SUN-324 Kidney derangements during chronic Hepatitis-C infection – interim results from the HCVKID study

Abstract

Hepatitis C infection is known to cause kidney derangements. HCV-related nephropathy may show different histopathologic patterns and both glomerular and tubulointerstitial damage have been described. Kidney injury may result from immune-mediated tissue damage or from direct effects of HCV and other, yet unknown mechanisms may be involved. HCV-related nephropathy may appear at any time during the natural history of HCV infection. Objective of the prospective, observational HCVKID-study is to assess the prevalence of renal manifestations among patients suffering from chronic HCV in Finland cross-sectionally, complemented by long-term analysis to identify changes from baseline. Assessments of renal variables are made at baseline and one year after the eradication treatment. HCV-negative control group is enrolled by an occupational healthcare provider and will be used for comparisons between HCV-positive and HCV-negative groups. This analysis compares baseline characteristics between HCV-positive patients with renal manifestations and HCV-positive patients without renal manifestations. The outcome of interest, renal deterioration, is evaluated using urine and blood testing. Baseline data includes clinical and treatment characteristics. For this analysis, 145 HCV-PCR-positive male and female patients (≥ 18 years old) were eligible for the study. Exclusion criteria were HIV or Hepatitis B positivity and other underlying diseases that may influence kidney function and had emerged before the transmission of HCV. Renal manifestation was stated if s-creatinine was > 100 µmol/l in male or > 90 µmol/l in female or eGFR < 60 ml/min/1.73m2 or spot urine analysis revealed hematuria (u-erythrocytes ≥ 20 x10(E6)/l), tubular proteinuria (u -A1Miglo ≥ 12 mg/l) or glomerular proteinuria (u-AlbCrea in men ≥ 2.5 mg/mmol, in women ≥ 3.5 mg/mmol). Prevalence of any renal finding was 15.2 %. Baseline characteristics between HCV-positive patients with and without renal manifestations did not differ significantly (Table 1). HCV-genotype profile was significantly different in patients with renal manifestations, genotype 3 being the most usual genotype. Route of infection, stage of fibrosis, estimated time since HCV-transmission or viral load did not differ significantly (Table 2). Basic laboratory tests showed no significant differences (Table 3). Dipstick proteinuria and hematuria were more common in renal manifestation group as could be expected. The most common renal manifestation was tubular proteinuria (p<0.0001 vs. without renal manifestations). The amount of glomerular proteinuria was not statistically different between those with renal manifestations and those without. The level of proteinuria did not generally exceed the level necessitating kidney biopsy. Serum creatinine was not different between the groups, but eGFR was significantly less in those with renal manifestations. Serum cystatin-C was statistically higher in males with renal manifestation (Table 4). Tubular proteinuria marker was deranged reflecting renal lesions due to tubulointerstitial damage. It may be postulated that HCV could infect several renal cell types including also renal tubular cells. Tubular cell damage may even be the earliest sign of renal dysfunction caused by HCV and warrants testing when HCV patients are being evaluated.