We have studied coagulation and fibrinolysis in renal diseases in childhood. In active stage, patients with nephrotic syndrome were in the hypercoagulable state. Various types of renal diseases in active stage have generally been assumed to have high anti-plasmin activity. Fibrinogen in active stage in acute glomerulonephritis was within normal limits, in contrast to hyperfibrinogenemia in nephrotic syndrome. As shown in Fig. 1, 2 and 3, there were significant correlations between fibrinogen and urinary protein, fibrinogen and cholesterol levels, fibrinogen and cholesterol levels, fibrinogen and a2-globulin levels in nephrotic syndrome. These findings, as in arteriosclerosis, may suggest that hyperlipemia, hypercoagulability, and high anti-plasmin activity associated with the pathogenesis of vessels in nephrotic syndrome. We have not observed typical DIC (Disseminated Intravascular Coagulation) in renal diseases. Urinary FDP (Fibrin/Fibrinogen Degradation Products) was not correlated with serum FDP. Urinary FDP reflected the progression of renal disease. High level of urinary FDP was also observed in urinary tract infection, suggesting that urinary FDP was produced from the lower urinary tract. Urinary FDP was noted in the majority of the patients with lower urokinase activity. Urokinase activity has the significant correlation with urinary osmolarity and urinary creatinine. This correlation which we observed seems to be related to the progression of the disturbance of renal function.

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In some cases of membranous nephropathy a renal tubular epithelial (RTE) antigen is detected in epimembranous deposits by immunofluorescent technique using specific rabbit anti-RTE antiserum. In this report immunochemical and physicoehemical characterization of urinary RTE is described. RTE antigen was prepared from normal human kidney cortices by trypsinization (tr-RTE). Rabbit antiserum against this tr-RTE was raised by immunizing a rabbit with the material in complete Freund's adjuvant. The resulting antiserum did not react with serum components and other renal tissue antigens and other than RTE antigen. The excreted urinary RTE was also purified from patient's urine by a similar immunochemical and physicochemical procedures, and antisera against urinary antigens were prepared as stated above. 1) RTE antigen was detected in normal urine and the RTE of normal subjects had some different characteristics from tr-RTE antigen with respect to the immunochemical and physicochemical properties: it had an additional antigenic determinants to the tr-RTE antigen and its molecular weight was greater than urinary 7s IgG. 2) 5 cases out of 32 renal diseases had 2 different characteristic components of RTE antigens in their urines. One had almost the same characters to normal urinary RTE and another had some different properties from normal urinary RTE : its molecular weight was smaller than its nolmal counterpart and it was eluted with human albumin on Sephadex G-200 column. 3) 2 Cases of membranous nephropathy out of these 5 cases had deposits in the glomeruli which contained both tubular antigen and host antibody. These findings suggest that some cases of membranous nephropathy are induced by the deposition of immune composed of RTE antigen antibody, and this low molecular RTE antigen in patient's urine would be associated to the immune complexes.

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When one of the authors, T. Takeuchi visited Dr. Vasilije Ivanovic, clinic for renal diseases Bergrad University during his travel through the South Europe in August, 1974, Dr. v. Ivanovic promised him to send articles on Endemic Nephropathy. Then after we have received two monographs titled "Endemska Nefropatija" which were published in 1967 and 1971 and contain many reports in symposium style written in Yugoslavian., Russian, Germany or English. We here introduce what the Endemic Nephropathy is, according these publications.

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A 60-year-old man had a renal stone of uric acid component with the laboratory findings of hypouricemia (1.1-2.0 mg/100 ml), hyperuricosuria (700-1600 mg/day), and an increased uric acid clearance (43 ml/min). This combination of metabolic abnormalities may be the results of hyperexcretion of uric acid associated with the tubular reabsorptire defect. Similar case with renal stone has not yet been reported to date.Although it has already been known that a significant group of patients with uric acid calculi do not have hyperuricemia or increased uric acid excretion, uric acid renal stone is occasionally formed in hyperuricosuric condition. Hyperexcretion of uric acid associated with hypouricemia is an infrequent abnormality of uric acid metabolism. We herein present a rare case of renal stone with the laboratory findings of both hypouricemie hyperuicosuria, and tubular reabsorptive defect of uric acid.

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