透析方式不影响红细胞生成素在慢性肾功能衰竭患者体内的代谢

重组人类红细胞生成素（ＥＰＯ）的问世是治疗肾性贫血的一个突破性进展。早期主要在血液透析患者中使用，因当时的研究认为慢性肾功能衰竭患者血清中存在着对ＥＰＯ及红细胞生成抑制作用的物质，此物质仅可经血液透析清除，而未透析患者或腹膜透析患者则可能因此而ＥＰＯ...     

慢性肾功能衰竭患者性功能障碍机制的研究进展

性功能障碍在慢性肾功能衰竭患者中发病率很高,但目前在治疗效果上除了男性勃起功能障碍外均不够理想.为了取得更好的治疗效果,首先要明确性功能变化的发生机制、本文就近年来对慢性肾功能衰竭患者性功能变化的机制研究的进展作一综述.     

CD146与慢性肾功能衰竭的研究进展

CD146又被称作Mel-CAM,MUC18等,是膜糖蛋白作为钙离子依赖的细胞粘附分子,最早被发现存在于黑色素瘤中,因其对血管内皮功能损伤有影响,因此在肾脏疾病发生发展过程中的作用亦引起众多学者的重视.慢性肾衰患者的CD146水平较健康人群显著上升,与冠心病的发生同样存在理论上的相关性,同时发现肾脏移植后的CD146恢...     

慢性肾功能衰竭腹膜透析患者的出凝血紊乱

为了阐明慢履肾功能衰竭患者腹膜透析治疗中出血倾向和血栓形成倾向并存的矛盾状态，对２６例慢性肾功能衰竭行ＰＤ治疗患者，１７例慢性肾功能衰竭保守治疗患者，３６例慢性肾功能衰竭行血液透析治疗患者与２０例正常对照者的凝血，抗凝血，纤维蛋白溶解及血小板功能进行了综合研究。     

肝移植术后慢性肾功能衰竭的研究进展

随着肝移植患者例数逐渐增加和生存期延长,术后慢性肾功能衰竭（chronic renal failure,CRF）也逐渐增加。Ojo等报道肝移植术后1年和5年CRF发生率为8%和18%。     

瘦素与慢性肾功能衰竭

瘦素是ｏｂ基因编码的具有调节体重和代谢的激素作用的循环因子，它通过旁分泌／自分泌的方式调节脂肪代谢。新近研究表明在慢性肾功能患者血浆中瘦素水平升高，可能是尿毒症患者营养不良的原因之一。     

脂质代谢紊乱与慢性肾功能衰竭

脂质代谢紊乱是慢性肾衰(CRF)患者心血管疾病发生的重要危险因素，同时也会进一步加重肾脏损伤，参与造成CRF的进展。本文就CRF患者与各种脂质、脂蛋白、载脂蛋白及脂质颗粒等异常综述如下。     

瘦素与慢性肾功能衰竭营养不良研究进展

营养不良影响慢性肾功能衰竭病人生活质量和增加病死率的重要因素。Leptin是新近发现的具有调节食物摄入和能量代谢的激素样蛋白。研究表明慢性肾衰病人血Leptin水平明显升高，提示Leptin可能对慢性肾功能衰竭营养不良的发生起重要作用。     

一氧化氮与慢性肾功能衰竭

一氧化氮（ＮＯ）在细胞信息传递、细胞防御和细胞损伤中起着重要作用，对ＮＯ的深入了解改变了心血管、神经及免疫系统生理和病理生理的观点。本文综述了ＮＯ的来源，代谢、作用机制；ＮＯ对肾脏血液动力学的影响及ＮＯ在慢性肾功能衰竭中的作用     

