It is well known that heavy metals are sometimes causative agents of a toxic nephropathy. The present study is described the presence of a toxic tubulopathy in the patient with organic mercury poisoning (Minamata disease) based on the analyses of urinary protein excretion patterns. The urine of 19 Minamata disease patients and 3 control groups (10 healthy subjects, 10 tubular proteinuria, 15 glomerular proteinuria) was examined. The concentrated urine of patient with Minamata disease was examined by gel chromatography. The elution pattern of urinary proteins in the patient was different from healthy controls, and the difference was mainly caused by the abundance of low molecular weight proteins (i. e., β₂-microglobulin and free light chains) in the urine. The elution pattern in the patient was similar to that of tubular proteinuria. The urinary excretion values of β₂-microglobulin (β₂μ), free light chains (L-chains), renal tubular epithelial antigen (RTE) and albumin (alb) were measured by immunochemical methods. Then the ratios of alb/β₂μ, alb/L-chains and RTE/alb in the uirne of Minamata disease patients were compared with those of the 3 control groups. The ratios of alb /β₂μ and alb/L-chains in the Minamata disease group were significantly different from healthy control. The RTE/alb ratio in the Minamata disease group was also significantly different from healthy control group. These ratios in the Minamata disease were identical to those in tubular proteinuria group. The results suggest that the patient with Minamata disease is not only affected with the nervous system but also affected the renal tubules, and that the nephropathy may be caused by the organic mercury poisoning.

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The patient, a 45-year-old female, with membranous glomerulonephropathy was treated with urokinase, dipyridamole, indomethacin, prednisolone or thiamphenicol individually. These all drugs except for indomethacin reduced urinary protein. Laboratory examinations showed a hypercoagulable state not only in the blood but also in the glomeruli.;
•Platelet function tests revealed increased adhesiveness and ADP aggregation. In thromboelasto-glam, k=2.75min, ma=63.0mm, ms=170.27%, r=6.0min
•Increased plasma antiplasmin activity was obserbed on fibrin plate.
•Immunohistologically a large amount of fibrin deposits were detected in the glomerular capillary lumens.
•The level of urinary FDP was 3μg/ml. It is said that the treatment with anticoagulants or fibrinolytic agents is not indicated for membranous glomerulonephropathy because of little connection with the blood coagulation mecha-nism on the course of its development. However, in this case with hypercoagulable state, both the therapies with anticoagulant or fibrinolytic agent (dipyridamole, urokinase) and other types of treatments (prednisolone, thiamphenicol) resulted in the decrease of urinary protein. These interesting findings indicate the multiplicity of factors which cause the renal damage and the variety of the treatments of glomerulonephritis and also offer a lot of suggestion to the disscussion on the blood coagulation system as one of the damaging factors in glomerulonephritis. At the same time these facts are significant and usefull when thinking about the indication of anticoagulant and/or fibrinolytic therapy.

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Renal micropuncture experiment was performed to clarify the mechanism of various segments of rat nephron with respect to regulation of urinary potassium excretion. Free flow samples of tubular fluid were collected from the superficial tubules and analyzed for inulin and potassium concentrations. Wistar rats were divided into the following five groups. A) control group B) low potassium diet group C) high potassium diet group D) intravenous KCI solution infusion group. F) nephron population reduction (NPR) group Filtered potassium is almost completely reabsorbed along the proximal tubule and loop of Henle both in control and K depleted rats. More than 90% is reabsorbed both in K loading and NPR group. Net secretion of potassium in distal convoluted tubule occures even in potassium depleted rat, and increment of K secretion is observed both in potassium loading and NPR group. Potassium transport mechanism beyond the distal convoluted tubule is evaluated by the difference in distal potassium delivery and urinary potassium excretion. At the collecting duct, the extensive net potassium reabsorption is observed in potassium depleted rats, whereas K absorption might be reduced or even secretion is seemingly taking place in potassium loading rat. In conclusion, distal convolution and collecting duct have the major role in the regulation of urinary potassium excretion.

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An adult case of an unusual type of MPGN, termed intramembranous electron dense direare, e laminal glomerulonephrltir or dense deporit disease, is reported here. The patient, 55 year-old, male began with edema, proteinuria and severe hypertension, The clinical course were rapidly progressive, and after 5 months dialysis were started because of his increased azotemia and severe edema. The months later from the onset, he suddenly died with apoplectic sign. Percutaneous renal biopsy was performed in one and half month from the onset, and electronmi-croscopically revealed MPGN with intramebranous lineal dense deposits in the capillary loops. There was, however, no any deposit in epimembraneum nor subendothelium, except a few fibrin which appeared with paracrystal periodicity, Neither serum complement level nor immunofluore-scent study was performed on this case. This is a first case from Japan, where it seems to be very rare as compared with European people.

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Eleven cases of the renal parenchymal tumor (10 cases of malignant tumors, including 5 of renal cell carcinoma, and 1 of angiomyolipoma) were examined The renal venous blood flow measured by the local thermodilution method was compared with the renal arteriographic findings in each involved kidney. 1. In the hypervascularized renal tumors (6 tumors) on the renal arteriograph.y the renal venous blood flow increased significantly compared to the noninvolved kidneys and the renal vascular resistance decreased. Futhermore, the arteriovenous oxgen difference became small in all tumor kidneys. 2. On the contrary, however, in oligo-or avascular ranal tumors (5 tumors) the renal venous flow was low and the renal vascular resistance was high. Futhermore, the arteriovenous oxygen difference was almost equal to the contralateral noninvolved kidneys 3. Therefore, the findings in the hypervascularized renal tumors were thought to be the functional proof of the appearance of the arteriovenous shunt in the tumor of the kidney.

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