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Biomedical subjects

O Sakai

Publications and source records attributed to O Sakai.

At least 109 records · Page 6Linked to original sources
PubMed1995

Attenuation of immune complex nephritis in NZB/WF1 mice by a prostacyclin analogue.

Although prostaglandins have been shown to inhibit the evolution of the nephritis in NZB/W mice, the mechanisms of this effect are unknown. To characterize such inhibition, we injected the prostacyclin (PGI2) analogue, beraprost, into NZB/W mice, using 0.5 mg, 1.0 mg or 5.0 mg beraprost/kg body weight of test animals three times in 1 week when the mice were 2 months old. Evaluation included measurement of urine albumin excretion, serological parameters and splenic T cell subset, as well as examination of renal histology by light and fluorescence microscopy. Mice given beraprost showed a marked decrease in urine albumin excretion and in glomerular hypercellularity compared with untreated controls. Maximal beneficial effects occurred when the dose was 5.0 mg/kg of beraprost. These effects correlated with a reduction of immune complex deposition in glomeruli. In addition, beraprost reduced serum levels of immunoglobulins and anti-double-stranded DNA antibodies, and decreased the number of helper (L3T4+) T cells in splenocytes. These results indicate that beraprost attenuates the nephritis of NZB/W mice, and that the source of this effect is the reduced production of autoantibodies and deposition of immune complexes in glomeruli.

Albuminuria↗
PubMed1995

Newly discovered familial juvenile gouty nephropathy in a Japanese family.

Our attention was initially called to 2 young Japanese sisters with gout and renal insufficiency, which led to an investigation of members of their family with similar conditions. One sister, a 26-year-old woman who had suffered from polyuria since infancy, suffered from gout and renal insufficiency. Her younger sister also had a history of polyuria, hyperuricemia, and moderately reduced renal function. Their urinary uric acid levels were reduced but purine enzyme activities in the erythrocytes were normal. A renal biopsy specimen from the younger sister showed severe interstitial fibrosis with tubular atrophy. An investigation of the family revealed an autosomal dominant transmission pattern. We believe these are new familial cases of juvenile gouty nephropathy found in a Japanese family.

Adult↗
PubMed1995

Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy.

Studies conducted over the last decade demonstrated variable therapeutic efficacy of angiotensin converting enzyme (ACE) inhibitor on the progression of glomerular diseases, including IgA nephropathy. In this study, among patients with biopsy-proven IgA nephropathy, 53 patients in whom creatinine clearance had been monitored over 5 yr were recruited for study. These patients were classified into two groups according to whether or not renal function had declined as determined by the slope of creatinine clearance against time: group 1 had stable renal function; group 2 had declining renal function (average: -6.7 +/- 1.3 ml/min/yr). 21 of 53 patients were treated with ACE inhibitor and followed for 48 wk. Gene polymorphism consisting of insertion (I) or deletion (D) of a 287-bp DNA fragment (presumed to be a silencer element) of the ACE gene was determined by PCR. 46 age-matched individuals without history of proteinuria were analyzed as controls. The DD genotype was significantly more frequent in group 2 (43%) than in controls (7%) or group 1 patients with stable renal function (16%). 48 wk after ACE inhibitor administration, proteinuria significantly decreased in patients with DD genotype but not in those with ID or II genotypes. The results indicate that deletion polymorphism in the ACE gene, particularly the homozygote DD, is a risk factor for progression to chronic renal failure in IgA nephropathy. Moreover, this deletion polymorphism predicts the therapeutic efficacy of ACE inhibition on proteinuria and, potentially, on progressive deterioration of renal function.

Adult↗
PubMed1995

A new family of Boucher-Neuhäuser syndrome: coexistence of Holmes type cerebellar atrophy, hypogonadotropic hypogonadism and retinochoroidal degeneration: case reports and review of literature.

The association of familial hypogonadism with progressive cerebellar ataxia is only rarely encountered, and the exact link between the symptoms remains unknown. We report here two sisters presenting with Holmes type cerebellar ataxia, hypogonadotropic hypogonadism and retinochoroidal degeneration recently diagnosed as Boucher-Neuhäuser syndrome. There was consanguinity between the parents of the affected individuals and the condition seemed to be inherited as an autosomal recessive defect. On endocrinological examinations, in both cases, the responses of LH and FSH to LH-RH (100 micrograms) were impaired even after repetitive stimulation with LH-RH (400 micrograms, 7 days), suggesting that the hypogonadism was due to a primary pituitary disturbance. Impaired GH responses to GRF (100 micrograms) and insulin-induced hypoglycemia (0.1 U/kg) were also noted. The two sisters shared an almost identical clinical and endocrinological picture. Their karyotypes were 46, XX. They had been treated for primary and secondary amenorrhea at the age of 20 years and neurological problems had started at the age of 30 years. This unique family displays clinical evidence of a possible common mechanism responsible for a progressive hypothalamo-pituitary and cerebellar impairment of late onset.