慢性肾功能衰竭患者机体成分研究的进展

本文综述了近年来慢性肾功能衰竭者机体成分分析研究情况，指出了各种方法的优缺点。     

Calcitriol metabolism in patients with chronic renal failure

We studied calcitriol metabolism in white patients with chronic renal failure and in age- and sex-matched normal subjects. The plasma levels of calcitriol (21.9 +/- 1.6 pg/mL, n = 7, v control, 37.4 +/- 2.9 pg/mL, P less than 0.001), metabolic clearance rate (MCR) of calcitriol (0.45 +/- .01 mL/min/kg v control, 0.58 +/- .02 mL/min/kg, P less than 0.001), and production rate (PR) of calcitriol (14.2 +/- 1.0 ng/kg/d v control, 31.8 +/- 3.2 ng/kg/d, P less than 0.001) were significantly lower in patients with moderate renal failure (average creatinine clearance, 0.59 +/- 0.01 mL/s [35.1 +/- 6.1 mL/min]) when compared with the respective values of normal control subjects. The MCR of calcitriol was determined again in patients with renal failure after they received calcitriol, 1 microgram/d, for 1 week. The MCR remained unchanged (0.46 +/- .04 mL/min/kg, n = 7) and plasma levels of calcitriol were increased to 34.6 +/- 2.77 pg/mL. The mechanism by which the MCR of calcitriol decreases in renal failure is partly due to the presence of inhibitory factors of degradation enzymes in uremic plasma. When the ultrafiltrates of uremic plasma obtained from hemodialysis patients were infused to normal Sprague-Dawley rats, the MCRs of calcitriol (0.20 +/- .01 mL/min/kg, n = 6) were markedly suppressed in comparison to those of rats infused with the ultrafiltrates of normal plasma (0.37 +/- .01 mL/min/kg, n = 6, P less than 0.001). The uremic plasma also contained factors that inhibit the synthesis of calcitriol. We conclude that metabolic degradation of calcitriol is decreased in patients with renal failure, and uremic plasma contains inhibitory factors that suppress the synthesis and degradation of calcitriol.     

Dyslipidemia and the progression of renal disease in chronic renal failure patients

Dyslipidemia is a common complication of progressive kidney disease and contributes to the high cardiovascular morbidity and mortality of chronic kidney disease (CKD) patients. Recent evidence also suggests a role for dyslipidemia in the development and progression of renal disease. Experimental studies have demonstrated that lipids may induce glomerular and tubulointerstitial injury, and that lipid-lowering treatments ameliorate renal injury. Various lipid abnormalities have been associated with the development and progression of renal disease in diabetic and nondiabetic patients. Population-based studies and studies of diabetic patients have reported associations of various lipid abnormalities with the development of renal disease. In patients with CKD, lipid abnormalities have also been associated with renal disease progression. Post hoc analyses of some large clinical trials on patients with vascular disease, diabetes, or dyslipidemia, and a meta-analysis of small, prospective, controlled studies on patients with CKD (diabetics and nondiabetics) suggest that statins may slow the progression of kidney disease. It is unclear whether the beneficial renal effects of statins are due to the reduction of serum cholesterol levels and/or their pleiotropic effects. There is also evidence for synergistic renoprotective effects between statins and renin-angiotensin system inhibitors. According to the results of post hoc analysis of several studies, treatment with fibrates does not seem to confer renoprotection, but evidence is scarce. In summary, there is growing evidence that lipid abnormalities may be a risk factor for renal disease, and that statins appear to confer a renoprotective effect.     

Dyslipidaemia and the progression of renal disease in chronic renal failure patients.

BACKGROUND: Dyslipidaemia is common in patients with chronic renal failure (CRF), and there is increasing evidence to support the role of dyslipidaemia as a contributing factor in the progression of chronic renal disease. However, few prospective studies have been carried out which address the possible relationship between dyslipidaemia and the rate of progression of renal disease in patients with renal failure. METHODS: Between January 1985 and December 1997, we prospectively assessed the risk of CRF progression to dialysis in a cohort of 138 patients. Forty CRF patients reached end-stage renal disease (ESRD) and had to start supportive therapy during the follow-up period [group ESRD(+)]. The remaining 98 CRF patients served as controls [group ESRD(-)]. Potential clinical and laboratory risk factors for more rapid CRF decline to dialysis, including lipid abnormalities and baseline creatinine clearance were determined at the start of the follow-up period. RESULTS: Several significant differences were found in univariate analysis between the two groups of CRF, ESRD(+) and ESRD(-), namely a shorter follow-up period, a lower level of baseline creatinine clearance, a faster rate of creatinine clearance decline, a higher level of serum triglycerides, fibrinogen, total homocyst(e)ine and proteinuria, and a lower level of serum high-density lipoprotein in the ESRD(+) group than in the ESRD(-) group. However, by multivariate Cox analysis proteinuria [relative risk (95% confidence interval) 1.32 (1.16-1.50) for each g/day P = 0.001], baseline creatinine clearance [0.53 (0.40-0.70) for each 10 ml/min, P = 0.001] and chronic interstitial nephritis and hypertensive nephrosclerosis [0.38 (0.17-0.84) for presence, P = 0.005] were the only significant risk factors for CRF progression to dialysis. Hypertriglyceridaemia and male gender were selected in the final model, but were of borderline significance. CONCLUSIONS: These results suggest a limited role for dyslipidaemia in the progression of chronic renal disease to dialysis in CRF patients, in contrast with the powerful influence of proteinuria, baseline creatinine clearance and nephropathy type in predicting this progression.     

