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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Risk factors for renal and cardiovascular disease in diabetic patients. 165 64

Increased urinary albumin excretion rate (AER) in the microalbuminuric phase of diabetic nephropathy has been attributed to intraglomerular hypertension. This could be caused by constriction of efferent glomerular arterioles, which carry alpha-adrenoceptors. We tested the hypothesis that insulin-dependent diabetes mellitus (IDDM) patients with microalbuminuria are hypersensitive to vasoconstriction induced by norepinephrine (NE). We studied 15 IDDM patients with microalbuminuria (AER 32-295 mg/24 h), 13 IDDM patients with normal AER (5-24 mg/24 h), and 9 nondiabetic subjects (AER 8-22 mg/24 h). All were normotensive. NE-induced vasoconstriction was measured in dorsal hand veins, which carry alpha-receptors similar to those of glomerular efferent arterioles. Vein diameter was measured with a linear displacement probe during a stepped NE infusion (1-32 ng/min) into the vein, and venoconstriction was expressed as a percentage of the maximum passively distended venous diameter. Microalbuminuric IDDM patients exhibited significantly greater vasoconstriction (P less than 0.005) at all NE infusion rates than both other groups. The NE infusion rate producing 50% of maximal venoconstriction (ED50) in the microalbuminuric IDDM group (median 1.1 ng/min, range 0.2-25.2 ng/min) was significantly less than in both the normoalbuminuric IDDM group (median 12.5 ng/min, range 4.9-40.5 ng/min, P = 0.00007) and the nondiabetic group (median 17.7 ng/min, range 5.9-42.2 ng/min, P = 0.0003). Dose-response curves and ED50 did not differ significantly between normalbuminuric IDDM and nondiabetic groups. IDDM patients with microalbuminuria are hypersensitive to NE-induced vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exaggerated sensitivity to NE-induced vasoconstriction in IDDM patients with microalbuminuria. Possible etiology and diagnostic implications. 173 11

Hypertension and renal disease are major causes of morbidity and mortality in the diabetic population, with the presence of microalbuminuria established as a predictor of excess mortality. Numerous attempts, both pharmacologic and nonpharmacologic, have been made to intervene in the disease process. Experimental and clinical evidence suggests that the converting enzyme inhibitors and, more recently, certain calcium antagonists have beneficial effects on renal function above and beyond those simply due to blood pressure control. These effects are likely attributable to favorable systemic and renal hemodynamic changes as well as to direct cellular effects. However, intervention with these agents in various rat models of diabetes or hypertension is initiated very early. Hence, some of the beneficial renal effects may not be as dramatic in clinical practice because of the more commonly advanced stage seen at the time of intervention. We present an overview of the histologic, renal hemodynamic, and antiproteinuric effects of these agents in the experimental setting, as well as the clinical evidence supporting the use of angiotensin-converting enzyme inhibitors and certain classes of calcium antagonists in diabetic renal disease.
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PMID:A perspective on converting enzyme inhibitors and calcium channel antagonists in diabetic renal disease. 174 90

In this article, we analyze the blood pressure (BP) threshold for the start of antihypertensive treatment in insulin-dependent diabetes mellitus (IDDM) patients, with particular emphasis on those with persistent microalbuminuria or proteinuria (incipient and overt nephropathy, respectively). In such individuals, there is a clear increase in the prevalence of hypertension and in actual measured BP values that is not observed in normoalbuminuric patients. In 94 young healthy adults (less than 45 yr of age), average mean +/- SD arterial pressure (MAP; diastolic + 1/3 pulse pressure) was approximately 90.0 +/- 8.1 mmHg, closely corresponding to large population studies. In microalbuminuric IDDM patients, MAP values between approximately 105 and approximately 95 mmHg have been found in different studies, and the level has progressively decreased in various studies between 1984 and 1990 with similar BP-measuring techniques. Somewhat higher values are seen in patients with proteinuria, who are also consistently characterized by reduced glomerular filtration rate (GFR). A clear correlation is found between MAP plotted against the increased rate of microalbuminuria (%/yr) in incipient nephropathy and against fall rate of GFR (ml.min-1.mo-1) in proteinuric patients. In the natural history of renal disease, different cutoff points in MAP for start of progression are observed: greater than 95 mmHg for the start of progression of microalbuminuria and greater than 105 mmHg for the decrease in GFR. During antihypertensive treatment, there is reduction or no progression in microalbuminuria with MAP of approximately 90-95 mmHg and only a limited fall in GFR with MAP of approximately 100 mmHg. However, certain antihypertensive drugs (angiotensin-converting enzyme inhibitors) may have specific renoprotective actions, reducing microalbuminuria at rather low BP levels or even independent of BP reduction. The optimal way of monitoring BP may be by 24-h ambulatory recording.
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PMID:Renal factors influencing blood pressure threshold and choice of treatment for hypertension in IDDM. 174 53

