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T Ideura

Publications and source records attributed to T Ideura.

At least 37 records · Page 2Linked to original sources

Simvastatin suppresses glomerular cell proliferation and macrophage infiltration in rats with mesangial proliferative nephritis.

Inhibition of 3-hydro-3-methylglutaryl coenzyme A reductase inhibits the production of mevalonate and has been shown to suppress proliferation in many cell types. Therefore, 3-hydro-3-methylglutaryl coenzyme A reductase inhibitors may have a beneficial effect in glomerular disease, because glomerular cell proliferation is a central feature in the active glomerular injury. This study examines the effect of simvastatin on glomerular pathology in a rat mesangial proliferative glomerulonephritis (GN) induced by anti-thymocyte antibody (anti-Thy 1.1 GN). There was no difference in the degree of the antibody and complement-mediated initial injuries between simvastatin-treated and control GN rats. The most pronounced feature of simvastatin-treated GN was the suppression of the early glomerular cell proliferation. The proliferative activity was maximal at day 4 after disease induction (26.5+/-7.0 of proliferating cell nuclear antigen-positive cells/glomerulus); however, approximately 70% of proliferation was suppressed by simvastatin treatment. At day 4 after disease induction, simvastatin administration also decreased alpha-smooth muscle actin expression in the glomerulus, which is a marker for mesangial cell activation. Inhibition of monocyte/macrophage recruitment into glomeruli by simvastatin was also a prominent feature. There was a 30% decrease in the number of glomerular ED-1+ cells by simvastatin treatment at day 2 after disease induction. Furthermore, simvastatin remarkably suppressed subsequent mesangial matrix expansion and type IV collagen accumulation in glomeruli. We also found that the platelet-derived growth factor expression was reduced in simvastatin-treated nephritic rats, which might simply reflect the reduction in mesangial cell proliferation and mesangial cellularity. There was no significant difference in plasma cholesterol or triglyceride levels between simvastatin- and vehicle-treated nephritic rats at day 2 and day 4, which corresponded to the times when simvastatin treatment resulted in a reduction in mesangial cell proliferation. In conclusion, this is the first report to find that mesangial cell proliferation and matrix expansion have been blocked by simvastatin in vivo. The protective effect of simvastatin in the matrix expansion in anti-Thy1.1 GN was partly by inhibition of mesangial cell proliferation and monocyte/ macrophage recruitment into glomeruli, which were independent of a change in circulating lipids.

Actins↗

Elimination study of silver in a hemodialyzed burn patient treated with silver sulfadiazine cream.

Silver sulfadiazine (SSD) cream is a potent agent for the treatment of burns. In a patient with end-stage renal disease, we observed a marked elevation in serum silver concentration in the course of 2 weeks of SSD cream therapy (200 g/d). Serum concentration of silver reached a maximum of 291 ng/mL in association with a rapid deterioration of mental status. SSD therapy was discontinued, and hemodialysis, hemofiltration, or plasma exchange was continually performed. Four months later, the patient died. At autopsy, profoundly elevated levels of silver were found in brain tissues of this patient (617.3, 823.7 ng/g wet tissue weight in the cerebrum and cerebellum, respectively). To determine the most efficient therapy to remove silver from serum, we compared hemodialysis (HD), hemofiltration (HF), and plasma exchange (PE). Both plasma exchange and hemofiltration were effective in decreasing serum silver, and their effects were additive. By contrast, HD was ineffective in reducing serum silver. This case illustrates that, on SSD cream therapy, burn patients with disturbed renal function are at risk of accumulating silver in serum and tissue to the level that may cause neuralgic decompensation. Removal of serum silver can best be effected by PE, particularly when combined with HF. In contrast, HD per se does not appear efficacious. None of these blood purification modalities improves deterioration of neurological status potentially attributable to silver deposition in brain tissues.

Adult↗

Clinical significance of hepatitis G virus infection in patients on long-term haemodialysis.

