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Purpose To Investigate the effect of diet-induced hyperchole sterolemia on the kidney ofWistar rats. Methods Male Wistar rats were fed with normal chow supplemented with 5 % cholesteroland observed biochemical changes in plasma lipid concentration, urinary microalbumin excretion, renalfunction, lipid component in renal cortices and morphological changes at 30,60 and 90 days. ResultsTotal plasma cholesterol (TCh) and low density lipoprotein (LDL) concentration were significantly elevatedin the group E (P＜0.05)at 30 days, and progressively increased thereafter, but during the entire study,there ere no differences in plasma urea nitrogen(BUN),creatinine(Cr), and endogenous creatinine clearance(Ccr) between the two groups. Quantitative urinary microalbumin excration was markely elevated in group E( P ＜ 0.05 ). Cholesterol (Ch), phosphatidylcholine(PC) and phosphatidylethanolamine(PE) levels of t he renalcortices were sigificantly increased in the group E at 12 weeks. Progressive development in mesangialhypercellulary, increased mesangial matrix, glomerular capillaries collapes were observed in the group E. Noelectron dense deposits were observed in any of the glomeruli examined. There was a siginificant positivecorrelation for the urinary microalbumin, Ch in the renal corticres, and glomerular size with plasma TCh andLDL concentration. Conclusions The diet-induced hypercholesterolemia may cause lipid nephrotoxicity inWistar rats.
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Objective To solve the hemodialysis in patients at risk for bleeding. Methods A 1.6 mol/L trisodium citrate solution, a standard calcium-containing bicarbonate dialysate and a standard hollow fiber capillary dialyzer were used. Results 72 dialysis were performed successfully with this technique on 6 stable and 17 high bleeding risk patients. Systemic anticoagulation didn't occur as a result of any dialysis procedure, and in no instance bleeding was observed. No severe dialyzer clotting was observed. There was a significant decline in whole blood ionized calcium during citrate dialysis (0.981?0.11 vs 0.907 ?0.12 mmol/L, P
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Objective To study the effects of insulin resistance on the occurance of hypertension in uremia. Methods With use of the oral glucose tolerance test (OGTT) and the insulin release test (IRT) , insulin glycoregulatory activity, including insulin sensitivity index (ISI) , glucose uptake rate (M) and the total areas under the glucose and insulin curves during OGTTs (AUCG, AUCINS) were investigated in 29 hypertensive (CRF-H) and 21 normotensive (CRF-NH) urernic patients and 12 healthy controls (C), and their plasma renin activity (PRA), angiotensin Ⅱ (AT Ⅱ) levels were investigated too. Results (1) Uremic patients had significantly higher blood glucose and serum insulin levels after glucose load, much higher AUCG and AUCINS values and significantly lower ISI and M values than the controls, compared with the CRF-NH patients, CRF-H patients had significantly higher blood glucose levels at 30', 60', 120', and higher serum insulin levels at 120' during OGTTS, significantly higher AUCG and AUCINS values, significantly lower ISI and M values and significantly increased incidences of insulin resistance and glucose intolerance; (2) Insulin resistant patients had more frequency and severe hypertension than the non-insulin resistant ones; simple regression showed that arterial blood pressure (SBP, DBF, MBP) had significant negative correlation with ISI and M, significant positive correlation with AUCG and AUCINS; (3) The levels of PRA, ATⅡbetween two CRT groups were not different; (4) Multiple linear regression showed that AUCG and AUCINS had significant positive correlation with MBP independent of age、 sex、 obesity、 the degree of real failure and plasma renin-angiotensin activity. Conclusion Insulin resistance 、 hyperinsulinemia and glucose intolerance or hyperglycemia may be one of the important mechanisms of uremic hypertension.
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To investigate the hepatitis C virus (HCV) infection in hemodialysis patients. Methods Sixty patients were tested for anti-HCV IgG and anti-HCV IgM using a second generation enzyme-linked immunosorbent assay (ELISA); for HCV-RNA using a nested polymerase chain reaction (PCR) assay. Results Twenty seven patients were positive for anti-HCV IgG, 24 for anti-HCV IgM and 37 for HCV-RNA. The total positive rate of HCV markers was 63.3% in 60 hemodialysis patients. In transfused group, the positive rate of HCV markers was 69.9% , while in non-transfused was 42.9% . Conclusion The prevalence of HCV infection in hemodialysis patients is serious. Blood transfusion is the main way to transmit HCV. However, there may be other transmitting routes by the dialysis equipment.
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Objective To investigate the cardioprotective effect of losartan o n subtotal nephrectomy renal failure rats. Methods Renal failure rats were estab lished by subtotal nephrectomy, and then divided into RF group with subtotal nep hrectomy,RF+Los group with additional losartan(10 mg?kg-1?d-1) gavage. Rats underwent sham operation(sham group) with normal saline gavage as control. Hear t changes of experimental rats were observed 12 weeks after operation. Results T he RF group developed hypertension of arterial systolic blood pressure(SBP) and myocardiac myocytes hypertrophy. The levels of collagen type Ⅰ,type Ⅲ,and fi bronectin in endocardium and surrounding intracardial coronary arteries adventit ia of the RF group were significantly increased as compared to those of the sham group. The SBP and the levels of collagen type Ⅰ,Ⅲand fibronectin were marked ly decreased in the RF+Los group as compared to those of the RF group.Expressio n of angiotensin Ⅱsubtype 1 receptor (AT1R) mRNA in the myocardium of the RF+L os group was significantly down regulated as compared to that of RF group. Concl usions Losartan can prevent the cardiac ventricular remodeling with left ventric ular hypertrophy (LVH) and myocardial interstitial fibrosis by the depression of renin-angiotensin system through the down-regulation of myocardiac AT1R mRNA.