From a recent review:
The most common histopathologic presentation of HBV-GN is HBV-associated membranous nephropathy, which usually manifests clinically with varying grades of proteinuria and microscopic hematuria. The pathogenesis is likely to be immune complex mediated; however, other host and viral factors have been implicated. The treatment of HBV-GN revolves around antiviral therapy. Various histologic types of glomerular diseases are reported in association with HCV infection, the most frequent being Type 1 membranoproliferative glomerulonephritis, usually in the context of Type 2 mixed cryoglobulinemia. The pathogenesis of HCV-GN can be attributed to glomerular deposition of cryoglobulins or noncryoglobulin-immune complexes. Cryoglobulins typically comprised immunoglobulin Mκ with rheumatoid factor activity. Clinically, patients may present with proteinuria, microscopic hematuria, hypertension, and acute nephritic and/or nephrotic syndrome. The treatment of HCV-GN, especially cryoglobulinemic membranoproliferative glomerulonephritis, encompasses various options including contemporary antiviral therapy with or without conventional and novel immunomodulatory agents.
Mentioned in the body of the paper are several other glomerular diseases that have been associated with hep B as well as polyarteritis nodosa which, though not a cause of glomerulonephritis, can cause renal damage as part of the vasculitis.