Infection with the newly discovered hepatitis G virus (HGV) was analysed in 163 patients on long-term haemodialysis to clarify its prevalence and clinical significance. Hepatitis G virus RNA in serum was measured by polymerase chain reaction with primers corresponding to the putative non-structural 5' region. Of the 163 patients, three (1.8%) were positive for hepatitis B surface antigen, 40 (24.5%) were positive for hepatitis C virus (HCV)-RNA and 16 (9.8%) were positive for HGV-RNA. Five of the 16 patients with HGV-RNA were also positive for HCV-RNA. Patients with HCV and HGV coinfection had undergone a longer duration of haemodialysis (P = 0.001) and had higher units of transfusion (P = 0.031) compared with those without hepatitis virus infection. Transfusion history was significantly higher (P = 0.039) in patients with only HGV infection than in those without hepatitis virus infection. Hepatitis C virus RNA concentration was higher (P = 0.032) in patients with HCV and HGV coinfection than in those with HCV infection only, but alanine aminotransferase (ALT) levels were similar between these two groups. In conclusion, about 10% of patients on haemodialysis were infected with HGV and the infection was closely associated with transfusion history.

Adolescent↗

[Proposal on new formulas for renal depth in the technetium-99m-mercaptoacetyltriglycine (MAG3) scintigraphy].

UNLABELLED: Recently, camera-based techniques to measure effective renal plasma flow (ERPF) have become more popular than single plasma sample techniques because camera-based measurements avoid the necessity of delayed plasma samples and in vitro techniques. The measurements of ERPF are used to estimate the clearance of technetium-99m-mercaptoacetyltriglycine (MAG3). However, camera-based techniques are dependent on an accurate estimate of renal depth to correct for soft-tissue attenuation. Then, new formulas for renal depth correction of technetium-99m-MAG3 clearance in place of Tønnesen's, M. Ito's, K. Itoh's, and Taylor's methods were tried to establish in this paper. PATIENTS AND METHODS: Eleven hundred and seventy patients without any renal disease were objected. The data from measurement of renal depth using X-ray CT in supine position were analyzed statistically. RESULTS: The depths of right kidney (Dr) and left kidney (Dl) were 7.33 +/- 1.27 and 7.07 +/- 1.27 cm. The correlation coefficients between Dr and height (H) body weight (W), body surface area (BSA: W0.425 x H0.725 x 0.007184 m2), age, and abdominal thickness (Ta) were 0.275, 0.709, 0.615, 0.087, and 0.743. The correlation coefficients between Dl and H, W, BSA, age, and Ta were 0.269, 0.732, 0.629, 0.029, and 0.812. Ta had best correlation with both Dr and Dl. The calculation formulas for Dr and Dl using Ta were as follows: Dr = 0.32 x Ta + 0.87 cm, and Dl = 0.36 x Ta - 0.08 cm. On the other hand, the multiplex calculation formulas of Dr or Dl with H, W, and Ta were as follows: Dr = 0.18Ta + 8.54 x (W/H) + 0.75 (r = 0.768), and Dl = 0.26Ta + 5.90 x (W/H)-0.16 (r = 0.823). CONCLUSION: The new regression equations provide superior estimates of renal depth compared to conventional equations. Application of these new formulas into camera-based protocols to determine renal clearances may lead to more accurate measurements of ERPF using technetium-99m-MAG3 scintigraphy.

Adolescent↗

[A case of posterior nutcracker syndrome occurring in pregnancy].

We have encountered a 23-year-old pregnant woman with macrohematuria, which occurred from the 8th or 9th week of gestation. Blood pressure and renal function were normal during the total course of pregnancy. Macrohematuria did not disappear after childbirth. Cystoscopy was conducted and the excretion of hematuria from the left ureter was confirmed. Therefore, a left renal venogram was performed although abdominal ultrasonography and CT scanning showed no abnormality. There were two branches of the left renal vein (LRV), such as the anterior and posterior branch. The pressure gradient was 4.4 cm H2O between the anterior branch of LRV and the inferior vena cava (i.v.c.). However, a significant pressure gradient (6.6 cm H2O) was demonstrated between the posterior branch of the LRV and IVC. From these findings we diagnosed this patient as venous hypertension in the posterior branch of the left renal vein (= posterior Nutcracker syndrome, PNS). Enlargement of the uterus in pregnancy might not be important in the occurrence of PNS because macrohematuria was observed from the 8th or 9th week of gestation. Functional hemodynamic change in pregnancy might cause a widening of the diameter or a shift of the aorta, that might result in compression of the posterior branch of the left renal vein. Persistence of macrohematuria after childbirth might have been due to irreversible hemodynamic alteration by the development of co-lateral circulation. To the best of our knowledge, this is the first case of PNS occurring in pregnancy.

