RENAL DISEASE ASSOCIATED WITH HEPATITIS C VIRUS INFECTION

RENAL DISEASE ASSOCIATED WITH HEPATITIS C VIRUS INFECTION

 

RENAL DISEASE ASSOCIATED WITH HEPATITIS C VIRUS INFECTION

 

There’s a strong & possibly causal relation between chronic hepatitis C viral infection (HCV) and the evolution of glomerular diseases. Major glomerular lesions highly related to HCV infection may include:

1)    Mixed cryoglobulinemia syndrome  

2)    Membranous nephropathy (MN).

3)    Polyarteritis nodosa (PAN)  

 

All ptns with mixed cryoglobulinemia syndrome, membranoproliferative GN (MPGN) type I, MN (membranous nephropathy), & PAN should be rigorously evaluated for the possibility of the presence of an underlying HCV infection. Furthermore, HCV-infected ptns should be thoroughly investigated for proteinuria, haematuria, HT, and a decline glomerular filtration rate (GFR). Ptns presented with renal functional alterations should undergo lab testing for cryoglobulins, hypocomplementemia, as well as a +ve rheumatoid factor. A kidney biopsy should be regulated in view of the presence of significant proteinuria and/or diminished kidney function. Generally, ptns with severe & progressive HCV-related GN should commence antiviral therapy. Most ptns with less severe glomerular disease observed with HCV should also start antiviral therapy in condition that they do not have decompensated cirrhosis. In ptns who are selected for antiviral therapy, its specific protocol primarily relies upon the estimated GFR (eGFR).

 

Mixed cryoglobulinemia syndrome (MCS):  a systemic vasculitis. Ptns typically show {nonsp. systemic Sms, palpable purpura, arthralgia, fever, neuropathy, etc}. Clinical features of renal disease may include haematuria, proteinuria (may be nephrotic range), + renal dysfunction. Lab studies show: {low C + circulating cryoglobulins (CG)}. Complement (C) components, C3, C4, & C1q, are typically low; lowering in C4 is usually greater than that in C3. CG are mostly type II, characterized by polyclonal IgG & IgM kappa RF directed against Fc portion of IgG. Most ptns with MCS hv HCV infection, & there’s strong evidence that HCV-containing immune complexes are directly involved in MCS pathogenesis. HCV RNA & HCV IgG Ag-AB complex is highly concentrated in the cryoppt. Moreover, HCV Ags have been detected along glomerular capillary wall & in the mesangium of ptns with HCV-related GN, mainly in those with MPGN & +ve HCV RNA. Despite HCV is primarily correlated with type II MCS, it may also be responsible for some cases of type III MCS. Type III CG is characterized by CG comprised of polyclonal IgG & polyclonal IgM. kidney biopsy: glomerular infiltration by activated macrophages. Glomerular basement membrane (GBM) shows double contours caused by interposition of monocytes between GBM & endothelium. Subendothelial deposits of IgM, IgG & C components are seen by IF & EM.

 

Membranoproliferative GN without cryoglobulins: The relation of HCV infection and MPGN type I in the absence of CG is debatable. Despite such ptns have been reported, most of these ptns eventually developed measurable CG, although not certainly in conjugation with extrarenal manifestations of cryoglobulinemia. Circulating CG are usually difficult to detect, and cryoglobulinemia may be undetectable.

 

Membranous nephropathy: It’s not certain there’s a clear relation between MN & HCV infection. Many small reports- although conflicting- have suggested: MN may be induced by chronic HCV infection. One report: MN was significantly prevalent in HCV-+ve as compared to HCV-negative KTx ptns. These findings suggest but do not approve a possible relation of👉 HCV in MN evolution. However, in contrary to in MCS or MPGN, C levels tend to be normal, & neither CG nor RF is present in HCV-related MN.

 

Polyarteritis nodosa: PAN is well reported with HBV infection, but it also seen in HCV ptns in absence of CG. Certain series: 161 ptns with HCV-related vasculitis, 31 (19 %) were diagnosed with PAN that’s called secondary PAN. Ptns infected with HCV who develop PAN may have more intense systemic manifestations of vasculitis as compared to those HCV ptns with MCS vasculitis. In the study cited above, compared with ptns with HCV-related MCS, HCV-related PAN is more commonly show fever, weight loss, HT, GIT affection, severe mononeuropathy, & higher CRP levels.