Abstract: FR-PO0415
Monoclonal IgM-Associated Pseudohypercreatininemia Mimicking Rapidly Progressive Kidney Dysfunction After COVID-19
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
- Shimanaka, Yusuke, Dokkyo Ika Daigaku Nikko Iryo Center, Nikko, Tochigi Prefecture, Japan
- Kawamoto, Shinya, Dokkyo Ika Daigaku Nikko Iryo Center, Nikko, Tochigi Prefecture, Japan
Introduction
Paraprotein-related assay interference is a recognized but underappreciated cause of pseudohypercreatininemia. In the post-COVID era, apparent rapid declines in kidney function may prompt aggressive diagnostic evaluation, including kidney biopsy. We report a case of monoclonal IgM-associated pseudohypercreatininemia that mimicked rapidly progressive kidney dysfunction after COVID-19 infection.
Case Description
A 76-year-old Japanese man developed apparent rapidly progressive kidney dysfunction several months after COVID-19 infection. Plasma creatinine increased progressively from 0.90 to 2.53 mg/dL, with estimated glomerular filtration rate decreasing from 64.5 to 20.3 mL/min/1.73 m2. However, urinalysis showed minimal abnormalities, blood urea nitrogen remained relatively preserved, and cystatin C elevation was disproportionately mild relative to the apparent creatinine-based decline in kidney function. Because COVID-19-associated nephropathy was suspected, kidney biopsy was performed but demonstrated no significant glomerular or tubulointerstitial abnormalities. Histologic findings were inconsistent with the apparent severity of kidney dysfunction. Further evaluation revealed marked discrepancies among creatinine assays. Creatinine concentrations measured using serum samples and high-performance liquid chromatography were near normal, whereas falsely elevated values were observed exclusively in heparinized plasma using a specific enzymatic assay. Serum immunoelectrophoresis identified monoclonal IgM-κ paraproteinemia. Additional analyses performed in collaboration with the assay manufacturer demonstrated precipitation during the enzymatic reaction caused by interaction between monoclonal IgM and heparinized plasma, confirming paraprotein-mediated pseudohypercreatininemia.
Discussion
This case highlights an important diagnostic pitfall in evaluating rapidly progressive kidney dysfunction in the post-COVID era. Discordance between creatinine values and the clinical picture, particularly preserved cystatin C levels, minimal urinary abnormalities, and unremarkable kidney histology, should prompt consideration of paraprotein-related assay interference. Early recognition of pseudohypercreatininemia may prevent unnecessary invasive procedures, including kidney biopsy.