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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney disease is a primary cause of morbidity and mortality in diabetic patients. Factors that predetermine development of nephropathy remain unknown. Poor glycemic control, insulin requirement, duration of diabetes and family history of hypertension appear to be associated with an increased risk. Arterial hypertension, which is twice as common in diabetic patients as in the normal population, accelerates the progression of diabetic nephropathy. The pathophysiologic mechanisms responsible for hypertension appear to be different in IDDM and NIDDM. In IDDM, hypertension occurs usually as a consequence of diabetic renal disease. Conversely, the pathogenesis in NIDDM appears to be multifactorial. In either condition, aggressive blood pressure control is the single most important intervention proven to retard the progression of nephropathy. A stepped-care approach similar to that for essential hypertension with slight modifications is indicated in the treatment of the hypertensive diabetic patient with nephropathy. Nonpharmacological therapy, including dietary protein restriction, should be used as first step. Selection of the ideal antihypertensive must be based not only on efficacy but also on its side effect profile. Angiotensin converting enzyme inhibitors and calcium antagonists have a low incidence of side effects and do not induce metabolic disturbances. Therefore, they are the agents of choice for patients who do not respond to nonpharmacological therapy alone. Thiazide diuretics and beta-blockers should be used as first line therapy only for specific indications. Antihypertensive therapy combined with good glycemic control and dietary protein restriction constitute the standard of care for diabetic patients with hypertension and renal disease.
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PMID:Hypertension and kidney disease of diabetes mellitus. 176 55

Several lines of evidence suggest that hypertension is a contributing factor to diabetic nephropathy, a major cause of mortality in diabetes mellitus patients. The present study tested the hypotheses (1) that insulin dependent diabetes (IDD) causes hypertension, and (2) that simultaneous hypertension and IDD causes greater renal damage than would be expected from the independent contributions of each disease. IDD was induced by injection of streptozotocin (STZ, 65 mg/kg i.p.) into male Wistar rats, causing severe hyperglycaemia within 4 days. Seven days after the STZ treatment, hypertension was initiated by subcutaneous implantation of deoxycorticosterone acetate and administration of 1% saline in the drinking water (DOCA-NaCl). IDD rats not receiving DOCA-NaCl displayed a small elevation of blood pressure one week after STZ treatment, but thereafter displayed significant hypotension. The IDD rats receiving DOCA-NaCl displayed elevated systolic arterial pressure throughout the study, but by the end of the experiment, their mean systolic arterial pressure was significantly lower than that of the rats treated with DOCA-NaCl alone. Only the IDD/DOCA-NaCl rats displayed significant signs of renal dysfunction, i.e. greatly increased proteinuria and morphological renal damage, including marked distension of distal tubules and occasional casts. No other group displayed these abnormalities.
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PMID:Effects of simultaneous diabetes and hypertension in an insulin dependent diabetic model. 176 11

Alacepril is a new angiotensin-converting enzyme (ACE) inhibitor that possesses sympatho-inhibitory action. We evaluated the effect of alacepril on blood pressure and progression of diabetic nephropathy in hypertensive type II diabetics in an open multicenter trial. Eighty-nine type II diabetics with mild hypertension were treated with 50 mg of alacepril daily and observed for 12 weeks. Blood pressure was reduced significantly at 4 weeks; this reduction continued throughout the study. Urinary excretion of albumin also was reduced significantly at 12 weeks. Glycosylated hemoglobin (HbA1c) and serum total cholesterol showed significant reduction with alacepril. We confirmed the beneficial effect of alacepril on blood pressure and diabetic nephropathy, and found that glucose and lipid metabolism improves in the diabetic state with this ACE inhibitor.
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PMID:Beneficial effect of alacepril, a new angiotensin-converting enzyme inhibitor on albuminuria and glycemic state: an open multicenter trial. Alacepril Study Group. 177 32

The major renal pathologic changes of diabetes include thickening of all renal extracellular basement membranes and mesangial matrix and, to a lesser extent, mesangial cell expansion. Two renal lesions appear critical in diabetic nephropathy. Mesangial expansion out of proportion to the size of the glomerulus is closely and inversely related to measures of peripheral capillary wall filtration surface and to clinical features of proteinuria, hypertension, and decreasing glomerular filtration rate (GFR). Arteriolar hyalinosis is related to global glomerulosclerosis, and both are correlated with the clinical features of nephropathy. These lesions are markedly advanced by the time renal dysfunction is clinically detectable. Relationships of structure and function early in the course of the diabetes have not been examined satisfactorily.
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PMID:Structural-functional relationships in type I insulin-dependent diabetes mellitus in humans. 177 56

