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  • 1
    ISSN: 1432-5233
    Keywords: Abnormal albuminuria ; ACE-inhibition ; Hypertension ; Microalbuminuria ; Diabetic nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is general agreement that a fall rate in glomerular filtration rate (GFR) is the principal endpoint in diabetics with renal disease, and that abnormal albuminuria (including microalbuminuria) is an important intermediate end-point. The relative roles of blood pressure (BP) elevation and abnormal albuminuria in the prediction and genesis of renal disease are a matter of debate, and are further analysed in this paper. New studies show that neither genetic predisposition to hypertension (parental BP) nor parental abnormal albuminuria can be used to predict renal disease in patients with type 1 (insulin-dependent) diabetes. However, parental predisposition to proteinuria seems to be important to certain types of patients with type 2 (non-insulin-dependent) diabetes. Cross-sectional as well as follow-up studies document that GFR is generally well preserved in microalbuminuria (in both type 1 and type 2 patients), while the transition to clinical proteinuria is associated with a decline in GFR. Thus, prevention of overt proteinuria is important in clinical trials in microalbuminuric patients. In type 1 diabetes clear ultrastructural changes have been documented with microalbuminuria and a good correlation between abnormal albuminuria and structural damage is seen. Structural damage in normo- and microalbuminuric patients correlates poorly with BP. New studies in type 1 diabetes document that microalbuminuria (but not elevated BP) predicts not only clinical diabetic nephropathy but also end-stage renal failure and mortality. In type 2 diabetes microalbuminuria is the strongest predictor of mortality, whereas BP elevation is not a predictor. Several studies now document that antihypertensive treatment, especially with inhibitors of angiotensin converting enzyme, is able to reverse or reduce abnormal albuminuria, even in non-hypertensive type 1 patients, and possibly preserve GFR. Therefore, microalbuminuria may be the main indicator for starting antihypertensive treatment in these patients. With respect to organ damage in the retina, abnormal albuminuria is an important indicator of the risk of severe diabetic retinopathy. BP elevation seems not to be an initiating factor, but rather aggravates established retinopathy. Left ventricular hypertrophy has a stronger correlation with BP elevation than normoalbuminuria, suggesting that left ventricular hypertrophy is at least partially a phenomenon secondary to elevated BP in diabetic patients with abnormal albuminuria. Generally, abnormal albuminuria is a strong indicator of cardiovascular renal damage in diabetic patients and in most organs is a stronger factor than elevated BP.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-5233
    Keywords: Angiotensin converting enzyme inhibition ; Microalbuminuria ; Renal haemodynamics ; Type 1 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The renal effects of intravenous injection of 40 mg enalapril were investigated in 16 normotensive microalbuminuric type 1 (insulin-dependent) diabetic patients. After enalapril the following changes were observed: fractional albumin clearance (Θ Alb) decreased from 9.9 (3.0–23.8) to 8.2 (2.0–18.3)×10−6 (2P〈0.01); filtration fraction (FF) decreased from 0.260 (0.225–0.312) to 0.253 (0.190–0.297) (2P〈0.01); renal plasma flow (RPF) increased from 565 (411–690) to 623 (449–785) (2P〈0.01); and glomerular filtration rate (GFR) remained stable at 149 (128–181) versus 150 (124–185) ml · min−1 (NS). These values were unchanged after placebo (n=8), except for RFP which decreased from 606 (401–701) to 559 (381–677) ml · min−1 (2P〈0.05) and GFR which was reduced from 148 (111–173) to 138 (111–167) (2P〈0.05). A reduction in mean blood pressure from 94 (87–103) to 89 (79–101) mmHg (2P〈0.05) was found in the enalapril group and a minor reduction in the placebo group from 97 (83–106) to 96 (81–104) mmHg (2P〈0.05) was also noted. The relative changes in systolic blood pressure in the enalapril group correlated with changes in Θ Alb (Spearman'sr=0.66, 2P〈0.02) and FF (r=0.53, 2P〈0.05). Acute inhibition of angiotensin converting enzyme does not reduce the pathological hyperfiltration in these patients and a reduction in Θ Alb and FF can not be dissociated from the reduction in blood pressure.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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