SuPAR, an emerging biomarker in acute kidney injury in ICU patients
1 Military Medical Academy.
2 Department of microbiology and Immunology, Faculty of Medicine, Al-Azhar university, girls.
3 R & D Consultant for Armed Forces Pharmaceutical Factory.
4 R & D Consultant for PANAX Pharma - Egyptian Pharmaceutical Company.
Research Article
GSC Biological and Pharmaceutical Sciences, 2025, 30(01), 065-077.
Article DOI: 10.30574/gscbps.2025.30.1.0485
Publication history:
Received on 11 November 2024; revised on 22 December 2024; accepted on 25 December 2024
Abstract:
Acute kidney injury (AKI) is a critical condition with delayed diagnosis when relying solely on plasma creatinine levels. This study investigates the role of soluble urokinase plasminogen activator receptor (SuPAR) as a biomarker for early prediction of AKI in ICU patients. Results from a prospective observational study of 30 patients indicate that elevated SuPAR levels at 24- and 48-hours post-ICU admission strongly correlate with the incidence of AKI, demonstrating superior predictive power compared to traditional markers. These findings suggest that SuPAR measurements could be instrumental in the early detection and management of AKI, potentially improving patient outcomes. The mean age of participants was 51.13 ± 5.61 years; 60% were male. Hypertension (HTN) was the most prevalent comorbidity (43.3%), and the mortality rate was 30% in the entire cohort. No significant differences in age, gender, or medical history were found between AKI and control groups. SuPAR levels were significantly elevated in the AKI group across all time points. At 48 hours, AKI cases had SuPAR levels of 7.25 ng/dL compared to 5.3 ng/dL in controls (p < 0.001). A strong positive correlation was observed between suPAR levels and serum creatinine at 24 hours (r = 0.62, p < 0.001) and 48 hours (r = 0.678, p < 0.001). suPAR showed potential as a predictive biomarker for AKI progression. Mortality was higher in the AKI group (45.45%) compared to controls (21.05%), but the difference was not statistically significant (p = 0.225). The BUN increased from 8.49 mmol/L at 12 hours to 9.21 mmol/L at 48 hours. Serum suPAR levels rose from 5.14 ng/dL to 6.01 ng/dL during the 48-hour interval. No significant differences were identified between the control and AKI groups for age, gender, or medical history. No significant difference was seen between the groups concerning TLC and PLT levels at different time periods. BUN levels were markedly elevated in the AKI group relative to the control group at all time intervals, with the most pronounced disparity after 48 hours (10.93 vs. 8.21 mmol/L), yielding p-values of 0.007, 0.006, and 0.005 after 12, 24, and 48 hours, respectively. Serum creatinine levels were markedly elevated in the AKI group relative to controls at all time intervals. At 12 hours, creatinine levels in the AKI group were 1.22 mg/dL, but in the control group they were 0.85 mg/dL (p<0.001). suPAR levels were markedly increased in AKI sufferers relative to controls at all time intervals. At 12 hours, AKI cases exhibited suPAR levels of 5.67 ng/dL compared to 4.84 ng/dL in controls (p-value = 0.008). The disparity escalated after 48 hours, with AKI cases exhibiting 7.25 ng/dL in contrast to 5.3 ng/dL in controls (p-value <0.001).
Keywords:
SuPAR; Acute kidney injury (AKI); Serum creatinine; ICU patients
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