HCV cirrhotic patients treated with direct-acting antivirals: Detection of tubular dysfunction and resolution after viral clearance

Abstract

Bilotti et al's1 recent excellent report on the prevalence of tubular and glomerular dysfunction in patients with HCV infection on direct-acting antiviral (DAA) agents, and their evolution following HCV clearance adds to recent attempts at exploring the subclinical role of KIM-1 (among other markers of tubular dysfunction) as early biomarkers of tubular damage. Her report showed urinary KIM-1 thresholds (4.7 [3.4-11.3] vs 2.1 [1.0-3.4] ng/mg, P < .001) in patients with tubular injury compared to their normal counterparts. The median KIM-1 threshold for tubular dysfunction in healthy volunteers and across various morbidities within the general population ranged between 0.059 and 2.15 ng/L and 3.5 and 7.1 ng/L respectively.2, 3 The comparatively higher levels of urinary KIM-1 (corrected for creatinine excretion) reported by Bilotti et al is probably attributable to a combination of upregulation of KIM-1 excretion by HCV viral infection itself; additional effect of DAA’s (possibly other drugs such as Cisplatin, Carboplatin and Tenofovir2) and, as yet to be determined, factor(s) associated with polymorphisms of the KIM-1 receptor (Figure1).