Adult↗

Expression of epidermal growth factor and its receptor in rabbits with ischaemic acute renal failure.

Urinary immunoreactive epidermal growth factor (EGF) levels decrease, and renal immunoreactive EGF levels increase in rats with ischaemic acute renal failure (ARF). We investigated the immunohistochemical localization of EGF and EGF receptor in rabbits with ischaemic ARF to clarify the significance of renal EGF. Male New Zealand White rabbits underwent right nephrectomy prior to a 60 min renal artery clamp. At 3, 6, 24, 48, 72 and 96 h after ischaemia, serum urea nitrogen and serum creatinine were determined. Guinea pig anti-rabbit EGF antibody and monoclonal anti-EGF receptor antibody were used for the primary incubation. EGF was immunolocalized to the ascending limb of Henle and the distal convoluted tubule in the normal right kidneys. However, in the post ischaemic left kidneys at 6, 24, 48 and 72 h, immunoreactivity of EGF was associated with proximal tubules. In the normal kidneys, antibody to EGF receptor reacted with distal tubules and collecting ducts. In the ischaemic kidneys, EGF receptor was localized in the basolateral membrane in the proximal tubules. The expression of EGF and EGF receptor in renal tubules may play an important role in repair following ischaemic renal damage.

Acute Kidney Injury↗

rHuEPO enhances the production of plasminogen activator inhibitor-1 in cultured endothelial cells.

The direct effects of recombinant human erythropoietin(rHuEPO) on coagulation and fibrinolysis factors were evaluated in a cultured endothelial cell (EC) system. Confluent quiescent ECs were incubated with or without 5.0 U/ml rHuEPO for 1, 6, and 18 hours, and supernatant concentrations of plasminogen activator inhibitor-1 (PAI-1): antigen (Ag), tissue plasminogen activator and thrombomodulin, and supernatant activities of tissue factor pathway inhibitor and von Willebrand factor were measured. The results showed that only PAI-1 levels were increased by the presence of rHuEPO. In order to assess the effect of rHuEPO on PAI-1 production by EC more precisely, confluent ECs were incubated with various doses of rHuEPO (0, 1.0, 2.5, 5.0, 10.0 U/ml) for 1, 6, 12, and 18 hours, and PAI-1:Ag concentrations in the supernatants of media were measured. PAI-1:Ag in the supernatants were increased by the presence of rHuEPO at all incubation times (P < 0.01) and the increase in PAI-1:Ag was dependent on rHuEPO concentration. The increases in PAI-1:Ag by 5.0 U/ml rHuEPO were comparable to those by 0.1 U/ml tumor necrosis factor-alpha, 1.0 microgram/ml lipopolysaccharide, and 0.5 U/ml thrombin. The increase in PAI-1:Ag by rHuEPO was suppressed by pre-incubation with 10 micrograms/ml cycloheximide (P < 0.01) or 0.2 microgram/ml actinomycin D (P < 0.01). These results indicate that rHuEPO directly stimulates PAI-1 production in cultured EC via de novo protein and RNA syntheses.

Cells, Cultured↗

Dialysis membranes in the year 2000: performance and biocompatibility.

