Yasuhiko Sasaki

Effect of Captopril on Heavy Proteinuria in Azotemic Diabetics

We investigated whether captopril, an angiotensin-converting-enzyme inhibitor, would reduce proteinuria in patients with advanced diabetic nephropathy. Captopril (37.5 mg given in divided doses three times daily) was administered to 10 azotemic diabetics with heavy proteinuria. Urinary protein decreased promptly within two weeks (from 10.6 +/- 2.2 to 6.1 +/- 1.4 g per day [mean +/- S.E.M.]; P less than 0.01). The decrease in proteinuria did not coincide with a fall in systemic blood pressure or in the blood glucose concentration. Serum creatinine and potassium values did not change in any of the patients except one. We suggest that captopril caused a decrease in intrarenal hypertension, which contributed to the reduction of urinary protein excretion. The therapeutic value of this intervention remains to be established.

Sjögren's syndrome and renal tubular acidosis

Abstract Clinical studies were conducted in four cases of Sjogrens syndrome complicated by renal tubular acidosis (group I) and in ten cases of Sjogrens syndrome without this complication (group II). No differences between the two groups were noted in respect to the ages of the patients or the duration of the disease. Hyperglobulinemia and an increase in serum IgG were observed in three of the four cases in group I, but no difference was found in the degree of increase when comparing the two groups. No differences were observed between the two groups when compared using various serologic tests. Marked lymphocytic infiltration was noted in the biopsy specimens of the lacrimal and parotid glands. In the kidney biopsy specimens in three cases of group I lymphocytic infiltration interspersed with plasma cells was conspicuous in the interstitial tissues. No lymphocytic infiltration was noted in one case without hyperglobulinemia but a marked interstitial fibrosis was seen. No remarkable changes were seen in the renal biopsy tissue in four cases of group II. Accordingly hyperglobulinemia of itself does not appear to be the primary cause of renal tubular acidosis in Sjogrens syndrome. Renal changes appear to represent one of several systemic changes occurring in Sjogrens syndrome. Therefore renal tubular acidosis is probably an inherent result of the disease process responsible for the development of Sjogrens syndrome.

A family with nephronophthisis – medullary cystic disease complex

Abstract We report a family with nephronophthisis-medullary cystic disease complex (NPH-MCD). Case 1 was a 12-year-old girl with normal growth and development, who showed anemia and proteinuria at a health screening. A renal biopsy specimen showed chronic tubulointerstitial nephritis. Her renal function progressively decreased, and maintenance hemodialysis was started in January 1989. Case 2, the 29-year-old elder brother of case 1, had had anemia for 9 years and visited our hospital with symptoms of a common cold. Examination showed that he had chronic renal failure. A renal biopsy specimen showed chronic tublointerstitial nephritis. Case 3, a 27-year-old man, a first cousin of case 1, had had anemia for 1 year and was admitted to our hospital because of acute cardiac failure associated with chronic renal failure. Hemodialysis was started immediately. Two other people in the same family had chronic renal failure. Typing of the histocompatibility leukocyte antigen (HLA) was performed in four members of the family, but the results showed that there was no involvement of HLA in the pathogenesis of NPH-MCD.

Fever of unknown origin deu to sclerosing mediastinitis.

症例は51歳,女性.高熱を主訴に受診.各種抗生物質の投与を受けたが症状は軽快せず,不明熱の原因精査の目的で当科入院した. Gaシンチグラフィーでは前縦隔に著明な集積を認め,胸部CTにおいても同じ部位に腫瘤像を認めた.前縦隔腫瘍として,腫瘍摘出術を施行.病理組織学的にはリンパ球,形質細胞等の非特異的な細胞浸潤を伴う,広範な線維化を主体とした結節構造を認め, Sclerosing mediastinitisと診断した.術後は速やかに解熱し, CRPも徐々に低下した.一般にSclerosing mediastinitisは原因不明の疾患であり,上大静脈症候群等の胸部臓器圧迫症状で発症することが多いとされているが,本症例においては高熱以外の特異的な症状に乏しく,診断に苦慮した症例であり今回報告する.

Plasma renin activity in acute renal failure induced by norepinephrine infusion in unilaterally nephrectomized dogs.

Plasma renin activity was determined by bioassay prior to, during and following a 2-hour infusion of norepinephrine into the renal artery in unilaterally nephrectomized dogs in order to examine the role of renin-angiotensin system in norepinephrine-induced ARF. ARF was induced in 5 of 8 dogs receiving 0.75 microgram/kg/min of norepinephrine, but not in the remaining 3 dogs and 2 dogs infused with 0.6 and 0.4 microgram/kg/min of norepinephrine. There proved no difference in plasma renin activity in renal venous blood between the dogs with and without ARF when followed up to 2 h after the discontinuation of the infusion. The same results were obtained when the plasma renin activity in the foreleg vein was followed at 24, 48 and 72 h after the infusion. The renin-angiotensin system does not seem to contribute to the reduction of renal function in norepinephrine-induced ARF in dogs.