5613391 SUBCLINICAL NEPHROTOXICITY IN PATIENTS WITH BETA-THALASSEMIA: ROLE OF URINARY KIDNEY INJURY MOLECULE

Abstract

Background: Improved survival in thalassemic patients has led to the emergence of previously unrecognized complications, such as renal disease. Aim: We aimed to investigate the role of urinary kidney injury molecule-1 (KIM-1) in detection of subclinical nephrotoxicity in patients with Beta-thalassemia (β-TM) in relation to chelation therapy and to correlate the urinary KIM-1 level with other clinical and laboratory findings. Methods: We conducted a cross-sectional study on 66 thalassemic patients. Their ages range from 7 to 22 years. Routine kidney indices and novel urinary KIM/creatinine ratio (UKIM-1/Cr) were measured. Estimated glomerular filtration rate (eGFR) was calculated. Results: Results indicate that the level of serum creatinine was significantly higher in patients on deferasirox therapy than patients on deferoxamine and deferiprone therapy [median(IQR), 0.85(0.63–0.99), 0.50(0.34–0.58) and 0.44(0.36–0.45)] mg/dL, respectively, p < 0.001]. The median(IQR) level of eGFR was significantly lower in patients on deferasirox therapy than patients on deferoxamine and deferiprone therapy [63.3(56.5–92.1), 117.3(91.9–162) and 136.7(109.4–157.6)] ml/min/1.73 m2, respectively, p < 0.001]. The mean level of UKIM-1/Cr was significantly higher in patients on deferasirox therapy than patients on deferoxamine and deferiprone therapy (7.0 ± 1.9, 4.1 ± 1.7 and 4.2 ± 1.5) ng/mg creatinine, respectively, p < 0.001). Conclusion: We concluded that urinary KIM-1 is an early predictive biomarker for decline in eGFR in patients with β-TM on deferasirox therapy. The appropriate chelation therapy and good monitoring of those patients are intensely needed for early detection of renal dysfunction and timely intervention.