In order to obtain more information on the quality of metabolic control and presence of secondary complications in type 2 diabetic patients treated in a hospital outpatient-clinic, we studied 124 of our diabetic patients (56 males, 68 females, age 65 (SD 11) years, duration of diabetes 9, range 1-32 years). HbA1c levels were 7.9% in patients on oral hypoglycaemic agents (n = 56), and 8.2% in insulin-treated patients (n = 59). Cholesterol and triglyceride levels tended to be lower in the insulin-treated patients. The prevalence of vascular abnormalities was high: in comparison with a population of general practice patients more patients had hypertension (56% vs 38%), coronary artery disease (48% vs 40%), and cerebrovascular disease (15% vs 6%). In addition, 35% of our diabetics had signs of peripheral artery disease. Retinopathy was present in 35 patients, microalbuminuria was found in 31 patients, proteinuria in 18 patients. The presence of microalbuminuria and proteinuria was a strong indicator for cardiovascular disease, polyneuropathy and retinopathy. The use of cardiovascular medication was high: 57 patients used antihypertensive therapy, 37 used diuretics, and 26 long-acting nitrates. Only 25 patients took no medication apart from to their diabetes therapy.
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PMID:[Regulation of diabetes and late complications in the ambulatory treatment of patients with Type II diabetes mellitus]. 174 45

The aim of this retrospective study was to evaluate the prevalence of microalbuminuria in type 1 and 2 diabetic patients with or without high blood pressure levels. 653 patients were involved in the study [type 1: n = 413 (normotensive: n = 298; hypertensive: n = 115); type 2: n = 240 (normotensive: n = 93; hypertensive: n = 147)]. In type 1 diabetic patients, the prevalence of microalbuminuria was of 21 per cent. Microalbuminuria was also found in 28 per cent of type 2 diabetic subjects (p less than 0.10 vs type 1). The prevalence of microalbuminuria was significantly higher in hypertensive than in normotensive diabetic subjects (28 vs 20 per cent; p less than 0.05). Blood pressure in type 1 and 2 normotensive patients was significantly higher in subjects with than without microalbuminuria. We also observed higher HbA1 levels in microalbuminuric type 1 diabetic patients. Finally, we also assessed that the prevalence of diabetic chronic complications was higher in type 1 patients with than without microalbuminuria (p less than 0.05). This relationship was not evidenced in type 2 diabetic patients. In conclusion, the prevalence of microalbuminuria in a population of type 1 and 2 diabetic patients is high. We confirm in this study the relationship between microalbuminuria, blood pressure, and HbA1.
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PMID:[Microalbuminuria in a population of 653 patients with type 1 and 2 diabetes]. 175 48

23 living related kidney transplant donors were prospectively studied to determine the degree of hyperfiltration which occurs after uninephrectomy and to monitor potential consequences of this procedure such as hypertension, microalbuminuria or renal functional impairment. Standard inulin and PAH clearance studies were performed immediately before (n = 23), one week after (n = 22) and one year after nephrectomy (n = 12). Hyperfiltration was defined as the ratio of (post-nephrectomy inulin clearance)/(0.5 x pre-nephrectomy inulin clearance), hyperperfusion was defined in an analogous way for PAH clearance. One week after uninephrectomy, hyperfiltration averaged 134 +/- 6% (SEM) and hyperperfusion was 138 +/- 6%. The degree of hyperfiltration did not correlate with donor age. One year after nephrectomy, hyperfiltration was nearly unchanged (130 +/- 7%) whereas hyperperfusion had significantly decreased to 119 +/- 8% (p less than 0.05). Blood pressure did not increase after nephrectomy and no new cases of hypertension were observed during follow-up. In contrast, there were two new cases of microalbuminuria at one week and one year after nephrectomy. Further follow-up of these kidney donors is warranted.
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PMID:[Glomerular hyperfiltration following unilateral nephrectomy in healthy subjects]. 175 67

