1994年 · 第10卷第02期

In order to clarify the relationship of HBV infection and MPGN which shows the highest carrier rate of HBV among the Chinese patients with primary glomerulonephritis and general population, a clinicopathological study was conducted with 84 patients of MPGN involved. They were allocated to two groups, HBV carriers and non HBV carriers, according to the serological studies of HBV markers including HBV DNA. The results showed that HBV antigens, particularly HBsAg, were detected more commonly in the glomeruli in HBV carriers compared with non HBV carriers. There was a male predominance in HBV carriefs. Liver disease history and abnormal liver function tests could also be found in them. Depressed C4 or C3 and presence of autoantibodies in serum were detected more commonly in HBV carriers. There seemed to be a benign course in HBV carriers with less impaired renal function and hypertension, milder tubulo-interstitial lesions and glomerulosclerosis than those of non-HBV carriers. MPGN type 111 was often diagnosed in HBV carriers. The entity of HBV associated MPGN hence established which is characterized by HBV antigenemia, MPGN and deposition of HBV associated antigens in the glomeruli.

We observed the change of plasma Atrial Natriuretic Peptide (ANP) and Arginine Vasopressin (AVP) in 33 patients with chronic renal failure (CRF) during hemodialysis by means of specific radioimmunoassay. The results showed that the level of plasma ANP and AVP in the patients with CRF were significantly elevated. After hemodialysis the level of plasma ANP and AVP in the cases of normal blood pressure fell to normal level (P<0.001). It was demonstrated that ANP, AVP were lost from hemodialysis fluid and loss was closely oorrelated with ultrafiltration volume, but the level of plasma AVP in the cases of high blood pressure gradually elevated and was closely correlated with the elevation of plasmic sodium concentration (r=0.63, P<0.05), the hypertension may be related to the hyperreactive to the change in sodium concentration.

This study succeeded in establishing the experimental model of diffuse endocapillary proliferative glomerulonephritis by modified chronic serum sickness in rats. After 7 weeks immunizaiton, the pathological changes showed both endothelial cell and mesangial cell proliferations and typical hump under epithelium by EM. The experimental rats presented heavy protcinuria. The experimental model of endocapillary proliferative glomerulonephritis was first reported in China. This model is highly reproducible and practical.