Evidence suggested that hepatitis B surface antigen (HBs Ag) forms immune complex with its antibody (anti-HBs) in the circulation, and the soluble HBs Ag-antibody immune complex plays a major role in the pathogenesis of rashes and arthritis resembling acute serum sickness seen in the early stage of type B acute hepatitis. It has also been reported that glomerulonephritis, together with vasculitis, can be associated in viral hepatitis with chronic persistent antigenemia by the pathogenetic role of soluble immune complex formation, i.e. HBs Ag-antibody-C´3, in the circulation.
The occurrence of HBs Ag among healthy populations and the incidence of acute and chronic liver disease was reported high in Korea. It is then intended in this report to appraise glomerular damage in chronic liver diseases with persistent antigenemia in this country.
Among 111 patients with chronic active hepatitis (CAH), all histologically proven: 91 male and 20 female with mean age of 40.07 years, 30 cases (27.03%) had albuminuria at the time the-patients were first seen, and albuminuria with microscopic hematuria were found in 10-cases (9.01%) out of the 111 patients with CAH
Twelve cases (21.05%) o t of 57 - R who were followed up for over the pe iod of more than 3 months were shown to be asso iated wi - glomerular damage by the findings of m. ked al uminuria and hematuria. Renal biopsy ob ained from 2 patients out of these 12 cases revealed membrano-prolifenative and proliferative glomerulonephritis, respectively HBs Ag test by im une adherence hemagglutination assay (IAHA) was found positive in all of 12 cases of CAH associated with glomerular damage, and anti-HBs tested by passive hemagglutination assay (PHA) was also detected positive in all of the cases, but with low in titer. It was observed that the findings of glomerular damage were appeared or intensified as the elevated s-GOT activity was declined to its normal level (10 out of 12 CAH) with concomitent lowering of HBs Ag titer. The anti-HBs titer, however, as not evidently changed as with change of s-GOT activity. Among 94 patients with liver cirrhosis who were also followed up for over the period of more than 3 months, all with esophageal varix: 80 male and 14 female, 15 cases (15. 74%) were transiently and/ or eventually known to be associated with glomerular damage, among whom 2 renal biopsies showed proliferative and 1 membrano-proliferative glomerulonephritis and the other 2 died of chronic renal failure with hepatic coma. A 17 year old female patients with type B acute viral hepatitis complicated with memirano-proliferative glomerulonephritis and reflactory anemia with leukopenia during convalescent phase of relapsing hepatitis was also included in this report, and the clinical picture was depicted in figure 3. It is thought to be another interesting finding, probably also caused by immune mechanism,that the platelets which were initially normal in counts were markedly decreased as with appearance of glomerular damage in acute and chronic type B hepatitis. The significance of this change may be supported by the result that the platelet counts are lower in CAH with albuminuria than in CAH without albuminuria (p=0.05).
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