It had been suspected that the immunological mechanism participates in the pathogenesis of glomerul-onephritis scince the report of Longcope in 1913. Dixon described in 1963 that almost all of the glomerul-onephritis belong to the immune complex disease and Cochrane insisted the importance of IgE in immune-complex deposition in 1971, but there are only few reports concerning the attitude of IgE in renal diseases. Since 1971, studies on the behavior of immunoglobulins and complement in various renal diseases are carried on in our laboratory. IgE and complement (C′₃) levels in the blood and urine were analysed with that of IgG. The results obtained were as follow; 1. No positive correlation is obrerved in the serum levels of IgG and IgE. 2. Characteristic increase of serum IgE is observed in indeterminate group nephrosis. 3. The differences of complement fixation were suggested from the correlation between IgG, IgE and C'₃. 4. It was suggest ed that there are at least four immunological patterns in glomerulonephritis or nephrotic syndrome ; a) hyper-IgE an d hypercomplementemic patterns in indeterminate group nephrosis b) hypocomplementemic pattern in chronic membranoproliferative glomerulonephritis c) relatively by per-IgG pattern in membranous type nephrosis b) generally non-specific pattern 5. In the mesurement of selectivity patterns of protein excretion, it is important to consider the existence of splitted small molecular proteins having the same immunological behavior in addition to the ordinary protein molecules. 6. It was suggested that IgE protein is excreted through the glomerular basement membrane (GBM) as same as IgG protein.

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Immunological deficient state in chronic renal failure was studied by evaluating the subpopulation of peripheral lymphocytes, quantitatively and qualitatively in 54 patients treated with long-term hemodialysis. In addition, PPD skin reaction, hepatitis-B antigen and antibody, and immunoglobulins and beta 1 C/A globulin in sera were determined. By comparing these immunological parameters with the lymphocyte subpopulation, the following results were observed in the hemodialysis patients. 1) The percentages and counts of T-cells were significantly lower than in the healthy subjects (per 0.001).2) The PHA-induced lymphocyte transformation was significantly impaired (p<0.05). 3) There was, however, no demonstrable differences in percentages and counts of B-cells in contrast to the healthy group. 4) The immunoglobulins (IgG, IgA and IgM) and beta 1 C/A globulin were almost within normal ranges. These observations suggest that the cell-mediated immunity is particularly impaired in chronic renal failure while the production of circulating antibodies is essentially unaffected on the whole.

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A 24 year-old female patient with renal failure associated with sarcoidosis was reported. Diagnosis for sarcoidosis was based on the findings such as BHL on chest roentgenogram, turbidity of the retina, positive for Kveim test, epithelioid granuloma in the biopsy specimen from her leg nodule, high ESR, hypergamm-aglobulinemia and hypercalcemia. Other laboratory data disclosed mild renal insufficiency ; mild proteinuria, elevation of BUN and serum creatinine, and decreased GFR and RPF. X-ray examination of the kidney showed large kidneys with irregular contour, but without nephrocalcinosis. Renal scintigram showed many coin-like lesions bilaterally. Histologic examination of renal biopsy specimen revealed severe interstitial nephritis with hyaline necrosis, but without calcium deposition. It is reasonable to pressume that renal failure was due to the involvement of sarcoid granulomata to the kidney, although neither epithelioid nor giant cells could be found out in the renal biopsy specimen. Porcine calcitonin was administered prior to corticoid therapy which improved her general conditions. Calcitonin was effective to lower serum calcium and inorganic phosphate levels. Of particular interest was the decrease of urinary phosphate excretion as well as calcium excretion, despite of constant urine volume and creatinine clearance during calcitonin administration. Hypercalcemia in this case was assumed to be due to the increased state of bone resorption.

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