Published on July 13, 2014

Author: mohammed.abdelsattar



VIRAL HEPATITIS-ASSOCIATED GLOMERULONEPHRITIS: VIRAL HEPATITIS-ASSOCIATED GLOMERULONEPHRITIS PowerPoint Presentation: In cirrhosis Creatine production in the liver will then be significantly reduced this will lead to a lower muscle mass and a lower serum Creatinine PowerPoint Presentation: The typical serum creatinine is usually 0.5 to 0.6 mg/ dL in patients with cirrhosis chronic hepatitis B: chronic hepatitis B common nephropathies are described : membranous GN MCGN polyarteritis nodosa membranous nephropathy : membranous nephropathy most common glomerular pathology seen with active hepatitis B antigenemia is membranous nephropathy (MN ) membranous nephropathy : membranous nephropathy This lesion is a result of the deposition of immune complexes in the basement membrane of the glomerulus, specifically in the subepithelial space size of the immune complex is very small pass through the basement membrane and end up on the outside of the capillary underneath the podocyte foot processes ( subepithelial space) PowerPoint Presentation: The only immune complex from hepatitis B that can do this is the hepatitis B e Ag-antibody complex . Therefore , the vast majority of patients with chronic hepatitis B antigenemia who develop MN are also positive for the hepatitis B e antigen Mesangiocapillary glomerulonephritis: Mesangiocapillary glomerulonephritis Immune complexes involving HBsAg are too large to traverse the basement membrane so settle in the subendothelial space presenting with i ncrease BP, heavy proteinuria , microhaematuria , and progressive CKD (i.e. a more nephritic presentation than MN) Polyarteritis nodosa: Polyarteritis nodosa Occurs within 4 months of HBV infection in adults, presenting as a medium-vessel vasculitis attributed to immune complex deposition ANCA – ve . Relapse never once viral replication has stopped/ seroconversion has occurred. PowerPoint Presentation: These patients can also develop IgA nephropathy , and focal segmental glomerulosclerosis (FSGS). ttt: ttt primary goal of therapy is to directly treat the source of the antigens—the hepatitis B virus . Initially , lamivudine was the treatment of choice for suppressing the viral load Treatment of HBV-related liver disease: Treatment of HBV-related liver disease when HBV DNA levels are above 2,000IU/mL Serum ALT is above the upper limit of normal with evidence of active liver inflammation or fibrosis . ttt: ttt Interferon alfa 5 million U x 6/week or 10 million U x 3/week SC for 4 months leads to undetectable HBV DNA levels and HBeAg clearance in 30 – 40%. 5 – 10% of patients relapse after treatment. PowerPoint Presentation: Peginterferon alfa A 48-week regimen has similar efficacy to interferon alfa . Peginterferon alfa 2a has an more half-life and a more stable plasma concentration, Allowing fewer injections and better patien t tolerability PowerPoint Presentation: Nucleoside/nucleotide analogues Associated with lower rates of HBe and HBs seroconversion . Most evidence for extra-hepatic manifestations lies with lamivudine Usual dose 100mg PO daily, but dose reductions for d erease GFR PowerPoint Presentation: No steroids or other forms of immunosuppression are needed and these agents may actually worsen the prognosis by increasing viremia . chronic hepatitis C: chronic hepatitis C The most common histologic change in the glomerulus of patients with chronic hepatitis C Infection is type I membranoproliferative glomerulonephritis as a consequence of type II cryoglobulinemia PowerPoint Presentation: These patients may also develop membranous nephropathy Fibrillary glomerulonephritis IgA nephropathy diabetic nephropathy Other HCV-related glomerulopathies: Other HCV-related glomerulopathies Non- cryoglobuminaemic MCGN occurs . It will still be associated with HCV antibodies and HCV RNA . HCV-associated PAN is well described type I MPGN as a consequence of type II cryoglobulinemia: type I MPGN as a consequence of type II cryoglobulinemia Hepatitis C results in the unique production of cryoglobulins that deposit in the kidney leading to MPGN The cryoglobulins in hepatitis C are so large that they can not filter through the basement membrane, thereby becoming trapped in the subendothelial Space PowerPoint Presentation: MN would typically cause only the nephrotic syndrome whereas MPGN would be accompanied by the nephritic syndrome with an “active” urinary sediment showing red cells casts, granular casts, dysmorphic red cells, and renal tubular epithelial cells PowerPoint Presentation: Hepatitis B is a hepatotropic virus , meaning it selectively enters hepatic tissue but no other organ tissue Hepatitis C is not only hepatotropic , but it is lymphotropic , having an affinity to bind to select receptors on B cell PowerPoint Presentation: S0 Over time, patients with hepatitis C who have cryoglobulinemia are at higher risk for the development of B-cell lymphoma PowerPoint Presentation: A positive rheumatoid factor assay coupled with a low C3 and C4 is typical of active cryoglobulinemia . treatment for MPGN in hepatitis C: treatment for MPGN in hepatitis C the only effective therapy for hepatitis C is the use of interferon with or without adjunctive ribavirin However Ribavirin is not recommended if GFR <50 ml/min PowerPoint Presentation: KDIGO guidelines for HCV treatment in CKD: - CKD stages 1 and 2 : peginterferon and ribavirin - CKD stages 3 and 4 : peginterferon monotherapy - HD : standard interferon alpha PowerPoint Presentation: In certain circumstances, additional, more aggressive immunosuppressive therapy may be warranted in hepatitis C-related MPGN . These exceptions include the following : (1) a rapid decline of renal function with biopsy evidence of crescentic changes (2) systemic vasculitis with life-threatening organ dysfunction PowerPoint Presentation: Corticosteroids : Given as pulsed methylprednisolone 0.5- 1 gm IV for 3 days then oral Cyclophosphamide: 1.5-2 mg/kg daily oral for 2-4 months PowerPoint Presentation: Plasmapheresis : has become the treatment of choice for severe cases of cryoglobulinemia and will effectively remove these immune complexes from the circulation 3 times per week for 2-3 weeks to remove cryoglobulins PowerPoint Presentation: In addition to the lymphotropic effect of hepatitis C, this virus also appears to bind to b islet cells . The interaction of the virus surface antigens with b islet cells in the pancreas initiates a sequence of events that leads to islet dysfunction and secondary diabetes. PowerPoint Presentation: The treatment of diabetic nephropathy in patients with hepatitis C is similar to that of diabetic nephropathy in the general population and includes inhibition of the renin-angiotensin-aldosterone system (RAAS ) anti-hypertension control strict glucose control PowerPoint Presentation: Differentiating hepatitis B or C glomerulonephritis from HRS can be done using routine laboratory and urinalysis tests PowerPoint Presentation: Is there proteinuria Patients with HRS by definition have to have 500 mg of protein excretion in 24 hours patients with either hepatitis B– or C –related glomerulonephritis where the nephrotic syndrome is common PowerPoint Presentation: What does the urine sediment show In patients with HRS , the urine sediment is bland with no cells or casts . In hepatitis C MPGN , the urine will be nephritic with red cell casts, dysmorphic red blood cells, white blood cells, and renal tubular epithelial cells hepatitis B MN the urine will be nephrotic with fatty casts and oval fat bodies. PowerPoint Presentation: What about serum complement levels In hepatitis C MPGN the levels of C3 and C4 will be very low , indicating active consumption by the cryoglobulins , and the rheumatoid factor will be elevated . For hepatitis B MN and HRS, the serum complement levels and rheumatoid factor will all be within normal limits PowerPoint Presentation: THANKS

Related presentations

Other presentations created by mohammed.abdelsattar

03. 05. 2014