Cystatin C May Predict Outcomes in AKI and Liver Cirrhosis
In patients hospitalized with acute kidney injury (AKI) and liver cirrhosis, higher levels of peak serum cystatin C were associated with an increased risk for inhospital mortality, whereas lower baseline levels of the biomarker predicted better odds of renal recovery.
METHODOLOGY:
Cystatin C, a 13-kDa nonglycosylated protein produced by all nucleated cells, has been reported as an early predictor of AKI development in patients with liver cirrhosis; however, little is known about its role in predicting AKI recovery in this population.
Researchers conducted a retrospective cohort study to investigate whether serum levels of cystatin C could predict kidney function recovery and mortality in adults with liver cirrhosis and AKI (N = 209; 97 women; mean age, 56 years) hospitalized between May 2017 and May 2023.
Serum creatinine and cystatin C were measured within 7 days of admission, with the peak cystatin C level corresponding to the values taken on the same day as peak creatinine level; medical history and data on admission laboratory parameters were also retrieved.
Outcomes included inhospital mortality, renal recovery, length of hospital stay, and the need for renal replacement therapy. Complete renal recovery was defined as serum creatinine levels returning to within 50% above baseline, and partial renal recovery was defined as discharge without the need for renal replacement therapy but not meeting the complete recovery criteria.
TAKEAWAY:
Overall, 31% of patients died during hospital admission, 34.9% achieved complete renal recovery, and 30.1% achieved partial renal recovery.
Higher peak level of serum cystatin C emerged as a significant predictor of inhospital mortality (odds ratio [OR], 2.808; P ≤ .001); other predictors were serum albumin level (OR, 0.364; P = .013) and white blood cell count (OR, 1.085; P = .021).
Lower baseline serum levels of cystatin C predicted renal recovery (OR, 0.446; P ≤ .001); other predictors were hypertension, along with higher serum albumin, and baseline serum creatinine levels (P < .05 for all).
A peak serum cystatin C threshold of 2.77 mg/L predicted inhospital mortality with 79% sensitivity and 62% specificity, whereas a baseline threshold of 2.62 mg/L predicted renal recovery with 65% sensitivity and 64% specificity.
IN PRACTICE:
'Integrating serum cystatin C assessment into the management of AKI patients can help identify those with elevated levels who may benefit from targeted medical interventions to improve their outcomes,' the authors of the study wrote.
SOURCE:
This study was led by Eman Nagy, Mansoura University, Mansoura, Egypt. It was published online in BMC Nephrology.
LIMITATIONS:
This study was retrospective and conducted at a single center. Improvement of kidney function was defined only by serum creatinine levels without considering urine output. The causes of AKI or underlying etiology of liver cirrhosis were unknown.
DISCLOSURES:
This study did not receive any specific funding. The authors declared having no competing interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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