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Biomedical subjects

A Hishida

Publications and source records attributed to A Hishida.

At least 37 records · Page 2Linked to original sources
PubMed2001

Dominant effect of supplemented-sucrose on the low protein diet-induced increase in blood pressure of Sprague-Dawley rats.

A low-protein diet (LPD) is known to affect the regulation of hemodynamics, and could contribute to the genesis of hypertension. We investigated the mechanism for the LPD-induced elevation of blood pressure in 52 Sprague-Dawley rats. Rats fed the LPD for 8 weeks showed a significantly higher blood pressure than those fed on a normal-protein diet (NPD) when the LPD included sucrose as a predominant component of carbohydrate (LPD with a high sucrose content, 135 +/- 2 mmHg; NPD, 124 +/- 2 mmHg; p<0.05). However, LPD with a low sucrose content, in which corn starch was the main component of carbohydrate, did not have a hypertensive effect (125 +/- 2 mmHg). Urinary epinephrine and norepinephrine excretion was significantly higher in the LPD high-sucrose group than in the NPD and LPD low-sucrose groups, and there was a significant positive correlation between urinary norepinephrine excretion and systolic blood pressure. Urinary nitric oxide excretion was no different between these groups, and 2 % L-arginine administration exerted no antihypertensive effect on the LPD-induced elevation of blood pressure. Sodium restriction also did not attenuate the LPD-induced elevation of blood pressure. These results suggest that the effect of LPD on blood pressure could be interpreted as the effect of the high sucrose content supplemented to the LPD rather than the direct effect of protein restriction, and that the stimulation of sympathetic nervous activity was associated with this elevation of blood pressure.

Animals↗
PubMed2001

Complication of oliguric acute renal failure in patients treated with low-molecular weight dextran.

Acute renal failure (ARF) is a well-documented but infrequent complication in patients treated with low-molecular weight dextran (LMWD). We herein report 3 cases of oliguric ARF following the administration of dextran-40. One case developed ARF totally after 1.200 g of LMWD administration. In contrast, two cases having increased serum creatinine developed oliguria despite the acceptable therapeutic doses (totally 450 and 650 g). Contrast media was also co-administered in these patients. Plasma exchange (PE), double filtration plasmapheresis (DFPP), or continuous hemodiafiltration (CHDF) but not hemodialysis (HD) reduced circulating dextran concentrations by 35-44% during a single session. All patients completely recovered from ARF by 14-32 days after the treatment. Our cases suggested that radiocontrast could predispose to the development of LMWD-induced ARF especially in patients having pre-existing renal dysfunction. In addition, PE, DFPP and CHDF afforded a beneficial effect for removing accumulated LMWD from the circulation.

Acute Kidney Injury↗
PubMed2001

Amelioration of post-ischaemic renal injury by contralateral uninephrectomy: a role of endothelin-1.

BACKGROUND: Previous studies showed that unilateral renal damage is attenuated by prior contralateral uninephrectomy (Nx) in ischaemia-induced acute renal failure (ARF). Since renal ischaemia increases endothelin-1 (ET-1) production in the kidney, we examined whether the alteration of renal ET-1 content may contribute to the nephrectomy-induced attenuation of renal injury. METHODS: Ischaemic renal injury was provoked by 60-min left renal artery occlusion (RAO). Removal of the right kidney was performed just before RAO in the Nx group. Forty-eight hours after release of the clamp, renal ET-1 content was measured in both non-nephrectomized and unilaterally nephrectomized rats. We also examined the effects of a selective ET(A) receptor (FR139317) and monoclonal ET antibody (AwETN40) on the RAO-induced changes in renal haemodynamics at 2 and 48 h after RAO respectively. RESULTS: The plasma concentration of ET-1 did not change in the two groups of ARF rats, but the cortical content of ET-1 increased to a lesser extent in Nx animals after ischaemia. Prior removal of the right kidney significantly facilitated the percentage recovery of left renal blood flow (RBF) during the first 2 h after release of the clamp. The percentage recovery of inulin clearance (Cin) by the kidney was also significantly better in Nx than sham-Nx rats at 48 h after RAO. Continuous administration of FR139317 (50 mg/kg/day) using osmotic minipumps for 3 days significantly attenuated exogenous ET-1-induced decrease in Cin and RBF. Infusion of FR139317 restored the decrease in RBF to control values during first 2 h in sham-Nx rats. However, FR139317 and AwETN40 did not ameliorate the RAO-induced decline of Cin in sham-Nx or Nx rats at 2 and 48 h after ischaemia respectively. CONCLUSIONS: Contralateral uninephrectomy prior to ischaemia-induced ARF attenuated the increase in cortical ET-1 content and subsequent renal response to ischaemic injury. This beneficial effect of unilateral nephrectomy, however, was not mediated through well-preserved RBF due to reduced intrarenal ET-1 action.