Atrophy↗
PubMed1995

Cholesterol emboli following percutaneous transluminal coronary angioplasty as speculated by toe skin biopsy.

A 55-year-old man required hemodialysis for acute renal failure 3 days after repeat percutaneous transluminal coronary angioplasty (PTCA). Bilateral acrocyanosis and necrotic lesions of the toes occurred 10 days after PTCA. Skin biopsy samples revealed needle-shaped cholesterol crystals of the intraluminal clefts in his small arteries. He was diagnosed with cholesterol emboli presenting as blue toe syndrome. The conditions improved with anticoagulation and vasodilation, but improvement in renal function was temporary. He later required maintenance hemodialysis. Cholesterol emboli following PTCA are life threatening because they are difficult to diagnose and can cause severe complications.

Angioplasty, Balloon, Coronary↗
PubMed1995

Boucher-Neuhauser syndrome associated with hypocalciuric hypercalcemia.

A 52-year-old woman was diagnosed as having cerebellar ataxia, hypogonadotropic hypogonadism and retinochoroidal degeneration, the so-called, "Boucher-Neuhauser" syndrome proposed by Limber et al (Am J Med Genet 33:409, 1989). In addition, laboratory findings showed the elevation of serum calcium (Ca) levels, low urinary Ca excretion, and exaggerated reabsorption of filtrated Ca (FECa:0.14%), suggesting complication of hypocalciuric hypercalcemia. This is a very rare case of Boucher-Neuhauser syndrome associated with hypocalciuric hypercalcemia.

Calcium↗
PubMed1995

Familial thyroxine-binding globulin deficiency associated with hyperthyroidism.

A 24-year-old woman with familial thyroxine-binding globulin (TBG) deficiency associated with hyperthyroidism is reported. Thyroid-stimulating hormone (TSH)-binding inhibitor immunoglobulin (TBII) was negative, whereas thyroid-stimulating antibody (TSAb) was positive. Serum thyroxine-binding globulin (TBG) levels were extremely low, and remained low even after the normalization of thyroid function with methimazole (MMI) treatment. The serum TBG level of the mother of patient was also below the normal lower limit. Genetic analysis revealed single nucleotide deletion, common among Japanese with complete TBG deficiency (TBG-CD), from the allele-specific amplification of the TBG genes of the patient.

Adult↗
PubMed1995

Changes in renal function with aging among Japanese.

Renal function was assessed in 329 inpatients who were presumably free of renal disease or water-electrolyte imbalance and the relationship between renal function and aging and sexual differences were investigated. Serum creatinine levels were slightly increased with aging, and were significantly higher in males than in females. Urinary creatinine excretion significantly decreased with aging; this decline was more pronounced in males. Urinary creatinine excretion was significantly higher in males. Creatinine clearance also decreased significantly with aging and this tendency was still observed after correction for body surface area. Sexual differences played no part in creatinine clearance. There was a significant increase in the serum beta 2-microglobulin level with aging. In addition, the Cer of the aged Japanese population was lower in comparison with western counterpart. The findings suggest the need for special consideration in conducting clinical tests or administering drugs to this segment of the population in Japan.

Age Factors↗
PubMed1995

Rhabdomyolysis associated with bacteremia due to Streptococcus viridans.

A 25-year-old man was admitted with complaints of fever and macrohematuria. Laboratory tests showed a substantial increase in serum creatine phosphokinase and creatinine in association with myoglobinuria and proteinuria. Blood culture grew Streptococcus salivarius and Streptococcus oralis. Findings of renal biopsy were compatible with IgA nephropathy. The glomeruli had a mild mesangial proliferation without crescentic lesions. Changes of the interstitium and tubules were not evident. The clinical course and laboratory results strongly suggested a possible link between Streptococcus salivarius/oralis infection, and rhabdomyolysis. Rhabdomyolysis is rarely seen as a complication of bacterial infection, and the present case emphasizes the importance of suspecting bacteremia due to Streptococcus salivarius/oralis in the presence of rhabdomyolysis.

Acute Kidney Injury↗
PubMed1995

[Treatment of secondary hyperparathyroidisms of predialysis chronic renal failure with low doses of 1.25(OH)2D3].

