In order to delay the introduction of dialytic procedures, 11 patients with chronic renal failure due to chronic glomerulonephritis (8 cases), chronic pyelonephritis (1 case), polycystic kidney (1 case) and bilateral renal cortical necrosis (1 case) were treated with high dose of furosemide and sodium. They were given orally. Blood urea nitrogen was decreased in four cases, and serum creatinine in two, including one case of bilateral renal cortical necrosis in whom some improvement in renal funetion was ensued. In these 6 successful cases, when serum creatinine level was 8mg /dl or more, daily urine output was increased from an average volume of 1.3L to more than 2.4L by the use of 320mg of furosemide per day and 205mEq of sodium per day. When the level was less than 8mg/dl, mean daily output of urine was increased from 0.9L to 2.0L or more by the use of 547mg of furosemide per day and 189mEq of sodium per day. In unsuccessful cases daily urine output did not reach volume described above, and mean furosemide dose and mean sodium intake were 456mg/day and 147mEq/day, respectively. These results suggest that the use of sufficient amount of sodium in concomitance with furosemide is essential to the nondialytic treatment of end-stage chronic renal failure. During the treatment, bilateral perceptive hearing loss was noted by audiometric test in all 7 cases examined. They had not been treated with any aminoglycoside antibiotics. In the control group of 8 patients of chronic renal failure maintained with hemodialysis during 1.7 to 6.2 years, there were three cases with bilateral perceptive hearing loss, and two of them had been treated with aminoglycoside. It was not decided whether this damage was due to furosemide, and if so, whether it was reversible after cessation of its administration.

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The number of peripheal blood lymphocytes and the proportion of T and B cells were determined in 71 patients with chronic renal failure. T cells were identified by rosette formation with sheep red blood cells (E-rosette formaion); B cells were detected by membane immunofluorescence. The following results were obtained I) The number of peripheral lymphocytes and the percentage of T cells were remarkably depressed in these patients, whereas the percentage of B cells did not differ significatly from normal subjects. II) The patients undergoing hemodialysis had significantly higher lymphocyte levels than untreated patients. III) The severly ill patients with chronic renal failure had signi ficantly lower lymphocyte and T cell levels compared with mild ones. IV) The decrease in the mean percentage of T cells could usually be accounted for by a corresponding increase in the mean percentage of so called “null nells”, which could not be classified as either T or B cells. These facts storongly suggested that diminution of peripheral lymphocyte number cuold be improved by hemodialysis treatmnt. Also the changes in peripheral lympocyte subpopulation must in some way be correlated with diminished immune response seen in patients with chronic renal failure.

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Two cases of hypocomplementemic chronic glomerulonephritis with reduction of early complement components were reported. Case 1- An 18 year old woman was admitted for the examination of proteinuria. The renal biopsy revealed membranoproliferative glomerulonephritis (MPGN). Serum C3 (β1C/A globulin) and Clq levels were significantly reduced, and C3proactivator (β2-glycoprotein II, C3PA) and C4 (β1E globulin) levels were below normal. Immunof luorescence studies demonstrated C3, C3PA and Clq deposition in the glomeruli, though IgG, IgM and IgA were not demonstrable. Case 2-A 64 year old woman was admitted with a three year history of proteinuria and hyperte-nsion, and demonstrated marked generalized edema on admission. The renal biopsy studies demonstrated the typical lobulation of MPGN. In additon to the decrease of serum C3 and C3PA levels below norml, early components, Clq and C4 were significantly reduced. Immunofluorescence studies demonstrated C3 and IgG deposition in the glomeruli, but C3PA, IgM and IgA were not detected. Observation for Clq was not done. Depression of serum C3-9 without decrease in C1, C2 or C4, suggesting that alternate pathway is activated unassociated with the activation of classical pathway, has been observed in many cases of chronic hypocomplementemic MPGN. In the present 2 cases, however, definite decreases in the serum levels of early components and the presence of early component in the glomeruli were demonstrated. These findings suggest that the activation of classical pathway may also be involved in some cases of MPGN.

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The study on clinical effect on tryptophan loading on protein and amino acid metabolism of patients undertaking long-term hemodialysis is carried out. Intestinal tryptophan transport is alsoivestigated in vitro by means of everted-sac method. The results are described as follows: 1. Mean serum tryptophan concentration uremic patient is 0.75 mg/dl, which is significantly lower than that of control group (1.54 mg/dl). In addition, the serum concentration increased to 7.3 mg/dl at 80 minutes following L-tryp-tophan loading in controles, whereas the Values are up to 2.08 pre-and 3.92 post-dialysis. 2. Rat intestinal effex of tryptophan is significantly inhibited by the medium containg serum of dialyed patients in comparison with control serum. Inhibitory effect is also observed by the medium containing ultrafiltrate of dialyed patients. 3. Intestinal efflux of tryptophan of the with exoerimental renal failure is pecreased. According to the results, it is concluded that disturbance of tryptophan absorption from the gut may be, at least, an important factor induceing decrease in serum tryptophan concentration of uremic patients.

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