Acute Kidney Injury↗
PubMed2001

High blood soluble receptor p80 for tumour necrosis factor-alpha is associated with erythropoietin resistance in haemodialysis patients.

BACKGROUND: Inflammation is one of the major causes of resistance to erythropoietin (rHuEpo) treatment. Tumour necrosis factor-alpha (TNF-alpha), one of the most potent proinflammatory cytokines, is known to inhibit human erythropoiesis directly in vitro. Although blood levels of soluble receptors for TNF-alpha (sTNFRs) are elevated in haemodialysis (HD) patients, the role of sTNFR for rHuEpo responsiveness in HD patients remains to be clarified. METHODS: We measured serum sTNFR (p55 and p80) levels in 83 stable outpatients undergoing regular HD (age 62+/-1, HD duration 15+/-1 years). After dividing the patients into three groups according to rHuEpo dose: (low (L) <60, n=31; moderate (M) > or =60 to <120, n=31; high (H) > or =120 U/kg/week rHuEpo, n=21), we examined the relationship between serum sTNFR levels and the degree of renal anaemia and rHuEpo dosage. RESULTS: Haemoglobin was significantly higher in patients receiving low rHuEpo dosage (L, 10.5+/-0.2; M, 9.7+/-0.1; H, 9.5+/-0.2 g/dl, P<0.01 vs M and H groups). There were no differences in blood TNF-alpha, sTNFR p55, C-reactive protein, albumin, ferritin, or intact parathyroid hormone levels among the three groups. Body mass index and creatinine generation rate, a marker of whole-body muscle volume, were significantly reduced in group H (P<0.01). Serum sTNFR p80 levels were significantly higher in group H (4.88+/-0.45 ng/ml) than in L (3.73+/-0.14 ng/ml) and M (3.67+/-0.21 ng/ml) groups (P<0.05). The blood interleukin (IL)-6 level was also increased in patients requiring high rHuEpo doses (L, 5.5+/-0.5; M, 6.4+/-0.5; H, 10.2+/-2.0 pg/ml, P<0.05 vs L and H groups). A stepwise regression analysis revealed that gender and sTNFR p80 were significant predictors of rHuEpo dosage. A significant direct relationship was found between rHuEpo dose and sTNFR p80 (r=0.499) and IL-6 (r=0.439) values in women (P<0.01) but not in men. CONCLUSIONS: These findings suggest that high blood sTNFR p80 may contribute to the development of rHuEpo resistance in female patients undergoing long-term HD.

Adult↗
PubMed2001

Potential therapeutic effect of simvastatin on progressive renal failure and nephrotic-range proteinuria caused by renal cholesterol embolism.

We report our experience with a 62-year-old Japanese man with cholesterol crystal embolism after angiographic procedures performed because of intermittent claudication. In addition to progressive renal failure and nephrotic-range proteinuria, cutaneous ischemia, consisting of livedo reticularis in the lower limbs and digital necrosis at the tip of the right toe, and fundoscopic findings showing several white spots in the branches of retinal artery were also observed. Progressive renal failure and nephrotic-range proteinuria were halted just after treatment with simvastatin. Thus, simvastatin can exert a beneficial therapeutic effect on renal cholesterol embolism.

