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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate the importance of risk factors such as hyperglycemia and elevated systolic and diastolic blood pressures on the progression of renal insufficiency in diabetics suffering from diabetic nephropathy. Seventeen patients with Type I, insulin-dependent diabetes mellitus (IDDM) (8 women and 9 men) undergoing chronic hemodialysis were investigated by retrospective follow-up and compared with 17 age and sex matched IDDM patients without diabetic nephropathy (controls). According to the time interval of creatinine increase from 200 to 600 mumol/l, the patients were divided arbitrarily into two groups with rapidly (group I less than 20 months) or slowly progressive (group II greater than or equal to 20 months) renal insufficiency. This period was 13.4 +/- 2.05 months in group I (age 36.67 +/- 2.47 years, diabetes duration 23.55 +/- 2.37 years) and 32.75 +/- 4.34 months in group II (age 40.62 +/- 2.63 years, diabetes duration 26.62 +/- 2.63 years, P.n.s.), respectively. The IDDM patients studied exhibited individually differing progressions of renal insufficiency at different times after manifestation of diabetes. After 15 years of diabetes duration, both risk factors, that is blood pressure and blood glucose concentrations, were elevated in nephropathic diabetics when compared with controls (p less than 0.01). During the phase of declining kidney function, mean blood pressures were found to be higher in IDDM patients with rapid progression of renal insufficiency when compared with slowly progressing diabetics. Although both risk factors were related to diabetic nephropathy, during the phase of renal insufficiency hypertension appeared to be more closely related to the further deterioration of kidney function.
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PMID:The progression of diabetic nephropathy in type I diabetics: relationship to metabolic control and blood pressure. 296 2

Twenty-seven patients with Type I diabetes and diabetic nephropathy were repeatedly tested (mean, 6 times per patient) for residual urine volumes with a noninvasive technique. Results in 43 of 162 investigations (27%) were abnormal, with residual volumes of greater than 15 ml. Twelve of 162 (7%) showed a residual volume greater than 100 ml. In any individual patient the occurrence of residual volumes was not a consistent finding, and the volumes varied. Pathologic residual volumes were more common in men, but all those with bacteriuria were women. All patients with residual volumes (N = 16) were given voiding instructions. There was no increase in residual volumes during the observation period (mean, 32 months), the median residual volume being 8 ml at the first observation and 5 ml at the last observation. The occurrence of residual urine could not be shown to correlate with progression of renal insufficiency. It is suggested that all patients with long-standing Type I diabetes should be tested by a noninvasive technique for residual urine volume and given voiding instructions to avoid acute retention episodes and complete atony of the bladder.
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PMID:Diabetic cystopathy--a risk factor in diabetic nephropathy? 297 63

We carried out sonographic examination of 160 type I diabetics measuring the renal volume, the parenchyma/renal pelvis index and the brightness of the parenchyma. Creatinine and beta-2-microglobulin in the serum, creatinine clearance and albumin excretion by urine were determined as functional parameters. In contrast to existing results, we were unable to find significant changes in kidney size or function in newly diagnosed diabetics (duration of diabetes up to 6 months). Both the parenchyma/renal pelvis index and the kidney parenchyma were unchanged compared to control persons of the same age. It was only if diabetes lasted from 6 months to 5 years, that the renal volume was 19% larger (192 +/- 37 cm3/1.73 m2) than that of recently diagnosed patients (p less than 0.01). The index had increased by 15%, whereas the creatinine clearance had increased by 18% to 121 +/- 27 ml/min as a result of increased perfusion. The renal volume decreased continuously over a five-year period of duration of diabetes. Initially, microalbuminuria became manifest, followed some time later by a decrease in creatinine clearance and a corresponding increase in creatinine and beta-2-microglobulin in serum. No change in parenchyma brightness was noted. Diabetics with moderate renal insufficiency (creatinine 1.2 to 2 mg/dl) compared to diabetics without insufficiency developed larger kidneys (207 cm3/1.73 m2; p less than 0.01). Only in case of severe insufficiency (creatinine greater than 2 mg/dl) did the kidneys did shrink significantly (121 cm3/1,73 m2, n = 8, p less than 0.01). The temporary enlargement of the kidneys could be a prognostically unfavourable sign pointing towards a developing diabetic nephropathy.
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PMID:[Sonographic changes in the size of the kidneys in type I diabetes as a method of early detection of diabetic nephropathy]. 307 Jul 48

