Visceral leishmaniasis‐associated nephropathy in hospitalised Brazilian patients: new insights based on kidney injury biomarkers

Objective To evaluate the usefulness of early acute kidney injury (AKI) biomarkers in clinical management of visceral leishmaniasis. Methods Prospective study with 50 hospitalised VL patients. AKI biomarkers, that is, serum and urinary neutrophil gelatinase‐associated lipocalin (sNGAL, uNGAL, respectively), urinary kidney injury molecule‐1 (uKIM‐1) and urinary monocyte chemotactic protein‐1 (uMCP‐1), were quantified by immunoassay (ELISA). Also, interferon‐gamma (INF‐y) and C‐reactive protein (CRP) were evaluated as inflammatory biomarkers possibly related to VL severity. Results VL patients had hyponatremia, hypoalbuminemia, hypergammaglobulinemia, haematologic and hepatic disorders. AKI was found in 46%, and one death (2%) occurred. The AKI group had significant longer hospital stay, lower levels of IFN‐y and higher levels of CRP, more clinical renal abnormalities and higher levels of sNGAL, uNGAL, uKIM‐1 and uMCP‐1. Overall, sNGAL, uKIM‐1 and uMCP‐1 showed correlations with important clinical renal abnormalities, such as proteinuria, albuminuria, serum creatinine and glomerular filtration rate using adjusted correlations with CRP and IFN‐y. Only sNGAL showed an early association with AKI development (OR = 2.78, 95% CI = 1.429–5.428, per each increase of 50 ng/ml), even after adjusting for clinical signals of VL severity and for immune biomarkers. Moreover, sNGAL showed a better performance in predicting AKI development (AUC‐ROC = 0.81, 95% CI = 0.69–0.93; cut‐off = 154 ng/ml, sensitivity = 82.6%, specificity = 74.1%, P