Literature as to the significance of IgE in nephritis and nephrotic syndrome is rare. Therefore, this study was undertaken to evaluate properties of IgE characteristic in the diseases. Twenty-six patients with nephritis, 16 nephrotic syndrome, along with 14 of chronic renal failure in Hospital were chosen As the controls, 24 normal adults were examined. Measurement of IgE as well as immuno-histological study using fluorescent-antibody technique were made. For the former, IgE-Kit (radioimmunosorbent test) of Pharmacia and for the latter, anti-IgE serum (rabbit) labelled with FITC of Behringwerke were used. There was no significant cliff erece found between nophritis, chronic renal failure, treated nephrotic patients and controls. On the contrary, 7 subjects of untreated nephrotic syndrome had a mean value of 1132+698 ranging from 220 to 2400, significantly higher than that of controls (P<0.05). Kidney specimens were obtained by biopsy from all patients except chronic renal failure patients. They were frozen in dry-ice n-Hexane, and then localization of IgE was investigated by fluorescent-antibody technique. According to Gerber, IgE was demonstrated in conmma-like pattern in the glomeruli of patients with minimal change, while a diffusely granular pattern was shown in those of membranous nephropathy. In our investigation, however, no specific fluorescent positive materials were recognized. The serum IgE levels of nephrotic patients reduced in most cases, after trearment with steroid or azathioprine. But that has nothing to do with the therapeutic effects.The urine IgE levels in nephrotic syndrome corresponded to extent of proteinuria. As above mentioned, there are still many problems unsettled, as to the intrinsic nature of IgE in nephritis and nephrotic syndrome. The high level of serum IgE in nephrotic syndrome may suggest some correlation between them

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The aim of this study was to investigate the clinical significance and the pathogenesis of hyperuricemia in some of patients with chronic glomerulonephritis. 1. Nineteen of fifty-two patients with chronic glomerulonephritis showed hyperuricemia, in whom GFR and BUN level were almost normal. The incidence of hyperuricemia associated with chronic glomerulonephritis was 36.6 per cent. 2. No significant correlations were observed between plasma uric acid level and the value of renal function tests such as GFR, RPF and PSP excretion rate in these patients. Moreover, no significant differences were observed in the degree of hypertension and the changes of renal histology between the hyperuricemics and the normouricemics. 3. In the hyperuricemics, the uric acid excretion and the uric acid clearance were characteristically diminished, and the urinary ammonium excretion after oral load test of NH₄Cl was significantly lower compared to the normouricemic patients and the normal subjects. 4. These results were also different from the gouty patients in respect to that the urinary excretion of uric acid in the gouties was significantly higher than in normals, and the ammonium excretion was not significantly lower. 5. The pathogenesis of hyperuricemia seen in some patients with chronic glomerulonephritis seemed to be different from that of gouty hyperuricemia, and it is assumed to be concerned with the abnormality of uric acid transport in the renal tubules, which is closely related to renal ammonium excretion.

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An attempt was made to investigate the mechanism of denervation natriuresis and its relation to Intrarenal hemodynamics. Twenty mongrel dogs were studied under pentobarbital anesthesia. Urine volume, urinary sodium and potassium excretion, blood pressure, renal blood Low (RBF), renal plasma flow (RPF) and glomerular filtration rate (GFR) of the left kidney were measured before and after homolateral renal denervation. Simultanously, intrarenal distribution of blood flow was measured by ¹³³Xe-washout method in 10 animals, and in other 10 animals, intracortical blood flow distribution was measured by radioactive microsphere method before and after denervation. The following results were obtained. 1) Denervatidn resulted in significant increase in urine volume, urinary sodium and potassium excretion, fractional excretion of sodium (FE_Na) and fractional excretion of potassium (FE^K). 2) There occurred no significant change in blood pressure, RBF, RPF, GFR, filtration fraction (FF) and renal vascular resistsnce (RVR) after denervation. 3) Intrarenal distribution of blood flow measured by ¹³³Xe-washout method and intracortical distribution of blood flow determined by radioactive microsphere method did not show any significant change after denervation. 4) We suggest that the mechanism of denervation natriuresis might be independent of changes in GFR, redistribution of intrarenal blood flow and presumably peritubular physical factors, i, e, hydrostatic pressure and oncotic pressure, and that it might be caused by the elimination of a direct nervous control on the renal tubule.

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