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  • Articles: DFG German National Licenses  (6)
  • rat  (3)
  • Microalbuminuria  (2)
  • (Mouse)  (1)
Source
  • Articles: DFG German National Licenses  (6)
Material
Years
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism 836 (1985), S. 312-320 
    ISSN: 0005-2760
    Keywords: (Mouse) ; Bone marrow macrophage ; Extracellular enzyme ; Phospholipase A"1 ; Secretion
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Diabetes ; growth hormone ; hypertrophy ; kidney ; rat ; streptozotocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Normal and diabetic rats were given daily injections of human growth hormone for four days (5 mg per rat per day). Injected rats showed no differences from uninjected controls with respect to kidney weight or renal content of protein, RNA or DNA. Kidney weight increased by 7% after two days of diabetes and by 20% after four days, but growth hormone caused no augmentation of the hypertrophy. It is concluded that growth hormone plays no role in the initiation of diabetic renal hypertrophy.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 14 (1978), S. 325-328 
    ISSN: 1432-0428
    Keywords: Diabetes ; hypertrophy ; kidney ; nephrectomy ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The kidney growth seen after the induction of experimental diabetes in rats has been compared to the compensatory renal growth after one-sided nephrectomy. After five days the kidney weight had increased from 650 ± 15 mg in a group of controls to 778 ± 21 mg in diabetic rats, and 764 ±17 mg in unilaterally nephrectomised rats. The increased weight was in both groups reflected in an increased DNA content and increased RNA/DNA and protein/DNA ratios. In a group of rats made diabetic and nephrectomised at the same time, kidney weight increased to 953 ± 22 mg after five days. When rats were unilaterally nephrectomised after 20 days of untreated diabetes, compensatory growth was much more pronounced than in non-diabetic rats, kidney weight rising from 780 ± 21 to 1144 ± 39 mg in five days. Similarly, in rats with established compensatory renal hypertrophy, diabetes induced a very rapid growth of the remaining kidney (1226 ± 46 mg after five days).
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 13 (1977), S. 141-143 
    ISSN: 1432-0428
    Keywords: Blood glucose ; diabetes ; DNA ; hypertrophy ; kidney ; rat ; Streptozotocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Streptozotocin diabetic rats have larger kidneys than non-diabetic rats. In the present study the rate of kidney growth during the first seven days of diabetes was correlated with the blood glucose concentration. Over a wide range of blood glucose concentrations (116–340 mg/100 ml) the kidney weight, protein content and protein/DNA ratio were closely correlated with the glucose values.
    Type of Medium: Electronic Resource
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  • 5
    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
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  • 6
    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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