Although disorders of renal calcitriol synthesis play an important role in the pathogenesis of secondary hyperparathyroidism in the early and moderate phase of chronic renal failure, the treatment of secondary hyperparathyroidism with vitamin D metabolite has not attained consensus from the view point that is accelerates the progression of renal disease. The aim of this study was to evaluate the efficacy and adverse effect of low-dose daily oral treatment of 1.25 vitamin D for patients with mild to moderate renal failure. Fifteen chronic renal failure patients with serum creatinine ranging from 2.5 to 6.1 mg/dl and serum intact parathyroid hormone ranging from 100 to 450 pg/ml, were treated with oral 0.25-0.5 micrograms of 1.25 vitamin D for six months, after a six month control periods. In the six months control periods, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein increased significantly, however after the treatment of 1.25 vitamin D, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein decreased significantly. Serum calcium concentration increased significantly after the initiation of 1.25 vitamin D treatment, so it could not be ascertained whether or not 1.25 vitamin D directly suppressed parathyroid hormone synthesis. Bone mineral densities did not change within one year. Renal function was evaluated from the slopes of the reciprocal serum creatinine concentration versus time. The slopes did not change after the administration of 1.25 vitamin D. In conclusion, 1.25 vitamin D treatment of secondary hyperparathyroidism in patients with mild to moderate renal failure had beneficial therapeutic effect on humoral bone parameters, and did not show any adverse effect on renal function.

Aged↗
PubMed1995

[RAEB in T with monosomy 7 after treatment of severe aplastic anemia with long term G-CSF].

A 19-year-old male who suffered from severe aplastic anemia had been treated with granulocyte colony stimulating factor (G-CSF) from September 1991. Marked increase of hematopoietic cells in his bone marrow was observed, and maintenance administration of G-CSF was continued. 15 months later, myeloblasts with nuclear abnormality increased, and 22 months later, myeloblasts with chromosomal abnormality presenting 46, XY, -7, +21 exceeded 20%, and aplastic anemia seemed to be transformed into refractory anemia with excess of blasts in transformation (RAEB in T). The usefulness of G-CSF in the treatment of aplastic anemia is now established, but there are some reports questioning the effect of long-term administration, especially transformation to MDS with monosomy 7. Leukemic transformation from aplastic anemia is very complex, but in some cases, long term administration of G-CSF may affect the natural course and may lead to the earlier development of leukemia.

Adult↗
PubMed1995

[Acute myelomonocytic leukemia complicated with syndrome of inappropriate secretion of antidiuretic hormone, nephrotic syndrome, and hemophagocytic syndrome].

A 59-year-old man was admitted to our hospital because of fever in August 1991. Bone marrow showed normocellularity with 41.5% of CD13, 14, 33 positive blasts, and a diagnosis of AMMoL was made. Laboratory investigation revealed hyponatremia and elevated serum ADH level, indicating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Intensive chemotherapy successfully induced hematological complete remission and his serum sodium level became normal. In February 1992, he developed proteinuria and findings were consistent with nephrotic syndrome (NS). Renal biopsy specimen showed membranous proliferative glomerulonephritis and massive infiltration of macrophages, and his serum interleukin 6 level was elevated. Five months later, he suffered from pancytopenia and elevation of biliary enzymes with increase of hemophagocytic histiocytes in his bone marrow (hemophagocytic syndrome). He transiently responded to low dose chemotherapy but he died due to severe infection. It is interesting that association between macrophages and/or cytokines with these various complications was suggested in AMMoL.

Fatal Outcome↗
PubMed1995

[Recent advances of studies on interstitial nephritis--definition and pathogenesis].

An abbreviated history describing our understanding of the interstitial nephritis was outlined in the present report. Interstitial nephritis has been recognized with increasing frequency. This nephritis is a diverse group of renal disorders in which the predominant morphologic changes occur in the interstitium included tubules. Recent explosive advances in immunological studies and molecular biological techniques have greatly expanded a study on the mechanisms of interstitial fibrosis.

Collagen↗
PubMed1995

[Effect of cyclosporin monotherapy on proteinuria in a patient with membranoproliferative glomerulonephritis].

A-34-year-old man with a 16-year history of proteinuria was successfully treated with cyclosporin A (CsA). He was diagnosed as having membranoproliferative glomerulonephritis (MPGN) by renal needle biopsy and was treated with dipyridamole. In July 1992, he was readmitted for the treatment of anasarka. Although conventional predonisolone was administered for 5 months after one cycle of methyl-predonisolone pulse therapy, his nephrotic state did not improve. Immediately after the cessation of this treatment, he was given CsA 3 mg/kg/day. A marked reduction in proteinuria and edema occurred during the use of CsA for 6 months, with a reduction in the fractional excretion of protein. The nephrotic condition of this patient was subsequently stable without massive proteinuria despite the discontinuation of CsA at least for several months. These findings suggest that CsA monotherapy may be useful in patients with MPGN and steroid-resistant nephrotic syndrome.

Adult↗
PubMed1995

[An epidemiologic study on pathogenesis of uric acid urolithiasis].

We reviewed 5477 patients with urinary calculi who presented during the years from 1975 to 1993. During this time the percentage of calcium stones has remained at approximately 86%. However over the same period the rate of urinary calculi composed of uric acid has increased and is now about 7.2%. The number of uric acid stones has increased 3.5 times compared to 1975. 355 of 394 (90.1%) with uric acid stones are male. We believe that the increase in the numbers of patients seen with gout, hyperurisemia of a high alcohol intake.

Alcohol Drinking↗