Abstract: PUB020
A Case of Masked AKI
Session Information
Category: Trainee Case Report
- 103 AKI: Mechanisms
Authors
- Iyer, Sitalakshmi Jayamani, NYU Langone Health, New York, New York, United States
- Block, Clay A., Dartmouth College Geisel School of Medicine, Hanover, New Hampshire, United States
Introduction
Despite wide recognition of pitfalls, changes in serum creatinine (Cr) and/or a decline in urine output (UO) remain the mainstay of AKI diagnosis. We report a patient whose extremely low Cr and preserved UO demonstrate the problem in reliance on these parameters.
Case Description
57 F was admitted for respiratory failure due to COVID-19. Her management included tocilizumab, mechanical ventilation, vasopressors, ECMO, and antibiotics. On entry she weighed 54kg and Cr was 0.5 mg/dL. After 5 days, Cr nadired at 0.1 then gradually rose to 0.6 where it remained (day 15). Net fluid balance was 20L. By Cr, her eGFR was 110 ml/min/1.73m2 but by cystatin C (CysC) it was 56.
Discussion
AKIN defines AKI by an absolute rise in Cr 0.3mg/dl within 48 hrs, a relative increase 150% of baseline within 1 week, or reduction in UO to <0.5mL/kg/hr for at least 6 hrs.
Cr is a flawed AKI biomarker due to uncertainty of the baseline, variability in rate of generation, and elimination by secretion and filtration. Cr generation falls rapidly with critical illness. The impact of volume expansion resulting in hyperfiltration or hemodilution are underrecognized. Antibiotics, diuretics, glucose, ketones and bilirubin may interfere with measurement. UO too is flawed since oliguria may occur in the absence of AKI due to antidiuretic hormone or conversely, UO may be maintained despite AKI due to osmotic diuresis, failure of tubular function or diuretic use.
The choice of baseline Cr influences our patient’s diagnosis. If 0.5 is chosen, she fails to meet AKIN criteria, but based on nadir Cr, she has severe stage III AKI. AKI can also be demonstrated by adjusting Cr for volume expansion: measured Cr x (initial total body water [TBW] + cumulative fluid gain) ÷ initial TBW = 1.4 in our patient.
Our patient received tube feeds, suffered hyperglycemia resulting in high osmolar load driving an osmotic diuresis. Also, periodic furosemide was given to mitigate her positive fluid balance.
Below normal Cr is generally seen in myopathies, cirrhosis or with drug interference, but hyperfiltration can occur with volume expansion contributing to low Cr. In his case, we believe a baseline small muscle mass, critical illness sarcopenia, and marked volume expansion conspired to mask significant AKI in our patient. Documentation of AKI by measuring CysC led to adjustments in drug dosing.