It is well known that hypertension (HT) is frequently accompanied with diabetic nephropathy (DN) and that HT contributes to progression of DN. Thus, proper anti-hypertensive therapy is required in hypertensive patients with DN. However, there is so far no consensus of optimal blood pressure (BP) level to maintain the renal function in these patients. In order to evaluate the optimal BP level in the patients with renal insufficiency, we investigated the relation between BP and renal function in 15 DN patients with HT (aged 56.9 +/- 11.7 years at the first medical examination; 6 male and 9 female, total 117 patient-years) and 20 patients with hypertensive nephropathy (aged 44.3 +/- 13.0 years at the first medical examination; 17 male and 3 female, total 207.5 patient-years) as the control, who receive antihypertensive therapy for more than 4 years as outpatients at the second department of internal medicine of Tohoku University Hospital between 1974 and 1990. During this period 7 patients with DN came to receive hemodialysis therapy 2 to 6 (average 3.8 +/- 1.3) years after the first medical examination. As a result, in patients with hypertensive nephropathy, there was a tendency to show that the lower the mean BP was, the better the renal function. On the contrary, in DN patients there was an optimal mean BP (MBP) range; i.e, when MBP was controlled in this range, the deterioration rate of renal function was delayed, while deviation of MBP from this range made the renal function worse (p less than 0.01). However, this range varied with the serum creatinine (SCr) concentration level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The treatment of hypertensive patients with renal insufficiency--a comparison of the blood pressure management in patients with diabetic nephropathy and patients with hypertensive nephropathy]. 177 Jun 21

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

Duplex Doppler ultrasonography may explore renal perfusion in frequent diseases such as renal obstruction, reno-vascular hypertension, acute or chronic renal failure or diabetic renal complications by measuring Pourcelot's resistive index (RI) of renal parenchyma arteries for each kidney. A statistical and prospective study was performed on 574 patients. In healthy patients, the RI values, equal for each kidney were included in 0.45 and 0.7 (mean RI = 0.59). For other values, there was a renal pathology. Patients with idiopathic hypertension (mean RI = 0.59) or non obstructive dilatation (mean RI = 0.61) did not have an RI significantly different from healthy patients. In cases of renal obstruction, there was a significant increase in the RI for the pathological kidney (mean RI of 0.73). The sensitivity and the specificity was 100% for acute obstructions examined during the first 48 hours. In contrast, in case of renal artery stenosis greater than 70% there was a significant decrease in the RI for pathological kidney. So the RI increased significantly in both kidneys: when there was renal failure with active disease within the tubulo-interstitial compartment (mean RI of 0.77); in all cases of diabetic nephropathy (mean RI of 0.74) where the RI increased early before laboratory signs. Duplex Doppler ultrasonography may be an original method for renal explorations by providing not only morphological data but also physiological data with the perfusion study.
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PMID:[Duplex Doppler ultrasonography of intra-renal arteries. Normal and pathological aspects]. 177 87

Urinary kallikrein (reliable reflexion of its renal excretion) is studied in a large group of diabetic patients with and without nephropathy (again subdivided following Mogensen stages) and in hypertense non-diabetic patients. It is observed that the urinary excretion of kallikrein is independent of the type of diabetes (insulin or non-insulin dependent). There exists a clear difference in the behaviour of this enzyme, in diabetic patients with and without nephropathy, increasing in the former and decreasing in the latter (p less than 0.001). The decrease in urinary kallikrein is parallel to the existence of diabetic nephropathy with arterial hypertension. Urinary kallikrein in hypertense non-diabetic patients who are not treated with diuretics (furosemide) has a behaviour as in normal controls, but it is much higher in patients treated with captopril, being this finding of great importance since it can suggest new therapeutic approaches to diabetic nephropathy.
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PMID:[Renal kallikrein in diabetic nephropathy]. 178 May 9

Diabetic nephropathy, clinically defined by overt albuminuria, hypertension and declining GFR, affects 25-35% of IDDM patients. The risk of nephropathy peaks during the second decade of IDDM and declines thereafter, suggesting that only a subset of IDDM patients is at risk for nephropathy. A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. Mesangial expansion is a characteristic lesion of diabetic nephropathology and correlates with renal function. Functional studies are not indicative of underlying renal pathology except relatively late, when glomerular injury is advanced. Microalbuminuria in the 'predictive' range (greater than 30 micrograms/min) and associated with hypertension and/or declining GFR is a marker of established diabetic glomerulopathy. Only carefully designed longitudinal studies of renal morphology and function with accurate blood pressure monitoring beginning early in the course of IDDM will clarify the relationships between blood pressure and renal damage in IDDM. In NIDDM the frequent presence of non-diabetic renal lesions, of hypertension at or before the onset of diabetes, and the relative paucity of clinical-pathological correlations currently make it difficult to understand the role of hypertension in the genesis and progression of nephropathy. Again, longitudinal studies of blood pressure and renal structure and function are required in NIDDM patients. Finally, animal models of hypertension and diabetes may aid progress in these areas.
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PMID:Hypertension and diabetic renal disease. 179 13

Arterial hypertension is present in 10-80% of newly diagnosed Type 2 diabetics, and in 30-50% of Type 1 diabetics after some years. In patients with overt nephropathy, correction of hypertension is associated with a reduction in the rate of decline of glomerular filtration rate. In most patients without clinical diabetic nephropathy, arterial pressure remains within normal limits as defined by usual criteria, whether or not microalbuminuria is present. Short-term studies of Type 1 diabetics with microalbuminuria suggest that angiotensin-converting enzyme inhibitors result in a fall in urinary albumin excretion rate more than calcium antagonists and diuretics. Additional studies assessing the long-term effect of different antihypertensive agents on the evolution of early diabetic nephropathy are needed before the superiority of any drug can be claimed. In addition, non pharmacological approaches, including optimal glycemic control as well as modification of dietary sodium and serum lipid profile, may alter the progressive course of elevation in arterial pressure and decline in renal function. The optimal level of blood pressure for diabetic patients remains to be determined.
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PMID:Blood pressure reduction as a preventive treatment of diabetic nephropathy. 179 16


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