scholarly journals Lower Rates Of Naturally Occurring Resistance-Associated Substitutions (RASs) In Hepatitis C Virus (HCV)-Infected Chronic Kidney Disease (CKD) Patients Than In HCV-Infected Patients With Only Liver Disease

2019 ◽  
Vol Volume 12 ◽  
pp. 3635-3640
Author(s):  
Ekta Gupta ◽  
Manish Chandra Choudhary ◽  
Nimisha Upadhyay ◽  
Gaurav Singh ◽  
Suman lata Nayak ◽  
...  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Abraham Cohen-Bucay ◽  
Jean M. Francis ◽  
Craig E. Gordon

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Fabrizio Fabrizi ◽  
Piergiorgio Messa ◽  
Paul Martin

The 2011 report of the World Health Organization General Assembly on noncommunicable diseases identified chronic kidney disease as a worldwide health issue posing a heavy economic burden. Hepatitis C virus infection, which is responsible for over 1 million deaths resulting from cirrhosis and liver cancer, is linked to chronic kidney disease in several ways; some forms of renal disease are precipitated by hepatitis C and patients with end-stage chronic renal disease are at increased risk for acquiring HCV. The aim of this review is to update the evidence on the relationship between hepatitis C infection and chronic kidney disease. Information has been accumulated in the last decade indicating that HCV plays an adverse effect on the incidence and progression of chronic kidney disease; a novel meta-analysis of observational studies (seven longitudinal studies; 890,560 unique individuals) found a relationship between hepatitis C seropositivity and incidence of reduced estimated glomerular filtration rate (adjusted relative risk, 1.70; 95% CI, 1.20; 2.39; P=0.002) in the adult general population. In addition to conventional risk factors, hepatitis C may be an additional factor for the development of chronic kidney disease, and an atheromasic activity of hepatitis C virus has been mentioned. The link between hepatitis C and atherosclerosis could also explain the excess risk of cardiovascular mortality that has been observed among hepatitis C virus seropositive patients undergoing maintenance dialysis. A number of biologically plausible mechanisms related to hepatitis C virus have been hypothesized to contribute to atherosclerosis. Implementation of effective treatment intervention towards hepatitis C is required to decrease the healthcare burden of hepatitis C and to prevent the progression of chronic renal disease.


QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Magdy M El Sharkawy ◽  
Lina E Khedr ◽  
Ashraf H Abdelmbdy ◽  
Mohamed T Mohamed

Abstract Background Anemia is a severe complication of chronic kidney disease (CKD) that is seen in more than 80% of patients with impaired renal function. Although there are many mechanisms involved in the pathogenesis of anemia of renal disease, the primary cause is the inadequate production of erythropoietin by the damaged kidneys. Aim of the work to assess hepcidin level in non dialysis patients (CKD stage 4 &5) treated from Hepatitis C virus and its relation to iron parameters. Patients and Methods This study was conducted on 20 CKD patients (stage 4 and 5) treated from hepatitis C virus. All candidates included in this study subjected to careful history taking, full clinical examination and investigations (including complete blood count, renal chemistry, HCVAb, serum iron, total iron binding capacity, TSAT%, ferritin and hsCRP. Serum hepcidin was analyzed by ELISA technique. Results Serum hepcidin was 26.35±7.26; 40% in stage III, 37.8% in stage IV and 22.2% in stage V. There was statistically significant difference between GFR stages according to Hb., Drug intake ACE inhibitor/ARB, Plt., Creatinine, BUN, Iron, TIBC, Ferritin, T SAT%, CRP and Serum Hepcidin. We showed significant correlations between serum hepcidin and TIC, Iron, TIBC, Ferritin and TSAT%. Conclusion Median hepcidin value is elevated in nondialysis CKD patients due to increased inflammation and decreased clearance of hepcidin. Furthermore, iron status modifies serum hepcidin level and its association with Hb. Increased hepcidin level leads to iron-restricted erythropoiesis and recombinant human EPO (rhEPO) resistance by inhibiting iron absorption from gut and iron recycling from macrophages. Hence, elevated hepcidin can predict need for parenteral iron to overcome hepcidin-mediated iron-restricted erythropoiesis and need for relatively higher rhEPO doses to suppress hepcidin.


2011 ◽  
Vol 20 (4) ◽  
pp. 326-330 ◽  
Author(s):  
Jonathan N. Hofmann ◽  
Anna Törner ◽  
Wong-Ho Chow ◽  
Weimin Ye ◽  
Mark P. Purdue ◽  
...  

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