Twenty-one patients with diabetes of type I and diabetic nephropathy with reduced glomerular filtration rate (GFR) were followed prospectively with regard to GFR, proteinuria, blood pressure and glucosylated haemoglobin (HbA1). All patients were on antihypertensive treatment. The mean rate of decline in GFR was only 0.38 ml/month = 4.6 ml/year. In one third of the patients, GFR remained constant at a reduced level for at least 24 months. Mean plasma clearance of 51Cr-EDTA in this group was 48.3 +/- 14.6 ml/min/1.73 m2 body surface at entry and 48.0 +/- 13.6 at the time of evaluation. The patients with constant GFR had significantly less proteinuria and lower systolic as well as mean arterial pressure during the study than patients with falling GFR. They also had significantly lower mean HbA1 and fewer very high HbA1 values than patients who deteriorated. The data thus indicate that a combination of good metabolic control and effective blood pressure control may strongly delay the progression of renal insufficiency in diabetic nephropathy. They also show that low degree of proteinuria is a marker of good prognosis.
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PMID:Constant glomerular filtration rate in diabetic nephropathy. Correlation to blood pressure and blood glucose control. 308 7

The effect of long term, aggressive antihypertensive treatment on kidney function in diabetic nephropathy was studied prospectively in 11 insulin dependent diabetics (mean age 30). During the mean pretreatment period of 32 (range 23-66) months the glomerular filtration rate decreased significantly and albuminuria and the arterial blood pressure increased significantly. During the 72 (range 32-91) month period of antihypertensive treatment the average arterial blood pressure fell from 143/96 mm Hg to 129/84 mm Hg and albuminuria decreased from 1038 micrograms/min to 504 micrograms/min. The rate of decline in the glomerular filtration rate decreased from 0.89 (range 0.44-1.46) ml/min/month before treatment to 0.22 (range 0.01-0.40) ml/min/month during treatment. The rate of decline in the glomerular filtration rate was significantly smaller during the second three years compared with the first three years in patients who received long term antihypertensive treatment (greater than or equal to 6 years). One patient died from acute myocardial infarction (glomerular filtration rate 46 ml/min/1.74 m2). Effective antihypertensive treatment postpones renal insufficiency in diabetic nephropathy.
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PMID:Effect of antihypertensive treatment on kidney function in diabetic nephropathy. 311 83

Plasma as well as renal clearance of 51Cr-EDTA, serum creatinine, plasma beta-2-microglobulin and endogenous creatinine clearance were compared and evaluated in patients with diabetic nephropathy and in control patients with renal disease of other origin. The difference between the plasma clearance and the renal clearance of 51Cr-EDTA, that is the extrarenal clearance, was found to be higher in diabetics than in control patients (7.0 vs. 3.5 ml/min; p less than 0.001). The serum creatinine correlated well with the glomerular filtration rate (GFR), but in the individual case the GFR was not at all predictable from serum creatinine. The plasma beta-2-microglobulin did not correlate better than serum creatinine to 51Cr-EDTA clearance, and did not permit an earlier diagnosis of renal insufficiency. Endogenous creatinine clearance overestimated GFR by 0-180%. Due to residual urine, the coefficient of variation was higher in diabetic patients than in controls, but the effect of this imperfection was reduced by using multiple collection periods. In conclusion, the renal clearance of 51Cr-EDTA was found to be preferable to the other methods.
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PMID:Estimation of renal function in diabetic nephropathy. Comparison of five methods. 311 57

