Predictors of Fibrosis Progression in Chronic Active Hepatitis C Related Nephropathy

Background: Hepatitis C virus (HCV) patients have a higher risk of developing renal impairment than health-matched controls. Fibrosis progression in HCV-related nephropathy could be accelerated. The role of angiopoietin 2 (Ang-2) in HCV-related nephropathy and its relationship with platelet parameters and thrombopoietin (TPO) is evaluated in this article. Methods: Three patient groups were selected: HCV without nephropathy (n=90), HCV-related nephropathy (n=90), and controls (n=60). Laboratory analysis included complete blood count to reveal mean platelet volume and platelet distribution width (PDW), albumin creatinine excretion ratio, estimated glomerular filtration rate, and cryoglobulins. Quantitative real-time PCR, serum Ang-2, and TPO by ELISA, abdominal ultrasonography, and liver stiffness measurement by fibroscan were all conducted. Results: Ang-2 was significantly higher in HCV-related nephropathy patients (43.0±36.9 pg/mL) when compared to healthy controls (16.6±4.3 pg/mL) (p=0.001). However, when compared to HCV without nephropathy (30.3±22.9 pg/mL), a statistically insignificant difference was noted (p=0.45). Logistic regression analysis revealed that significant fibrosis in HCV-related nephropathy is independently associated with platelet count (β: 0.98; p=0.000; odds ratio [OR]: 2.7), PDW (β: 0.722; p=0.000; OR: 2.1), serum TPO (β = 1.180; p=0.000; OR: 3.25), liver stiffness measurement by fibroscan (β: 1.29; p=0.000; OR: 3.63), and FIB4 (β: 1.07; p=0.000; OR: 2.9). Conclusion: Ang-2, TPO, PDW, FIB4, and liver stiffness measurement are markers of liver fibrosis and portal hypertension in HCV-related nephropathy.