How To Choose Treatment Plan for Kidney Disease With Hepatitis C
Hepatitis c virus (HCV) infection is common at clinic, and HCV mortality is higher in dialysis and kidney transplantation patients than in the general population. The risk of patients with HCV positive renal transplant recipients and liver failure is higher than in patients with negative HCV. Besides, HCV infection can increase the risk of diabetes and Chronic Kidney Disease (CKD) and the incidence of systemic complications (especially cardiovascular system) increases. Therefore, active management of HCV has important clinical significance for patients with kidney disease.
How does HCV damage the kidneys?
There are two main mechanisms for HCV infection to damage the kidney: immune-mediated tissue damage and virus direct damage.
HCV antigen activates T and B lymphocytes to produce a variety of autoimmune antibodies and cryoprecipitated and non-cryoprecipitated immune complexes. Deposition of immune complexes in the kidney can trigger glomerulonephritis, producing anti-HCV IgG antibodies, anti-endothelial antibodies, and activating complements, leading to glomerular fibrinoid necrosis, followed by inflammatory cell aggregation (e.g, dendritic cells, natural killer [NK] cells, T cells, and B cells), and platelet aggregation. HCV also targets kidney and perinephric B cells, which may be caused by the surface expression of CD81 receptor cells. Capillary lesion can make cryoglobulin enter the lumen and promote the occurrence of glomerular crescent and renal tubule type.
In addition to indirect damage to the kidney, HCV can also directly damage the renal tissue by infecting endothelial cells and renal tubular epithelial cells. Endothelial cell infection can cause apoptosis, while Bowman's cystic epithelial cell infection can cause podocyte injury. HCV can also infect mesangial cells, activate chemokines and affect cell proliferation and apoptosis.
Treatment for CKD with HCV infection
International guidelines recommend that all patients with HCV infection, especially those with HCV infection and CKD, should take treatment to reduce liver and extrahepatic complications (especially renal deterioration and diabetes).
Treatment for HCV infection in stage 1-3 CKD
The trePatients with glomerular filtration rate (eGFR)> 30 ml/min/1.73m2 CKD patients with HCV infection. Depending on the HCV genotype and subtype, these patients are typically treated with a combination of sofosbuvir/velpatasvir, sofosbuvir/ledipasvir, grazoprevir/elbasvir for 8-12 weeks. Patients without cirrhosis can be given pangenotype hepatitis c treatment regimens - sofosbuvir, velpatasvir, voxilaprevir or glecaprevir and pibrentasvir for 8 weeks, and patients with cirrhosis for 12 weeks.
Treatment for HCV infection in stage 4-5 CKD
Although protease inhibitors have limited application in patients with decompensated cirrhosis, they are still an important therapeutic agent for patients with stage 4-5 CKD because they are mainly metabolized by the liver and no dose adjustment is required for patients with stage 4 or 5 CKD. NS5A inhibitors are also metabolized by liver, which is also effective for these patients.
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