亚临床和显性糖尿病肾病的心血管和肾功能研究。

J Berglund
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引用次数: 0

摘要

研究人员对两组长期胰岛素依赖型糖尿病患者的心血管和肾功能进行了检测,其中一组为微量白蛋白尿,是早期亚临床肾病的征兆,另一组为临床表现为糖尿病肾病的患者。此外,还分析了可能对糖尿病肾病发生和预后有重要影响的临床变量。在16%的albustix阴性、血压正常、胰岛素依赖型糖尿病患者中发现了微量白蛋白尿,即夜间尿白蛋白平均排泄率超过20微克/分钟。微量白蛋白血症患者的仰卧位血压高于正常白蛋白血症患者。微量白蛋白血症患者的白蛋白排泄率与静息时血压相关,但与糖化血红蛋白无关。对五种不同试验操作的心血管反应显示,微量白蛋白尿患者比正常白蛋白尿患者有更明显的自主神经功能障碍迹象。然而,在精神压力下,两个亚组的循环反应几乎相同。尽管肾小球滤过率和肾血浆流量相似,微量白蛋白血症患者精神应激时白蛋白排泄量增加,但正常白蛋白血症患者保持不变。据推测,肾小球基底膜通透性的紊乱是微量白蛋白尿中白蛋白排泄升高的先决条件。自主神经功能障碍导致的肾小球血流动力学调节能力的丧失也可能是一个因素。这种功能障碍甚至可以解释为什么与正常白蛋白患者相比,微量白蛋白患者在休息时血压更高。在显性糖尿病肾病中,肾功能下降率与动脉血压相关,而血糖控制无相关性。快速进展肾病患者的生长激素值高于缓慢进展肾病患者。在糖尿病肾衰竭患者中,心导管检查显示运动期间卒中功减少和左心室舒张末期压升高。自主神经功能障碍和动脉高血压可能是导致心脏功能受损的原因。甚至必须考虑是否存在特定的糖尿病性心脏病。亚临床和显性糖尿病肾病均以男性为主。与蛋白尿正常者相比,糖尿病患者在微蛋白尿中发病年龄较低。糖尿病病程对亚临床或显性肾病的预后无影响。有明显肾病的患者死亡率高。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Studies of cardiovascular and renal function in subclinical and manifest diabetic nephropathy.

Cardiovascular and Renal function were examined in two populations of long-term insulin-dependent diabetics, those with microalbuminuria, a sign of early, subclinical nephropathy and those with clinically manifest diabetic nephropathy. In addition, clinical variables of possible importance for the occurrence and prognosis of diabetic nephropathy were analyzed. Microalbuminuria - a mean of three over-night urinary albumin excretion rates greater than 20 micrograms/min - was found in 16% of Albustix-negative, normotensive, insulin-dependent diabetics. The microalbuminurics had higher supine blood pressures than normoalbuminurics. The albumin excretion rate in microalbuminurics correlated to blood pressure at rest but not to glycosylated haemoglobin. The cardiovascular responses to five different test manoeuvres revealed more evident signs of autonomic nerve dysfunction in microalbuminurics than in normoalbuminurics. The circulatory reactions during mental stress however, were almost identical in the two subgroups. Despite similar glomerular filtration rate and renal plasma flow the albumin excretion during mental stress increased in microalbuminurics, but remained unchanged in normoalbuminurics. It is postulated that a disturbance of glomerular basement membrane permeability is a pre-requisite for the elevated albumin excretion seen in microalbuminurics. Inability to regulate glomerular haemodynamics, due to autonomic nerve dysfunction, may also be a contributing factor. Such dysfunction perhaps even explains why microalbuminurics have higher blood pressures at rest compared with normoalbuminurics. In manifest diabetic nephropathy the rate of renal functional decline correlated to arterial blood pressure, while glycemic control showed no such relation. Patients with rapidly progressive nephropathy showed higher values of growth hormone than slow progressors. In patients with diabetic renal failure, cardiac catheterization revealed reduced stroke work and elevated left ventricular end-distolic pressure during exercise. Autonomic nerve dysfunction and arterial hypertension possibly contributed to the impaired cardiac performance. The existence of a specific diabetic cardiopathy must even be considered. There was a male predominance both in subclinical and manifest diabetic nephropathy. Age at onset of diabetes was lower in micro- as compared to normoalbuminurics. Duration of diabetes had no prognostic implication in subclinical or manifest nephropathy. The mortality rate was high in patients with manifest nephropathy.(ABSTRACT TRUNCATED AT 400 WORDS)

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