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T Sakemi

Publications and source records attributed to T Sakemi.

At least 73 records · Page 4Linked to original sources
PubMed1993

[Severe proteinuria in IgA nephropathy. Clinicopathological study of 8 cases with 100 serial sections].

Using 100 serial sections for light microscopy, we studied the clinicopathologic characteristics of IgA nephropathy with severe proteinuria. Eight out of 128 cases with IgA nephropathy exhibited severe proteinuria of 3.0g/day or more. These cases consisted of 5 males and 3 females with an age range from 15 to 73 years. Daily proteinuria ranged from 3.3 to 7.1 g. At the time of biopsy, the serum creatinine level was 1.2 mg/dl or more in 6 cases; two of these developed end-stage renal failure during the follow-up period. In most of the cases, routine sections for light microscopy revealed moderate to severe mesangial proliferation and tubulointerstitial damage. In 7 cases, variable percentages of glomeruli, ranging from 20% to 95%, were involved by chronic lesion represented by sclerosis and fibrous crescents/adhesion, while only 2 cases exhibited active lesion characterized by segmental glomerular necrosis and/or cellular/fibrocellular crescents. In contrast, thorough observation of 100 additional serial sections disclosed the focal presence of active lesion in all except one case with features of endstage kidney. In addition, the highest percentage of glomeruli with active lesion in the serial sections correlated well with the severity of proteinuria. The results suggested that severe proteinuria in IgA nephropathy depends on, at least in part, focal outbreak of active lesion characterized by segmental glomerular necrosis and cellular/fibrocellular crescents.

Adolescent↗
PubMed1993

Castration attenuates proteinuria and glomerular injury in unilaterally nephrectomized male Sprague-Dawley rats.

BACKGROUND: To clarify the pathogenesis of focal and segmental glomerulosclerosis, we investigated the effect of castration on the development of proteinuria and glomerulosclerosis in unilaterally nephrectomized male Sprague-Dawley (SD) rats. EXPERIMENTAL DESIGN: At 5 weeks of age, group 3 was castrated, whereas groups 1 and 2 were sham-operated. At 6 weeks of age, groups 2 and 3 received unilateral right nephrectomy and group 1 received sham-operation. Body weight, blood pressure, urinary protein, serum albumin, cholesterol, blood urea nitrogen and serum creatinine were checked every 2 months from 2 through 12 months after right nephrectomy. Control group 1, Nx (nephrectomized) group 2 and castrated (nephrectomized + castrated) group 3 underwent morphologic study 6 months after nephrectomy. In an additional experiment, control group 4, Nx group 5, and castrated group 6 were followed for an additional 6 months and used for morphologic study. RESULTS: Growth was significantly stunted in the castrated rats as compared with control and Nx rats. Nx rats became proteinuric with age. Castration significantly reduced the proteinuria after 2 months of nephrectomy throughout the experiment. The proteinuria in castrated rats tended to decrease as compared with the controls. The glomerulosclerosis index was significantly higher in Nx rats than in either the controls or the castrated rats. The three groups showed no significant differences in blood pressure, plasma renin, activity and plasma aldosterone concentration. CONCLUSIONS: These observations suggest that sex hormones may contribute to the development of proteinuria and glomerulosclerosis in unilaterally nephrectomized male SD rats.

Animals↗
PubMed1992

Development of HTLV-I-associated myelopathy after blood transfusion in a patient with aplastic anemia and a recipient of a renal transplant.

We report the development of rapid progressive HTLV-I-associated myelopathy (HAM) after blood transfusion in two immunosuppressed patients, one of whom had aplastic anemia and the other was the recipient of a renal transplant receiving immunosuppressive chemotherapy. Spastic paraparesis developed 11 or 16 months after transfusion and rapidly progressed to a wheelchair-bound state. The present 2 cases suggest that the coexistent immunosuppression may play an important role in the rapid development of HAM in transfusion-acquired cases.

Adult↗
PubMed1992

Angiotensin-converting enzyme inhibition attenuates hypercholesterolemia and glomerular injury in hyperlipidemic Imai rats.