In 97 patients with type I diabetes mellitus, 155 patients with type II diabetes mellitus, and two matched control groups, serum concentrations of laminin P1, a non-collagenous component of basement membranes, were determined by radioimmunoassay to see whether laminin P1 might be a valuable indicator of microangiopathic complications in diabetics. Independent of the type of diabetes, serum laminin concentrations in patients without nephropathy or with early renal damage as assessed by microalbuminuria were comparable with those of the control subjects. Patients with macroproteinuria or with renal insufficiency had significantly increased serum laminin P1 concentrations. Diabetic retinopathy was not found to influence serum laminin P1 concentrations. These data indicate that serum laminin P1 concentrations are increased in advanced diabetic nephropathy.
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PMID:Serum concentrations of laminin P1 in diabetics with advanced nephropathy. 319 51

A third of all Type 1 diabetic patients will develop proteinuria as a clinical sign of diabetic nephropathy. A 100-fold increase in relative mortality is observed in patients with persistent proteinuria. Proteinuria is preceded by a microproteinuric phase, which is reversible upon optimized metabolic control. Thereby, progression towards clinically manifest nephropathy can be delayed. Macroproteinuria and progressive renal insufficiency are not influenced by metabolic control, but by aggressive antihypertensive therapy.
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PMID:[Proteinuria in diabetes mellitus]. 328 21

Recent clinical reports have suggested that hypertension accelerates the progress of diabetic nephropathy and retinopathy, whereas antihypertensive treatments may retard them. Thus, the effect of antihypertensive treatment in diabetes mellitus with hypertension was evaluated in rats. A model of diabetes mellitus with hypertension has been developed in spontaneously hypertensive (SHR) rats by unilateral nephrectomy and streptozotocin (STZ, 30 mg/kg, i.v. treatment). The rats were treated with four antihypertensive drugs orally for 12 weeks thereafter. STZ treatment induced chronic hypeglycaemia (300-400 mg/dl), decreased body weight and heart rate, and caused vascular changes of ophthalmic fundi and cataracta. The kidney of these rats showed proliferative changes such as periarteritis nodosa, hyperplasia, or fibronecrosis of the arterioles, exudative changes, mesangial proliferation, or thickening of the basement membrane of the glomeruli. Enalapril (10 mg/kg per day) and remipril (Hoe 498) (1 mg/kg per day), converting enzyme inhibitors, or arotinolol (20 mg/kg per day), a beta-adrenoceptor blocking drug, decreased blood pressure, prevented the development of renal and ocular lesions, and tended to increase creatinine clearance. Nisoldipine (3 mg/kg per day), a calcium-entry blocking drug, tended to decrease blood glucose, and prevented the decrease of body weight and development of ocular lesions. In conclusion, antihypertensive treatments were effective in preventing the progress of diabetic retinopathy and nephropathy, and renal insufficiency in this animal model.
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PMID:Antihypertensive treatment in spontaneously hypertensive rats with streptozotocin-induced diabetes mellitus. 329 54

Since the metabolic changes in normal pregnancy are diabetogenic, pregnancy imposes a severe stress on the metabolic milieu of diabetic patients. Moreover, many patients with long-standing diabetes have vascular complications, including retinopathy, renal insufficiency, nephrotic syndrome and hypertension, that represent separate risk factors for optimal fetal development. Recent experience has suggested that maternal hyperglycaemia, and associated fetal hyperinsulinaemia, may represent an important factor in the development of fetal complications. During the past two to three decades the incidence of perinatal deaths has been reduced in all cases of diabetics to a level that approaches the rate in healthy gravidas when severe congenital anomalies are excluded. Fetal and neonatal morbidity have also been reduced, although rates of congenital anomalies, polyhydramnios and respiratory distress syndrome remain high. In patients with significant vascular complications, especially nephropathy and retinopathy, there is no evidence that pregnancy alters the natural course of these complications. Although the morbidity associated with oedema formation and hypertension is elevated, with meticulous management of patients with diabetic nephropathy, especially in the absence of severe renal insufficiency and/or severe hypertension, pregnancy performance and outcome can be similar to other insulin-dependent diabetics.
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PMID:Managing diabetic patients with nephropathy and other vascular complications. 333 Apr 94


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