Anticholesteremic Agents↗
PubMed2001

Hypercalcemia in a patient with B-cell acute lymphoblastic leukemia: a role of proinflammatory cytokine.

The complication of hypercalcemia is reported to occur only in 2.5-4.8% of patients with acute lymphoblastic leukemia (ALL). We herein report a 53-year-old female patient with early B-cell ALL, complicated with extreme hypercalcemia (15.2 mg/dL). Bone X-ray revealed osteolytic changes in many locations. Serum 1,25(OH)2vitaminD3 and parathyroid hormone (PTH) levels were suppressed below normal ranges on admission. The circulating parathyroid hormone-related protein (PTHrP) value was within a normal range (< 1.1 pmol/L). Serum concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and soluble IL-2 receptor were increased to 72 pg/ml, 25.3 pg/ml, and 1469 U/ml, respectively. Following the induction chemotherapy, the serum calcium level was promptly normalized accompanied with decreases in serum TNF-alpha, IL-6 and soluble IL-2 receptor values to 34 pg/ml, 6.35 pg/ml, and 737 U/ml, respectively. Serum PTHrP values remained within detectable levels. To our knowledge, this is the first case of B-cell ALL in a patient who developed hypercalcemia with elevated concentrations of TNF-alpha, IL-6, and soluble IL-2 receptor, but not related to PTHrP. High circulating proinflammatory cytokines may have contributed to development of ALL-induced osteolysis and hypercalcemia in the present case.

Biomarkers, Tumor↗
PubMed2001

Tuberculous arthritis mimicking neoplasm in a hemodialysis patient.

Hemodialysis patients are known to develop the complication of extrapulmonary tuberculosis more frequently than the general population. Tuberculous arthritis is a rare form of extrapulmonary tuberculosis and is reported to occur in approximately 1% of cases in nonuremic patients. Only 3 cases in dialysis patients, who were not proven by a bacterial culture or had died before treatment, have been reported. We report herein a culture-proven case of tuberculous arthritis developing at the sternoclavicular joint, which initially mimicked an apparent neoplasm in a hemodialysis patient. A favorable outcome was obtained after antituberculous therapy. Tuberculosis must be considered one of the most significant diagnoses in hemodialysis patients who present with a tumor-like lesion.

Aged↗
PubMed2001

Elevation of blood (1-->3)-beta-D-glucan concentrations in hemodialysis patients.

Determination of the blood (1-->3)-beta-D-glucan (beta-DG) concentration is a sensitive marker to detect the presence of deep mycosis and fungal infections. Although cellulose material is known to contain beta-DG, the influence of a cellulose dialyzer membrane on the blood beta-DG level remains to be elucidated. In this study, we determined the plasma beta-DG levels in dialysis outpatients using either a modified regenerated cellulose (MRC) or a synthetic polysulfone (PS) membrane for more than 3 months. Plasma beta-DG levels were extremely high in patients using the MRC (2,778 +/- 549 pg/ml, n = 9) but not the PS membrane (18.8 +/- 3.7 pg/ml, n = 8) compared to normal ranges (<20 pg/ml). A single dialysis session using the MRC membrane further increased blood beta-DG values to 5,561 +/- 722 pg/ml (p < 0.01). After changing the membranes from MRC to PS, the blood beta-DG levels gradually decreased and reached 29.6 +/- 6.0 pg/ml at 6 months. In contrast, the PS membrane did not affect plasma beta-DG levels after a single dialysis session (16.0 +/- 3.9 pg/ml) or 4 months later (24.0 +/- 4.9 pg/ml). These findings suggested that a cellulose membrane could influence the measurement of blood beta-DG concentrations in the long-term. Careful assessment is required to diagnose the presence of fungal infection in HD patients using a cellulose membrane.

