Jakić Marko, Jakić Marijana, Zibar Lada, Mihaljević Dubravka, Stipanić Sanja, Teskera Tomislav
Klinicka bolnica Osijek, Klinika za unutarnje bolesti, Odjel za dijalizu, Ukrinska.
Lijec Vjesn. 2009 Jul-Aug;131(7-8):218-25.
There is an ongoing trend of a rapid increment in the frequency of diabetes mellitus, expecially the non-insulin dependent form. By the end of the 2nd millenium 150 million cases were recorded worldwide, while the estimations predicted doubling the number by the year 2030. Numerous chronic complications accompany the disease, among them micro-, as well as macrovascular prevail, affecting small and large blood vessels. This paper provides a literature review on the topic of diabetic nephropathy, the main microvascular complication of diabetic disease. Microalbuminuria is the earliest sign of the diabetic renal involvement, with more than 30 mg and less than 300 mg of albumins in 24 h urine sample. The reduction of renal function begins with albuminuria leaving microalbuminuria level and entering the pathologic proteinuria range. Renal failure advances through the 5 stages, the final fifth occurring fortunately only in a minor proportion of the patients. The final stage ensues in 232 of 100 000 diabetic patients, according to the US data. However, in many developed countries there are 30-40% of new patients entering chronic dialysis treatment for diabetic nephropathy. Pathogenesis of diabetic nephropathy is based on hyperglycemia and distinct hemodynamic changes, glomerular hyperfiltration and high intraglomerular pressure. The important role have oxidative stress, advanced glycation end products, some cytokines, growth factors and sorbitol pathway. Nevertheless, genetic influence is considered by far the most important risk factor for diabetic nephropathy. Heritage determines the susceptibility in one and the protection in another diabetic patient. At the moment of pathologic proteinuria occurrence, glomerular filtration rate begins to decline for 1.2 ml/min/monthly in some patients, making the annual reduction of 7-14 ml/min/1.73 m2 of body surface area. Improving glycemia, blood pressure control, renal anemia correction with rHu-Epo, dyslipidemia control, reduction in protein intake, i.e. management of the nongenetic factors, could slower the renal function loss in some of the patients. Hence, these measures could reduce the proportion of the patients reaching end-stage renal disease, having in mind that morphological and functional changes are reversible only within certain limits. Therefore, the success of kidney protection is better if commenced earlier.
糖尿病，尤其是非胰岛素依赖型糖尿病的发病频率呈快速上升趋势。到20世纪末，全球记录的病例达1.5亿例，而据估计到2030年这一数字将翻倍。该疾病伴有众多慢性并发症，其中微血管和大血管并发症占主导，影响小血管和大血管。本文对糖尿病肾病这一糖尿病主要微血管并发症的相关主题进行文献综述。微量白蛋白尿是糖尿病肾脏受累的最早迹象，24小时尿样中白蛋白含量超过30毫克且低于300毫克。肾功能减退始于白蛋白尿超过微量白蛋白尿水平并进入病理性蛋白尿范围。肾衰竭会经历5个阶段，幸运的是，最终阶段仅在一小部分患者中出现。根据美国的数据，每10万名糖尿病患者中有232人会进入最终阶段。然而，在许多发达国家，有30% - 40%的新患者因糖尿病肾病进入慢性透析治疗。糖尿病肾病的发病机制基于高血糖和明显的血流动力学变化，即肾小球高滤过和肾小球内高压。氧化应激、晚期糖基化终产物、一些细胞因子、生长因子和山梨醇途径也发挥着重要作用。然而，遗传影响被认为是糖尿病肾病迄今为止最重要的危险因素。遗传因素决定了一部分糖尿病患者的易感性，而对另一部分患者则有保护作用。在出现病理性蛋白尿时，一些患者的肾小球滤过率开始以每月1.2毫升/分钟的速度下降，即每年下降7 - 14毫升/分钟/1.73平方米体表面积。改善血糖、控制血压、用重组人促红细胞生成素纠正肾性贫血、控制血脂异常、减少蛋白质摄入，即对非遗传因素进行管理，可在一些患者中减缓肾功能丧失。因此，考虑到形态和功能变化仅在一定限度内可逆，这些措施可减少进入终末期肾病的患者比例。所以，如果更早开始肾脏保护会更成功。
