenal AKI
Session Information
- AKI: Biomarkers, Diagnostics, and Risk Prediction
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
- Lundberg, Evan Peter, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
- Lloyd, Granville Llewellyn, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
- Jani, Alkesh, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
Introduction
Serum Cystatin C (CysC) is a widely used biomarker alongside serum creatinine (sCr) for estimating kidney function. Prior studies suggest that CysC may detect injury sooner than sCr, enabling earlier diagnosis and intervention in acute kidney injury (AKI). We present an unusual case illustrating persistent discordance between sCr and CysC in evolving postrenal AKI.
Case Description
A 62-year-old male with stable metastatic prostate cancer presented with painless gross hematuria and clot passage. Initial sCr was 2.17 mg/dL (baseline 0.9) with mildly elevated CysC of 1.06 mg/L. Despite Foley placement with continuous bladder irrigation and daily urine output >0.5 mL/kg/h, sCr rose to 8.21 mg/dL with evidence of kidney failure including hyponatremia, hyperkalemia, uremia, and volume overload. During this time, CysC remained near baseline (0.87-1.08 mg/L). Imaging showed mild bilateral hydronephrosis. Cystoscopy revealed distorted bladder anatomy with inability to visualize the ureteral orifices. Following bilateral percutaneous nephrostomy tubes and ureteral stenting, rapid renal recovery occurred with postobstructive diuresis and sCr returning to baseline by discharge.
Discussion
Unlike creatinine, CysC is metabolized in the proximal tubule, and persistent metabolism despite impaired urinary drainage may partially explain the stable CysC levels observed in our patient. In contrast to postrenal AKI, proximal tubular injury in intrinsic AKI may limit CysC metabolism, while reduced renal blood flow and filtration in prerenal AKI may limit delivery of CysC to the proximal tubule, leading to increased CysC levels. This case illustrates persistent discordance between sCr and CysC in evolving postrenal AKI, suggesting that CysC may underestimate the severity of obstruction in certain clinical contexts. It also highlights that urine output can persist despite bilateral obstruction severe enough to cause severe AKI.