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 糖尿病腎病-Diabetic Nephropathy

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Statistical Increase in Diabetes
In the past 20 years, there has been a steady increase in the proportion of all patients with ESRD who have diabetes. According to the 1997 report of the USRDS, more than 40% of all newly treated patients with ESRD have diabetes.
Increasing Insulin Treatment in NIDDM
Renal Failure Cumulative Incidence.
Chronic renal failure was as likely to develop at a superimposable rate in both diabetic subsets. Numbers in parentheses indicate number of patients for each line.

Creatinine clearance. Further evidence of the similarity in course of diabetic nephropathy in type I (A) and type II (B) diabetes was presented in Ritz and Stefansky’s study of equivalent deterioration in creatinine clearance over the course of a decade. 
糖尿病腎病的發(fā)病機理（1）
腎內(nèi)血動力學改變：

腎內(nèi)血流動力學改變是指腎小球高濾過及腎小球高壓。

動物實驗，糖尿病模型建立后，即已存在腎小球的高濾過與腎小球肥大。

糖尿病腎病的發(fā)病機理（1）
高濾過是導致腎功能惡化的主要原因。在非糖尿病性5/6腎切除的動物模型中可見腎小球系膜基質(zhì)增多，GBM增厚及階段性腎小球硬化。
腎小球內(nèi)高壓是導致腎小球硬化的另一重要因素
糖尿病腎病的發(fā)病機理（2）
葡萄糖的毒性效應
高血糖可導致內(nèi)皮細胞，系膜細胞的結構及功能的改變。高血糖促使系膜細胞合成更多的胞外基質(zhì)。
持續(xù)的高血糖可使血漿蛋白及組織蛋白糖基化，導致晚期糖基化終末產(chǎn)物的生成。

糖尿病腎病的臨床表現(xiàn)
Ⅰ型及Ⅱ型糖尿病患者都有很大的可能發(fā)展為糖尿病腎病，Ⅰ型糖尿病患者其腎病更為顯著，進展也更為迅速，當發(fā)生了明顯糖尿病腎病后，兩型的臨床表現(xiàn)則無很大差別。
臨床上按照病理生理特點將Ⅰ型糖尿病腎病分為Ⅰ—Ⅴ期。
目前尚無Ⅱ糖尿病腎病的臨床分期，但其發(fā)生糖尿病腎病時也大體經(jīng)歷高濾過，正常白蛋白尿，微量白蛋白尿，臨床糖尿病腎病及慢性腎功能不全等幾個階段。

Stages of Nephropathy.
The interrelationships between functionaland morphologic markers of the stages of diabetic nephropathy are shown. Additional pathologic studies are needed to time with precision exactly when glomerular basement membrane (GBM) thickening and glomerular mesangial expansion take place. 
Diabetic Nephropathy in Types I & II.
Whereas microalbuminuria and glomerular hyperfiltration are subtle pathophysiologic manifestations of early DN, transformation to overt clinical DN takes place over months to many years. While not all microalbuminuric individuals progress to proteinuria and azotemia, the majorityare at risk for ESRD due to DN.
糖尿病腎病及慢性腎功能不全的預防
控制血糖
控制血壓
低蛋白飲食
對AGES的治療

Clinical recognition of diabetic nephropathy. The timing of reno-protective therapy in diabetes is a subject of current inquiry. Certainly, hypertension, poor metabolic regulation, and hyperlipidemia should be addressed in every diabetic individual at discovery.Discovery of microalbuminuria is by consensus reason to start treatment with an ACEI in either type of diabetes, regardless of BP elevation. However, nearly the entire course of renal injury in diabetes is clinically silent. Medical intervention during this “silent phase,” comprising BP pressure regulation, metabolic control, dietary protein restriction, and administration of ACEI is renoprotective, as judged by slowed loss of GFR.
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