Hyperlipidemic Imai rats spontaneously develop hypercholesterolemia, proteinuria and glomerulosclerosis. We investigated the effect of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneous hypercholesterolemia and the progressive renal injury in this rat strain. Male Imai rats (n = 7) were treated with enalapril at a dose of 50 mg/l in drinking water starting at 6 weeks of age. Body weight, blood pressure, urinary protein excretion and serum constituents were checked and compared with untreated controls (n = 5) up to 38 weeks of age. Enalapril treatment significantly reduced hypercholesterolemia (247 +/- 41 vs. 102 +/- 13 mg/dl, p < 0.01, at 38 weeks) and proteinuria (766 +/- 290 vs. 206 +/- 119 mg/kg/day, p < 0.01, at 38 weeks). The glomerulosclerosis index (SI) was significantly higher in untreated control rats than in the enalapril-treated group (227 +/- 57 vs. 27 +/- 9, p < 0.01). Although we could not clarify whether hypercholesterolemia is a primary event or secondary to the nephrotic syndrome, these results indicate that the ACE inhibitor has the property to protect remnant glomeruli from glomerulosclerosis in male Imai rats as well as in other animal models in which focal and segmental glomerulosclerosis is believed to represent a common pathologic pattern. This rat strain represents a unique model of a spontaneous proteinuria which can provide an important information on the pathogenesis of human focal and segmental glomerulosclerosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

[A case of acute interstitial nephritis and nonoliguria acute renal failure induced by cimetidine].

Cimetidine is a histamine H2-receptor antagonist. Widely it is prescribed, and then various side effects have been increasingly recognized. Acute renal failure as a result of acute interstitial nephritis is one of the most important adverse effect. We report a case of biopsy-proven acute interstitial nephritis following cimetidine therapy. Farther more, we review other reported cases of cimetidine-induced acute interstitial nephritis, and discuss the clinical features and a role of immunological mechanisms of these cimetidine-induced disorders. A 52-year-old woman was admitted because of fever and protenuria. A month before admission, she developed gastric ulcer and was given cimetidine 600mg orally a day by a near physician. Laboratory data on admission included the following: white blood cell count, 14700/microliters; eosinophils, 6%; BUN, 50.7mg/dl; Cr, 7.6mg/dl; CRP, 34.0mg/dl. All drugs were discontinued because we suspected drug-induced acute renal failure, especially by cimetidine. Renal biopsy performed on day 3 showed interstitial nephritis with lymphocyte infiltration which was composed mainly of T cell. T4/T8 ratio was determined to be 1. There was neither predominance of helper nor cytotoxic cells in T cell subpopulation. We reviewed 22 cases reported and discussed the features of cimetidine-induced interstitial nephritis. The most important thing is to monitor renal function periodically with the suspicion of this disorder. On the detection of abnormality of laboratory data, cimetidine should be discontinued.

Acute Kidney Injury↗
PubMed1992

[Clinicopathological study of membranous glomerulonephritis in patients with rheumatoid arthritis].

Of 103 patients with membranous glomerulonephritis proved by renal biopsy, 11 (10.7%) had rheumatoid arthritis. Nine of these 11 patients received systemic treatment with anti-rheumatic remedies including gold, D-penicillamine and bucillamine. Two others were administered only token of nonsteroidal antiinflammatory drugs. Renal function of the patients was well maintained and within normal limits. Four patients showed nephrotic syndrome, while mild to moderate proteinuria was found in the other 7. Hematuria was minimal to mild, and it was not a major symptom. Six patients resolved proteinuria completely and 2 patients incompletely after discontinuation of chrysotherapy. Nine cases of the membranous lesion in patients with rheumatoid arthritis were stage 1. Thus it was often difficult to identify the glomerular change only by light microscopy. IgA nephropathy and AA amyloidosis were associated in one patient respectively. Our data lead us to conclude that chrysotherapy would cause membranous lesions, but rheumatoid arthritis itself also induce membranous glomerulonephritis.

Adult↗
PubMed1991

Effects of the methylprednisolone pulse therapy on renal function.

The effect of the methylprednisolone (MP) pulse therapy on renal function was examined in 15 patients with renal or collagen disease. Three nephrotic patients who had reduced renal function and active renal disease with progressive deterioration of renal function prior to the use of MP developed transient renal failure following an MP pulse therapy. The renal failure in each case was reversed by discontinuation of MP and/or by forced diuresis using albumin and furosemide. We examined the correlations between the individual changes in serum creatinine (Scr), body weight (BW) and urine volume (UV) before and after the pulse therapy and other laboratory data such as Scr, total serum protein and albumin. There were significant correlations between a change in Scr on the one hand and changes in BW and UV, Scr and serum albumin on the other. These findings mean that the effect of the MP pulse therapy on renal function depends on the clinical state of the patient and that renal deterioration after the pulse therapy may be more marked in patients who are more nephrotic and more impaired in renal function and suggest that increasing sodium and water retention during an MP therapy and the associated renal interstitial edema, proposed as one of the mechanisms of acute renal failure occurring in patients with minimal-change nephrotic syndrome, may be responsible for the MP-induced transient renal failure.