Among many substances accumulated or generated by renal failure, much attention has focused on the pathogenetic effects of advanced glycation end-product (AGE)-bound proteins such as AGE-modified beta 2-microglobulin, and bioactive substances such as inflammatory cytokines. In order to remove these substances efficiently, dialysis membranes in the year 2000 should have a higher molecular cut-off point and a sharper cut-off curve, with less formation of concentration polarization, or a greater adsorbing capacity for target substances with less ensuing protein gel layer. Adequate supplementations for depleted substances by more efficient dialysis will be necessary as at present with carnitine and vitamins. Further, from now until the year 2000, membranes in which biocompatibility nearly corresponds to that of capillary endothelium, and safe and economical purification systems of dialysate should be realized.

Biocompatible Materials↗

[Role of apoptosis in the progression of secondary hyperparathyroidism].

In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2(apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperparathyroidism(2 degrees HPT), as compared with primary hyperparathyroidism(1 degree HPT) for clarification of the role of apoptosis in the development of 2 degrees HPT. The number of Ki-67+ cells was remarkably increased in 2 degrees HPT(12.02 +/- 10.87, mean +/- SD) compared to in 1 degree HPT(0.81 +/- 0.53) (p < 0.01). However, the number of apoptotic cells was significantly decreased in 2 degrees HPT(0.10 +/- 0.06) compared to in 1 degree HPT(0.31 +/- 0.19) (p < 0.05). To the contrary, Bcl-2+ cells were increased in 2 degrees HPT(0.35 +/- 0.23) compared to in 1 degree HPT(0.10 +/- 0.13) (p < 0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1 degree HPT and 2 degrees HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2 degrees HPT.

Adult↗

Endothelin-1 and endothelin B type receptor are induced in mesangial proliferative nephritis in the rat.

We studied whether endothelin-1 (ET-1) and its receptor subtypes (ETAR, endothelin A type receptor; and ETBR, B type receptor) were up-regulated in the glomerulus of a rat model of mesangial proliferative glomerulonephritis induced by anti-thymocyte serum (anti-Thy-1 GN). A marked increase in preproET-1 mRNA could be demonstrated in glomerular RNA 3 and six days after disease induction (4.1- and 4.9-fold vs. day 0, respectively), corresponding to the time of mesangial cell proliferation, to the time of macrophage infiltration into glomeruli, and also to the time of increase in glomerular PDGF B-chain mRNA expression. The localization of ET-1 protein in the mesangial area and along the inner aspect of the glomerular capillary wall was also demonstrated by immunohistochemistry from day 3 and maximal at day 6. The major source of the cells expressing ET-1 in glomeruli appeared to be mesangial cells, glomerular endothelial cells and monocyte/macrophages. Furthermore, both gene and protein expression of ET-1 were associated with increased urinary excretion of ET-1. There was no increase in the plasma ET-1 immunoreactivity. Glomerular expression of ETBR mRNA increased in anti-Thy-1 GN (1.5-fold vs. day 0 at day 3 after disease induction, 3.6-fold at day 6 and 2.7-fold at day 10), but there was minimal change in ETAR mRNA expression. These results suggest that preproET-1 mRNA, which is induced in anti-Thy-1 GN, is linked primarily with ETBR mRNA expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Immunochemical study of epidermal growth factor in rats with mercuric chloride-induced acute renal failure.

Urine contains high concentrations of epidermal growth factor (EGF), and EGF is a potent growth promoter for proximal tubular cells. In the present study, urinary and whole-kidney EGF levels were investigated in rats with mercuric chloride (HgCl2)-induced acute renal failure (ARF) using a specific radioimmunoassay for rat EGF to clarify changes in EGF after toxic injury. Male Wistar rats were given HgCl2 (2 mg/kg, subcutaneously) or saline. Serum urea nitrogen and creatinine levels were measured for 4 days after toxin administration. Forty-eight hours after toxic injury, urinary immunoreactive EGF levels in HgCl2-treated rats decreased significantly compared with control rats (1.62 +/- 0.15 versus 3.78 +/- 0.21 ng/mg creatinine; p < 0.01). Urinary immunoreactive EGF was at its lowest level 96 h after toxic injury (0.64 +/- 0.06 ng/mg creatinine; p < 0.001). Twenty-four hours after toxic injury, renal immunoreactive EGF levels increased significantly compared with control rats (22.04 +/- 2.12 versus 4.84 +/- 0.70 ng/g wet weight tissue; p < 0.001), and the increase persisted for as long as 48 h (13.36 +/- 1.61 ng/g wet weight tissue; p < 0.05). In summary, urinary immunoreactive EGF levels decreased and renal EGF levels increased in rats with HgCl2-induced ARF. These findings suggest that there is an impairment in the excretion of EGF in rats with HgCl2-induced ARF and that local paracrine production of EGF continues in ARF.