Cholesterol metabolism in patients with chronic renal failure on hemodialysis

Premature atherosclerosis is a major concern in patients on chronic dialysis and the identification of risk factors is important for preventive and interventional strategies. Other than the recognized atherogenic lipoprotein levels, little is known about overall cholesterol metabolism in patients on chronic hemodialysis (HD) and the best therapeutic intervention is still being debated. Therefore, we investigated intestinal cholesterol absorption, cholesterol and bile acid synthesis, and non-cholesterol plasma sterols in eight patients on dialysis and compared the results to those of 16 healthy male controls matched for body mass index and dietary cholesterol intake. Total, low-density lipoprotein (LDL) cholesterol, and triglycerides did not differ between the groups, but dialysis patients had a significantly lower high-density lipoprotein (HDL) cholesterol level (39 +/- 11 mg/dL vs. 48 +/- 10 mg/dL, p < 0.045). However, fractional cholesterol absorption, was significantly lower in dialysis patients (42.8 +/- 10.9% vs. 53.4 +/- 11%, p < 0.035), whereas plasma plant sterol concentrations and their ratios to cholesterol did not differ. Bile acid and total cholesterol synthesis were lower in dialysis patients (40% and -25%, respectively), although the differences were not significant. In contrast, lathosterol and its ratio to cholesterol in plasma was significantly lower in dialysis patients (0.176 +/- 0.084 mg/dL vs. 0.251 +/- 0.102 mg/dL, p < 0.024 and 0.733 +/- 0.353 microg/mg vs. 1.172 +/- 0.407 microg/mg, p < 0.017, respectively), indicating reduced hepatic de novo cholesterol synthesis. It is concluded that reduced HDL cholesterol and reduced bile acid synthesis contributes to atherosclerosis pathogenesis in dialysis patients, whereas intestinal cholesterol absorption and hepatic cholesterol synthesis did not seem dominant in this process at this stage of disease. Consequently, treatment with bile acid binding resins could be preferable to treatment with cholesterol absorption and synthesis inhibitors.     

Anemia management and chronic renal failure progression

Analysis of the biologic effects of erythropoietin and pathophysiology of chronic kidney diseases (CKD) suggests that treatment with erythropoiesis-stimulating agents (ESA) could slow the progression of CKD. By decreasing hypoxia and oxidative stress, it could prevent the development of interstitial fibrosis and the destruction of tubular cells. It could have direct protective effects on tubular cells through its antiapoptotic properties. It could help maintain the integrity of the interstitial capillary network through its effects on endothelial cells. Thus, suggesting that correcting anemia with ESA could slow the progression of CKD is biologically plausible. In patients with CKD, three small prospective studies and a retrospective study have suggested that treatment with ESA may have protective effects. Post-hoc analysis of the Reduction in Endpoints in Noninsulin-dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan study has also shown that anemia was an independent risk factor for progression of nephropathy in patients with type 2 diabetes. In addition, a large clinical trial, which had to be stopped prematurely because of labeling change for subcutaneous administration of epoetin alfa, suggests that complete normalization of hemoglobin levels is safe in CKD patients not on dialysis and without severe cardiovascular disease. Thus, it seems reasonable to advocate starting a large randomized, prospective study to determine if normalization of hemoglobin concentration can effectively slow the progression of CKD.     

Erythrocyte nitric oxide metabolism in patients with chronic renal failure.

AIMS: This study aims to investigate arginine-nitric oxide pathway in chronic renal failure (CRF) and to establish erythrocyte nitric oxide synthase (NOS) and arginase (ARG) activities in patients with CRF. MATERIALS AND METHODS: NOS and ARG activities were measured in erythrocytes from 30 patients with CRF and 12-control subjects. RESULTS: Erythrocyte NOS activity was found to be significantly lower and ARG activity higher in patients with CRF compared with controls. No differences were, however, found between patients with and without hemodialysis. A negative correlation (r = -0.7) was established between ARG and NOS activities in erythrocytes from patients. CONCLUSIONS: Results suggest that erythrocyte NO production is diminished in patients with CRF, possibly due to decreased NOS and increased ARG activities.