We measured the urinary excretion of albumin in 67 healthy primigravidae, at monthly intervals, from 16 to 36 weeks of gestation and 12 weeks postpartum. Of the 67 primigravidae, 55 completed a normal pregnancy and 12 developed pregnancy-induced hypertension. In the latter group, an additional measurement of urinary albumin excretion was performed at 24 weeks postpartum. The aims of the study were: to look for changes of urinary albumin excretion during the progression of normal pregnancy; to assess if microalbuminuria could be an early feature of pregnancy-induced hypertension; to evaluate the effects of physical activity on the excretion of albumin in normal pregnancy and pregnancy-induced hypertension. In contrast with glomerular hyperfiltration and increased urinary total protein, two recognized characteristics of the pregnant state, we found that normal primigravidae, during the day, excrete significantly less albumin (p between less than 0.01 and less than 0.001) in comparison with the postpartum period and nonpregnant women. Normal primigravidae, as a group, showed parallel changes of urinary albumin excretion and diastolic blood pressure throughout pregnancy and postpartum, suggesting an important physiologic role of hemodynamic factors in regulating glomerular permeability to albumin. The daytime urinary albumin excretion in patients developing pregnancy-induced hypertension was significantly higher (p between less than 0.005 and less than 0.001) than in normal pregnancy from the 28th gestational week onwards. The increased urinary albumin excretion preceded the onset of hypertension and tended to persist long after blood pressure had returned to normal levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary albumin excretion in normal pregnancy and pregnancy-induced hypertension. 175 31

The prevalences and risk factors of micro- and macroalbuminuria were surveyed in all 927 patients with diabetes mellitus who visited outpatient clinics in 27 hospitals in the Fukuoka prefecture on a designated day. The urinary albumin-creatinine ratio (UAI; mg/g Cr) of spot urine was determined in all patients except those with persistent macroproteinuria. The results were as follows: (1) The prevalences of microalbuminuria (UAI 30-299) and macroalbuminuria (UAI greater than or equal to 300) were 26% and 15%, respectively. (2) Hyperglycemia and high blood pressure synergistically increased the prevalences. (3) The independent risk factors of microalbuminuria were severities of retinopathy and neuropathy, duration of diabetes, blood pressure, and HbA1c, as determined by logistic regression analysis, although the explanation rate was low.
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PMID:One-day survey of albuminuria in diabetic outpatients in Fukuoka Prefecture, Japan. Fukuoka Diabetic Clinic Group. 177 29

The UK Prospective Diabetes Study (UKPDS) is a multi-centre, prospective, randomised, intervention trial of 5100 newly-diagnosed patients with Type 2 (non-insulin-dependent) diabetes mellitus which aims to determine whether improved blood glucose control will prevent complications and reduce the associated morbidity and mortality. Newly presenting Type 2 diabetic patients aged 25-65 years inclusive, median age 53 years, median body mass index 28 kg/m2 and median fasting plasma glucose 11.3 mmol/l, were recruited and treated initially by diet. Ninety five percent remained hyperglycaemic (fasting plasma glucose greater than 6 mmol/l) and were randomly allocated to different therapies. In the main randomisation, those who were asymptomatic and had fasting plasma glucose under 15 mmol/l were allocated either to diet policy, or to active policy with either insulin or sulphonylurea aiming to reduce the fasting plasma glucose to under 6 mmol/l. Over 3 years, the median fasting plasma glucose in those allocated to diet policy was 8.9 mmol/l compared with 7.0 mmol/l in those allocated to active policy. The Hypertension in Diabetes Study has been included in a factorial design to assess whether improved blood pressure control will be advantageous. Patients with blood pressure greater than or equal to 160/90 mm Hg were randomly allocated to tight control aiming for less than 150/85 mm Hg with either an angiotensin-converting enzyme inhibitor or a Beta-blocker or to less tight control aiming for less than 200/105 mm Hg. The endpoints of the studies are major clinical events which affect the life and well-being of patients, such as heart attacks, angina, strokes, amputations, blindness and renal failure. To date, 728 patients have had at least one clinical endpoint. Surrogate endpoints include indices of macrovascular and microvascular disease detected by ECG with Minnesota Coding, retinal colour photography and microalbuminuria. The studies also aim to evaluate potential risk factors for the development of diabetic complications such as smoking, obesity, central adiposity, plasma LDL- and HDL-cholesterol, triglyceride, insulin, urate and other biochemical variables. The studies are planned to terminate in 1994, with a median follow-up of 9 years (range 3-16 years) for the glucose study and 5 years (range 2-6 years) for the hypertension study.
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PMID:UK Prospective Diabetes Study (UKPDS). VIII. Study design, progress and performance. 177 53


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