Aged↗
PubMed2001

Effect of weekly or successive iron supplementation on erythropoietin doses in patients receiving hemodialysis.

AIMS: To conduct a 3-month prospective study to determine the optimal way for intravenous iron supplementation in hemodialysis (HD) patients with resistance to recombinant human erythropoietin (rHuEPO) therapy due to deficient iron storage. METHODS: Thirty-five HD patients with iron deficiency were divided into three groups: (1) patients receiving an intravenous infusion of 40 mg of iron during the first ten HD sessions (n = 12); (2) patients receiving 40 mg of iron injected once a week for 10 weeks (n = 12), and (3) patients without any iron supplementation (n = 11). The rHuEPO dosage was adjusted to maintain hemoglobin levels >10.0 g/dl, and the degree of anemia was assessed 3 months later. RESULTS: In group 1, the hemoglobin levels were significantly increased after 4 weeks and remained increased until the end of the study (p < 0.01). In group 2, the hemoglobin levels were gradually increased until the end of the study (p < 0.01). There was no difference in the final hemoglobin values between both groups. The rHuEPO dosage was significantly decreased from 131 +/- 18 to 90 +/- 17 U/kg/week in group 1 (p < 0.01), but could not be changed in group 2 during the observation period despite a similar elevation of the serum ferritin level. In group 3, the rHuEPO doses were rather increased at the end of the study (p < 0.05). CONCLUSION: Aggressive iron supplementation for the short term may be effective to restore rHuEPO hyporesponsiveness in HD patients with functional iron deficiency.

Aged↗
PubMed2001

Decreased plasma and cerebrospinal fluid glutamine concentrations in a patient with bialaphos poisoning.

A 47-year-old Japanese woman undergoing maintenance hemodialysis (HD) was admitted to our hospital because of poisoning with the herbicide bialaphos. Respiratory arrest and loss of consciousness ensued rapidly, accompanied by convulsions and nystagmus. Treatment with HD and direct hemoperfusion, followed by HD alone, effectively removed bialaphos and its chief toxic metabolite (L-AMPB) from the circulation (bialaphos decreased from 0.33 to < 0.05 microg/ml and L-AMPB from 14 to 0.86 microg/ml). The glutamate concentration improved gradually after the removal of bialaphos and L-AMPB from plasma (plasma glutamate concentration: 250.4 nmol/l on day 5 to 120.6 nmol/l on day 26). Decreased glutamine concentration in cerebrospinal fluid was demonstrated for the first time as well as in plasma, indicating glutamine synthetase inhibition not only in plants but also in humans by bialaphos poisoning.

Adult↗
PubMed2001

Progressive renal failure and blindness due to retinal hemorrhage after interferon therapy for hepatitis C virus-associated membranoproliferative glomerulonephritis.

We treated a 67-year-old Japanese woman with membranoproliferative glomerulonephritis (MPGN) and chronic active hepatitis associated with hepatitis C virus (HCV) infection. Treatment commenced with a daily dose of 6 MU IFN alpha-2b for 2 weeks, which was changed to three times weekly thereafter. After 2 weeks, HCV RNA in the serum was undetectable and there was a concomitant reduction in proteinuria. Treatment with IFN alpha-2b was discontinued because of severe headache and fever. Five weeks after the discontinuation of IFN alpha-2b, the patient experienced the sudden onset of visual loss due to retinal hemorrhage. Subsequently, proteinuria and renal function progressively deteriorated though HCV RNA was undetectable. This case exemplifies the need for careful monitoring of renal function and retinal lesions not only in patients receiving IFN but also in those following the discontinuation of IFN treatment.

Aged↗
PubMed2001

Stiff-person syndrome associated with cerebellar ataxia and high glutamic acid decarboxylase antibody titer.