Acute Kidney Injury↗

[Nephropathy in patients with primary antiphospholipid antibody syndrome].

Primary antiphospholipid antibody syndrome (APS) is characterized by abortion, thrombosis, thrombocytopenia and/or valvular disease and it is liable to complicate systemic lupus erythematosus (SLE). We carried out a study to investigate the clinical and renal pathological findings in five patients with APS, but not SLE. In the clinical findings, the patients had negative tests for proteinuria and hematuria, and their renal function and tubular function were within normal limits. In the light microscopic findings, three patients exhibited mild mesangial hypercellularity, and two had minor glomerular abnormalities. In immunofluorescent study, there were IgM and/or C3 depositions in the mesangial area in some cases, and in electron microscopic study, there were no special findings other than mesangial hypercellularity. In conclusion, nephropathy is a rare complication in patients with APS, unlike systemic lupus erythematosus.

Adult↗

Urinary epidermal growth factor levels in patients with acute renal failure.

To investigate the importance of epidermal growth factor (EGF) in patients with renal dysfunction, urinary human EGF (hEGF) levels were determined by radioimmunoassay in 16 patients with acute renal failure (ARF) and in 12 healthy controls. Seven patients with chronic renal failure also were studied. Urinary hEGF levels, corrected for urine creatinine concentrations, were significantly decreased in patients with ARF in the acute phase compared with normal control subjects (0.98 +/- 0.20 v 13.74 +/- 1.18 ng/mg creatinine, P < 0.001), and subsequently increased during the recovery phase (6.10 +/- 0.73 ng/mg creatinine, P < 0.001 v acute phase). A significant positive correlation existed between urinary hEGF levels and creatinine clearance in patients with ARF (r = 0.66, P < 0.001). Serum hEGF levels also were significantly lower in patients with ARF compared with normal control subjects (0.10 +/- 0.01 v 0.30 +/- 0.03 ng/mL, P < 0.001). No significant correlation was found between hEGF concentrations in serum and urine. In conclusion, measurement of urinary hEGF may be useful in the diagnosis of ARF and for following the recovery of the kidney after severe tubular injury.

Acute Kidney Injury↗

The distribution of 3H-labeled endotoxin in the kidney of liver cirrhotic rats.

Although the etiology and pathogenesis of progressive renal failure is largely unknown, endotoxin is supposed to be one of the contributory factors. However, the distribution of endotoxin in liver cirrhosis has not been clarified. Therefore we studied the distribution of 3H-labeled endotoxin in the kidney in rats with CCl4-induced liver injury. Daily inhalations of CCl4 on rats for 6 and 10 weeks produced liver fibrosis (LF group, N = 5) and cirrhosis (LC group, N = 5), respectively. At 6 or 10 weeks, animals were sacrificed 24 hours after an intravenous injection of endotoxin labeled with 3H at the galactose moiety (12,000 cpm/1 g body weight). In the liver, 3H-labeled endotoxin was taken up mainly by Kupffer cells as determined by autoradiography. Compared to control rats, in rats of the LC or LF group the measured amount of 3H-labeled endotoxin per gram kidney or ml blood increased, while that of the liver was significantly decreased. A positive correlation of the amount of 3H-labeled endotoxin per weight or volume respectively was shown between kidney and blood, but not between lung or spleen and blood. These results suggest that overflow of endotoxin due to decreased inactivation in the liver causes endotoxemia in liver injury and that the resulting endotoxemia may directly affect the kidney. The resulting endotoxin-induced vasoconstriction may be a contributory factor for the progressive renal failure frequently observed in liver cirrhosis.

Animals↗