Is HBV glomerular disease treatable

Is HBV glomerular disease treatable?

The immune complexes in all HBV kidney lesions require active viral replication, so the primary goal of therapy is to treat the source of the antigens: the active HBV. Lamivudine can suppress the viral load but needs to be continued indefinitely to maintain a sustained viral response. Patients experiencing a complete suppression of viral replication have a remission of MN with normalization of their proteinuria, improved kidney function, and a prolonged kidney survival. Unfortunately, as many as 50% of patients develop resistance to lamivudine and have a relapse of viremia. Current guidelines recommend entecavir as the primary agent for treatment of active hepatitis B antigenemia. For MN, this is the only therapy that is needed along with the typical antiproteinuria therapy, such as angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. No immunosuppression is recommended, although short-term immunosuppression may be used in severe cases of nephrotic syndrome with only a transient increase in systemic viremia.

For patients with MPGN, the data are not as clear; however, theoretically, control of viremia would be essential. Again, the use of steroids or other immunosuppressant agents are not efficacious in the treatment of this lesion. IgA nephropathy, as mentioned, is rarely clinically important, and the IgA deposits are a result of advanced liver disease; unless liver function improves, there will be a continuous presence of IgA in the kidney. If the IgA is directly related to active HBV, then antiviral therapy could lead to a stabilization of kidney function.

PAN is a systemic vasculitis that causes life-threatening widespread organ dysfunction. It results from HBV immune complexes, so once again, control of viremia is essential. However, if there is significant systemic vasculitis, then a temporary use of steroids and even immunosuppressive therapy may be needed. The risks of this option would be a further increase (temporarily) in the hepatitis B viral load at the expense of reducing end-organ damage. This decision must be weighed carefully based on the severity of the vasculitis.

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