Glutamic acid decarboxylase (GAD) is the main target of humoral autoimmunity in patients with insulin-dependent diabetes mellitus (IDDM) and stiff-person syndrome. We reviewed the case of a 46-year-old woman who had cerebellar ataxia before getting stiff-person syndrome and IDDM with high anti-GAD autoantibody titers. This was a rare case in which there were both the clinical symptoms of stiff-person syndrome and cerebellar ataxia. In western blot analysis her serum reacted with 65-kDa proteins from rat cerebellum, cerebral cortex, and spinal cord. Autoantibodies to GAD may cause functional impairment of gamma-aminobutyric acid (GABA) neurons in the spinal cord as well as in the cerebellum.

Autoantibodies↗
PubMed2001

Association between circulating leptin and soluble receptors for tumor necrosis factor-alpha in hemodialysis patients.

BACKGROUND: The expression of leptin, an adipocyte-derived protein, is regulated by tumor necrosis factor-alpha (TNF-alpha). Since circulating leptin levels adjusted for body fat mass are reported to be increased in dialysis patients, we examined if the TNF-alpha system may influence blood leptin levels in hemodialysis (HD) patients. PATIENTS AND METHODS: Sixty-three stable HD patients who had no signs of infection, collagen disease or malignancy were enrolled in the study (age: 63 +/- 1 years, duration of HD: 14 +/- 1 years, male/female = 34/29). We measured serum leptin, TNF-alpha, soluble receptors for TNF-alpha (sTNFR p55, p80) and interleukin-6 (IL-6) concentrations with ELISA kits. Body fat mass was determined using DEXA. To evaluate the potential association between serum leptin and the TNF-alpha system, we compared serum leptin and sTNFR levels, which has been validated as a sensitive marker of activation of the TNF-alpha system. RESULTS: Serum leptin levels were significantly higher in female patients compared to male patients (14.07 +/- 3.60 vs. 4.26 +/- 0.85 ng/ml, p < 0.005). A strong correlation was found between serum leptin levels and estimated body fat mass both in males (r = 0.742, p < 0.0001) and females (r = 0.769, p < 0.001), respectively. Serum TNF-alpha, sTNFR p55, p80 and IL-6 levels were significantly increased in HD patients compared to normal subjects. However, no association was found between serum leptin and serum TNF-alpha, sTNFR p55, p80 and IL-6 levels. Serum leptin levels were significantly correlated with the atherosclerotic index both in men (r = 0.382, p = 0.027) and women (r = 0.281, p = 0.041). In contrast, there was no relationship between circulating leptin values and serum albumin, transferrin, creatinine levels, or normalized protein catabolic rate in each sex. CONCLUSION: These findings suggested that serum leptin is independent of the TNF-alpha system, and is mainly correlated with body fat volume in HD patients. Elevation of circulating leptin may be associated with the disturbance of the serum lipid profile rather than malnutrition in patients receiving long-term HD.

Adipose Tissue↗
PubMed2000

Defective electron transfer in complexes I and IV in patients with aceruloplasminemia.

Aceruloplasminemia is a disorder of iron metabolism caused by mutations in the ceruloplasmin gene. It is characterized by progressive neurodegeneration of the retina, basal ganglia, dentate nucleus and cerebral cortex in association with iron accumulation in these tissues. Enzyme activities in the mitochondrial respiratory chain of the cerebral cortices of two patients were reduced to 62% and 71% for complexes I and IV. Malondialdehyde, a marker of lipid peroxidation, was three times higher than the control value and was accompanied by increased expression of superoxide dismutase 2 (Mn SOD). These findings suggest that iron-mediated free radicals contribute to the impairment of mitochondrial energy metabolism in aceruloplasminemia

Aged↗
PubMed2000

Short-term effect of vitamin K administration on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis.

