Plasma lipids fractions (cholesterol, triglyceride, β-lipoprotein, phospholipid and free fatty acids), postheparin lipolytic activity (PHLA) and immunoreactive insulin (IRI) were examined in 25 uremic patients undergoing intermittent hemodialysis over 6 years in duration. 1) Patients with 3 years hemodialysis (n=13) and 4 years hemodialysis (n=9) showed significantly increased triglyceride levels. Cholesterol did not change significantly and showed lower levels in those patients than control. Phospholipid had little changes within normal limit. β-Lipoprotein was normal, but slightly increased in patients with 6 years hemodialysis. Free fatty acids (FFA) level was significantly high throughout this study. However, patients with 5 and 6 years hemodialysis revealed rather low levels in IRI, compared to those of the early period of hemodialysis. 2) Any significant correlations between triglyceride, BUN, IRI, S-albumin and PHLA were not seen in the study. 3) In 12 patients with 4 years hemodialysis, the effect of hemodialysis to plasma lipids, PHLA and IRI was observed. None of these paramenters did not show any significant changes at the end of hemodialysis and the following morning. 4) The supplemental high caloric diet was given at every lunch time of each hemodialysis for 9 months. Triglyceride, phospholipid, FFA and β-lipoprotein significantly increased compared to the value of control and/or the value before starting this supplemental diet. 5) From this study, it can be assumed that low level of PHLA, as a cause of delayed clearing of triglyceride from blood and high level of IRI, as a cause of increased generation of triglyceride in liver, were indirectly related to the control of plasma triglyceride level in patients undergoing maintenance hemodialysis. Additionaly, a high caloric diet for hemodialyzed patients may contribute to high levels of plasma triglyceride and FFA.

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The insoluble renal tubular antigen (Tub-Ag) was obtained from normal rat kidneys by the modified method of Edgington et al. It was then solubilized by pronase-treatment and ultracentrifugation. The resulting supernatant containing soluble renal tubular antigen (Pron-Tub-Ag) was concentrated by negative pressure dialysis and subjected to gel filtration on Bio-Gel A 1.5 M which yielded six major peaks of optical density at 280 mμ. Among these, only the fraction C consisting of the third peak caused marked proteinuria when injected once into the homologous rat footpad mixed with the incomplete adjuvant. Proteinuria appeared 4-8 weeks after the injection and persisted for more than 12 months. Histological examination of the affected kidney revealed marked thickening of GBM without any significant celluar proliferation. Many deposits were noted in GBM on electron microscopy. By immunofluorescent technique granular deposits of rat γ-globulin were demonstrated along the glomerular capillary walls in the affected kidneys. When FITC-labeled antisera to Pron-Tub-Ag and fraction C were used, uniform granular fluorescence was observed along the glomerular capillary walls in a fashon similar to that of γ-globulin. These immunopathological findings of tie experimental glomerulonephritis were consistent with those of human membranous glomerulonephritis and suggested that renal lesion was mediated by the autologous tubular antigen-antibody complexes.

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A case of juxtaglomerular cell tumor was reported in a 17 year-old girl who clinically manifested hypertension (190-118 mmHg), high plasma renin activity (20.31 ng/ml/h), hypopotassemia (3.1 mEq/l) and aldosteronism (13.2 ng/dl). The patient received left nephrectomy because X-ray examination revealed a walnut-sized tumor in the hilar area of the left kidney. The tumor surgically removed was a well encapsulated, grayish white solid mass occasionally associated with haemorrhages and contained renin activity about 5000 times higher than the remaining cortical tissue of the same kidney. Microscopically the tumor consisted mainly of proliferation of polygonal epithelioid cells accompanying small-sized vessels and renal tubular-like structures. Silver impregnation disclosed epithelioid cells surrounded by fine fibrils radiating from the vascular walls. Fine granules positive for Bowie's stain were found in some epithelioid cells. From these findings it may be suggested that the tumor originates from the juxtaglomerular apparatus. Electron microscopic observation of the tumor cells showed varying types of intracytoplasmic granules specific for the juxtaglomerular cell. The rhomboid granules predominated in the Golgi area, presenting a grid-like crystalline with a periodicity of 90-120 Å. The round granules of varying diameters from 0.2-1 μ contained electron dense granular materials. Occasionally rhomboid crystallines which partly lost the gridlike structure were found in the round granules. These findings seem to be digestive processes of the rhomboid crystallines by lysosomal enzymes in the round granule. The round granules occasionally communicated with the outer-surface of the tumor cell cytoplasm through small canals. In addition, intracytoplasmic granules of mast cells diffusely scattered in the tumor were noted to be distinguished from the specific granules of the juxtaglomerular cells by performing various staining methods for detection of acid mucopolysaccharides, zinc and histamine, because mast cell granules were also positively stained with Bowie's staining.

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Clinical and histopathological (renal biopsy) studies were conducted in a series of 80 pediatric patients with acute glomerulonephritis (abbreviated as AGN) who were chosen for the study according to the following criteria of inclusion : (1) there is a preceding disease, (2) the onset is acute after a certain latent period, (3) the presenting symptom is hematuria or proteinuria or both, and (4) the duration of illness is up to one year. The male-to-female ratio of this series was 1.00 : 1.11; average age was 7 years and 10 months for males and 7 years and 7 months for females. There was a significant elevation of ASL-O titer in 56 (70.0%) of the 80 cases. The preceding illness was identified as upper respiratory infection in 70%, searlatina in 6.3%, lymphadenitis in 2.5%, viral infection in 3.8% and unknown in 11.3%. Initially, proteinuria was noted in 100.0% of the cases, hematuria was present in 97.3%, elevated blood pressure (systolic pressure of above 130 mmHg) in 47.4%, lowered β₁C level (50 mg) in 88.2%, decreased serum albumin (3.5 g/dl>) in 39.2%, and elevated BUN (20 mg/dl≤) in 37.0%. Renal function tests (PSP, GFR and RPF) did not correlate well with the clinical course, yielding no consistent results. Follow-up for an average of 2 years and 4 months revealed the disease to have become protracted in 15% of the cases, with one of the entire 80 cases showing histological evidence of chronicity of the disease. Renal biopsy done within 2 months of disease onset using fluorescent antibody technique demonstrated deposition of IgG in 1 (11.1%) of 9 cases and β₁C deposits in all of these 9 cases. The clinical course did not parallel but lagged behind histopathological findings, and no distinction could be made between healed cases, protracted cases and those with the disease becoming chronic with respect to clinical as well as histopathological findings initially. Some of those cases having an insidious onset with the only clinical symptom of microscopic hematuria exhibited histopathological changes similar to those seen in cases with acute manifestations. This implies the existence of subclinical AGN and permitted to presume that these two clinically distinct types of AGN are based on the same etiological substratum. What does the fact mean that the incidence of those cases with microscopic hematuria without concurrent proteinuria was unexpectedly high? To solve this problem would certainly be of help in the early diagnosis and early treatment of AGN.

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