Although the etiology and pathogenesis of IgA nephropathy is not fully understood, it has been classified as an immune-complex induced glomerulonephritis caused by an immunological mechanism. Forty-two patients with primary IgA nephropathy underwent tissue typing for HLA-A, B, and DR antigens by the standard method using a microlymphocytotoxicity test. There was no significant correlation between HLA-A and B antigens and this disease. However, the frequency of HLA-DR4 was 57.1% in the patients with normal renal function, 85.7% in those with decreased renal function, 100% in dialysis patients, and 39.2% in the control group. It is statistically significant in the patients with renal dysfunction (corrected P less than 0.05). Our results suggest that the HLA system may play an important role in the occurrence and exacerbation of IgA nephropathy in the Japanese population.

HLA-A, B, DR, and MT antigens were examined in 50 patients with idiopathic membranous nephropathy (IMN) by the standard microlymphocytotoxicity technique. The frequency of HLA-DR2 was significantly increased in the patients in comparison to the controls. Significant decreases in the frequencies were seen for HLA-DR4, DRw8 and DRw9 in the patients. The linkage disequilibrium between HLA-Bw52 and DR2 was noted in the controls, but it was significantly weaker in the patients. The frequency of MTl was significantly higher, and that of MT3 was significantly lower in the patients as compared with the controls. The findings suggest that an immunological disturbance under the influence of genetic factors may confer a susceptibility to IMN.

Human lymphocytes sensitized with HL‐A antibodies could not be killed by the addition of complement if the lymphocytes were incubated for periods of 1 to 5 hours at 37° C. This phenomenon was not produced by simple dissociation of the antibodies or by loss of antigens (modulation), but rather is postulated to result from an active release or pinocytosis of HL‐A antigens together with the attached antibody. “Escape from sensitization” is followed closely by reformation of antigens, for the cells can readily be resensitized and killed by addition of complement. Loss of sensitization is an active process, since one‐day‐aged lymphocytes or lymphocytes treated with actinomycin D or puromycin were unable to express this activity. A differential escape rate for different specificities was encountered indicating that HL‐A9 was produced more rapidly than several other specificities present on the same lymphocytes. A correlation was noted between the rate of HL‐A antigen synthesis by lymphocytes (indicated by escape rate) and the quantity of HL‐A antigen in the serum. Inhibition of lymphocyte cytotoxicity was used to detect the presence of HL‐A antigens in serum. Certain specificities, such as HL‐A9, were generally present in serum whereas others, such as HL‐A8, could not be detected. Cross‐inhibition tests with over 100 sera clearly showed an association of inhibition with specificity, although nonspecific inhibition was often observed. Sephadex fractions of sera tested at different concentrations revealed the greatest inhibitory activity in the 19S and 7S fractions.

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