Glucocorticoid-induced osteoporosis has been reported to be caused by enhanced bone resorption and suppressed bone formation. To clarify whether administration of vitamin K, which enhances bone formation, prevents prednisolone-induced loss of bone mineral density (BMD), a randomized, prospective, controlled study was conducted on 20 patients with chronic glomerulonephritis scheduled for treatment with prednisolone. All patients were initially treated with 0.8 mg/kg body weight/day of prednisolone (maximum of 40 mg) for 4 weeks, tapering to 20 mg/day over approximately 6 weeks. Ten patients received prednisolone alone (Group 1), and the other 10 patients received prednisolone plus 15 mg of menatetrenone, vitamin K, three times per day (Group 2). BMD of the lumbar spine measured by dual-energy X-ray absorptiometry (DXA) and biochemical markers of bone metabolism in blood and urine were evaluated before and 10 weeks after administration of prednisolone alone or with menatetrenone. In Group 1, treatment with prednisolone significantly reduced BMD of the lumbar spine from 1.14 +/- 0.12 to 1.10 +/- 0.11 g/cm2 (P = 0.0029). Serum intact osteocalcin and procollagen type I C-peptide (PICP) concentrations, biochemical markers of bone formation, were markedly reduced. A biochemical marker of bone resorption, urinary excretion of deoxypyridinoline, was significantly reduced. In Group 2, prednisolone-induced reduction of BMD was prevented by menatetrenone administration (1.09 +/- 0.09 to 1.07 +/- 0.07 g/cm2, P = 0.153). Menatetrenone prevented reduction of PICP concentration by prednisolone but not in serum intact osteocalcin concentration and urinary excretion of deoxypyridinoline. Thus, treatment with prednisolone resulted in loss of BMD of the lumbar spine associated with suppression of both bone formation and bone resorption. Menatetrenone is a useful agent in preventing prednisolone-induced loss of BMD.

Absorptiometry, Photon↗
PubMed2000

Possible involvement of myofibroblasts in cellular recovery of uranyl acetate-induced acute renal failure in rats.

Cellular recovery in acute renal failure is a form of wound healing. Fibroblast-like cells or myofibroblasts are involved in wound healing. We examined the serial changes in tubular damage and origin and kinetics of regenerating cells in uranyl acetate-induced acute renal failure, with a special emphasis on interstitial myofibroblasts. Acute renal failure was induced in rats by intravenous injection of uranyl acetate (5 mg/kg). All rats received bromodeoxyuridine intraperitoneally 1 hour before sacrifice. Serial changes in the distribution of tubular necrosis and bromodeoxyuridine-incorporated or vimentin-positive regenerating cells, and their spatial and temporal relation to alpha-smooth muscle actin-positive myofibroblasts as well as ED 1-positive monocytes/macrophages were examined. Necrotic tubules initially appeared around the corticomedullary junction after uranyl acetate injection, then spread both downstream and upstream of proximal tubules. Peritubular alpha-smooth muscle actin-positive myofibroblasts appeared and extended along the denuded tubular basement membrane, establishing network formation throughout the cortex and the outer stripe of outer medulla at days 4 to 5. Tubular regeneration originated in nonlethally injured cells in the distal end of S3 segments, which was confirmed by lectin and immunohistochemical staining using markers for tubular segment. Subsequently, upstream proliferation was noted along the tubular basement membrane firmly attached by myofibroblasts. During cellular recovery, no entry of myofibroblasts into the tubular lumen across the tubular basement membrane was noted and only a few myofibroblasts showed bromodeoxyuridine positivity. The fractional area of alpha-smooth muscle actin-positive interstitium reached a peak level at day 7 in the cortex and outer stripe of outer medulla, then gradually disappeared by day 15 and remained only around dilated tubules and in the expanded interstitium at day 21. ED 1-positive monocytes/macrophages were transiently infiltrated mainly into the region of injury. They did not show specific association with initially necrotic tubules, but some of them located in close proximity to regenerating tubules. Nonlethally injured cells at the distal end of proximal tubules are likely to be the main source of tubular regeneration, and the transient appearance of interstitial myofibroblasts attached to the tubular basement membrane immediately after tubular necrosis might play a role in promoting cellular recovery in possible association with monocytes/macrophages in uranyl acetate-induced acute renal failure.

Acute Kidney Injury↗