NUTRITIONAL THERAPY OF CHRONIC RENAL FAILURE IN OUTPATIENTS

门诊慢性肾功能衰竭患者的营养治疗

• 批准号: 6245405
• 负责人: MACKENZIE WALSER
• 金额: $ 2.23万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-03-05 至 1997-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6245405
• 关键词: chronic renal failure; clinical research; diabetic nephropathy; diet therapy; dietary proteins; glomerular filtration rate; hemodialysis; human subject; human therapy evaluation; interstitial nephritis; ketoconazole; kidney disorder chemotherapy; nephrotic syndrome; nutrition related tag; prednisone

Nutritional therapy of the nephrotic syndrome. We have found that a very low protein diet, supplemented by essential amino acids, may induce long-term remission of the nephrotic syndrome, even when it is caused by diabetes or by focal segmental glomerulosclerosis (disorders in which the nephrotic syndrome rarely remits spontaneously), provided that treatment is started before renal function has deteriorated severely. The mechanism of this surprising result remains to be determined by study of additional patients. Use of ketoconazole to slow progression of chronic renal failure. A randomized cross-over study of ketoconazole (to suppress cortisol production) plus low-dose prednisone (to prevent anterior pituitary escape) in patients with progressive chronic renal failure of various types has been completed. In diabetic nephropathy, glomerular disease, and interstitial nephritis, rate of decline of glomerular filtration rate slowed significantly; in polycystic kidney disease, rate of decline accelerated. Side effects or toxicity caused drug withdrawal in 20% of patients. Survival on dialysis of patients treated with a supplemented very low protein diet before dialysis. Extending our previously published finding that patients so treated generally enter dialysis with normal serum albumin levels, in contrast to the national experience, we determined the survival on dialysis of 46 such patients. During the first two years, survival on dialysis was markedly improved, compared with the national experience, correcting for age, sex, and diagnosis. Whether this was because these patients had higher serum albumin levels during dialysis could not be determined. Use of dehydroepiandrosterone to slow progression of chronic renal failure. Based on our unpublished finding that progression is negatively correlated with serum DHEA-S concentration, we hypothesized that DHEA supplementation may slow progression. Accordingly, a randomized, double-blind crossover study of sequential glomerular filtration rates in patients with all types of chronic renal failure given either a placebo or enough DHEA to raise serum DHEA-S level to about 12 ug/ml has been started. Renal production of nitric oxide as a determinant of progression. We have reported in abstract form that progression is positively correlated with the 24 excretion rate of nitrate (the stable end-product of nitric oxide). We have developed a method to determine renal (as opposed to systemic) production of nitrate, based on measuring nitrate and chloride clearances and glomerular filtration rate before and after an oral load of NANO3. We plan to extend these measurements and to determine whether the source of renal NO production is inducible nitric oxide synthase (as opposed to constitutive NOS) by repeating these measurements after giving a nearly specific inhibitor of iNOS (aminoguanidine).

肾病综合征的营养治疗。 我们发现， 极低蛋白饮食，补充必需氨基酸， 肾病综合征的长期缓解，即使它是由 糖尿病或局灶节段性肾小球硬化症（其中 肾病综合征很少自发缓解），前提是 在肾功能严重恶化之前开始治疗。 这一令人惊讶的结果的机制仍有待确定， 研究其他患者。 慢性肾功能衰竭的治疗方法有哪些 一 酮康唑（抑制皮质醇）的随机交叉研究 生产）加低剂量泼尼松（以防止垂体前叶 慢性肾功能衰竭的治疗方法有哪些 类型已经完成。 在糖尿病肾病，肾小球疾病， 和间质性肾炎，肾小球滤过率下降 多囊肾病的发病率有哪些？ 加快 20%的患者因副作用或毒性而停药 患者 接受补充极低剂量的 透析前的蛋白质饮食 扩展我们先前发布的 发现这样治疗的患者通常以正常的 血清白蛋白水平，与国家经验相反，我们 确定了46名此类患者的透析存活率。 期间 前两年，透析生存率明显提高， 根据全国的经验，校正年龄，性别和诊断。 这是否是因为这些患者的血清白蛋白水平较高 透析期间无法确定。 脱氢表雄酮在减缓慢性肾功能衰竭进展中的应用 失败 根据我们未发表的发现， 与血清DHEA-S浓度呈负相关，我们假设 补充脱氢表雄酮可能会减缓病情发展。 因此 随机、双盲、交叉研究，序贯肾小球 所有类型慢性肾衰竭患者的滤过率 给予安慰剂或足够的DHEA，以提高血清DHEA-S水平， 已开始约12 ug/ml。 肾脏产生一氧化氮作为疾病进展的决定因素。 我们 已经以摘要的形式报告了进展与 随着硝酸盐（硝酸盐的稳定终产物）排泄率的增加， 氧化物）。 我们已经开发了一种方法来确定肾（而不是 系统）生产硝酸盐，基于测量硝酸盐和氯化物 口服负荷前后的清除率和肾小球滤过率 关于NANO 3 我们计划扩大这些测量，并确定是否 肾NO产生来源是诱导型一氧化氮合酶（如 与组成型NOS相反）， 产生一种近乎特异性的iNOS抑制剂（氨基胍）。