Acute Kidney Injury↗
PubMed1991

[Membranous glomerulonephritis probably related to bucillamine therapy in two patients with rheumatoid arthritis].

We describe here two patients with rheumatoid arthritis who developed nephrotic syndrome after administration of bucillamine, a novel antirheumatic drug developed in Japan. The nephrotic syndrome occurred after six months' and five months' treatment of bucillamine, respectively. The renal biopsy showed early phase of membranous glomerulonephritis (stage 1) in both patients. The first patient was a 64-year-old man who had received gold therapy for two years, and penicillamine therapy for eight months before bucillamine therapy. The nephrotic syndrome occurred after one year's cessation of the gold therapy and six months' cessation of the penicillamine therapy. The other patient, 57-year-old woman, had no history of gold or penicillamine therapy. Our experience suggests that membranous glomerulonephritis might occur in relation to bucillamine therapy.

Anti-Inflammatory Agents↗
PubMed1991

Renal failure with nephrotic syndrome: reversal with large doses of furosemide.

The present study documents the occurrence of renal failure in 4 nephrotic patients including 3 with minor glomerular lesions and one with membranoproliferative glomerulonephritis. One patient died of sepsis at 3 months after onset of the acute renal failure. In the remaining 3, forced diuresis employing albumin plus furosemide in increasing doses to 600 mg/day reversed the renal failure independent of corticosteroid therapy. All of the 4 patients showed characteristic findings consisting of a remarkably low fractional excretion of sodium and an unexpectedly low urine osmolality at the onset of acute renal failure, although they were rather hypervolemic. Our findings suggest that the occurrence of a low fractional excretion of sodium and low osmolality may provide a good index of an absolute indication for intensive weight reduction therapy such as high-dose furosemide in nephrotic patients with acute renal failure in order to reverse the acute renal failure.

Acute Kidney Injury↗
PubMed1991

A comparative study of IgA nephropathy between two institutions in Japan and Korea.

As an approach to the geopathological evaluation of kidney disease, we conducted a comparative study on IgA nephropathy (IgANP) between Saga Medical School (SMS) in Japan and Kosin Medical College (KMC) in Korea for the period 1983-1987. The relative incidence of IgANP among primary glomerular diseases was significantly higher (P less than 0.05) at SMS (103 cases of IgANP among 250 cases of primary glomerular diseases, 41.2%) than at KMC (63 cases among 201 cases, 31.3%). Clinical and histological comparisons of the IgANP between the institutions revealed that the SMS series was generally milder than the KMC series. When the renal manifestations at the time of biopsy for all cases with primary glomerular diseases were compared, asymptomatic urinary abnormalities were more commonly found at SMS than at KMC. This suggests that certain differences in medical practice may exist between the two institutions, as follows: 1) the medical checkup system may be more efficient, 2) the accessibility to medical service may be easier, and 3) the biopsy criteria may be more liberal in Japan/SMS than in Korea/KMC. Thus, the real differences in incidence and severity of IgANP between the two institutions could be smaller than those reported here.

Adult↗
PubMed1990

[Malignant lymphoma with acute renal failure and nephrotic syndrome].

A case of non-Hodgkin's lymphoma with nephrotic syndrome and acute renal failure is described. A 60-year-old Japanese male was admitted to our hospital in November, 1988, because of lymphadenopathy, fever, night sweat, weight loss. On physical examination, lymphadenopathy was present in both cervical, submandibular, supraclavicular, axillary and inguinal regions. The leukocyte count was 9,700/microliters with 85% neutrophils and 2% atypical lymphocytes. Renal function was normal. Lymph node biopsy showed non-Hodgkin's lymphoma of diffuse, large cell type. Immunohistologic examination showed T cell type. A few days later, he fell into acute renal failure. After systemic chemotherapy, he showed prompt improvement in renal function. Echo and computerized tomography (CT) of abdomen revealed no compression of the ureters and bladder. Renal biopsy findings suggested mesangium proliferative glomerulonephritis without invasion of tumor cells. Our case seemed to be rare and was compared with previous reports.

Acute Kidney Injury↗
PubMed1989

Persistent wedge-shaped low-density lesions on computed tomography of the kidneys without infarction.

A patient with acute lymphoblastic leukemia, who developed acute renal failure, was imaged by computed tomography (CT). Persistent wedge-shaped areas of low attenuation in the kidneys were shown by sequential scans but not areas of infarction were found at autopsy. This case suggests that a wedge-shaped low-density lesion on CT may occur not only in infarcted areas, but also in areas where patchy vasoconstriction occurs.

Acute Kidney Injury↗
PubMed1988

Captopril-induced metabolic acidosis with hyperkalemia.

Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.

Acidosis↗