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

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44

Contrasting results have been reported regarding the prevalence of hypertension in insulin-dependent diabetes mellitus (IDDM), showing a slightly higher or normal percentage of IDDM patients with elevated blood pressure levels than in the general population. Most of the cross-sectional and prospective studies on the prevalence of hypertension in IDDM show an association between microalbuminuria and elevated blood pressure levels. However, it is not clear whether hypertension is simply secondary to kidney damage or whether hypertension occurs with or even before the development of impaired kidney function. Patients with IDDM have a higher exchangeable body Na+ pool. Na+ retention in IDDM is accounted for by several metabolic and hormonal abnormalities such as hyperglycemia, hyperketonemia, hyperinsulinemia, altered secretion, and resistance to atrial natriuretic peptide. High blood pressure appears to be dependent, at least at some phase, on expansion of extracellular fluid volume as a consequence of defects in the renal secretion of Na+ and water. On the other hand, a tendency toward Na+ retention characterizes all patients with IDDM, whereas hypertension develops only in a subgroup of diabetic patients. One possible explanation for these findings is that a genetic predisposition plays a role in creating susceptibility to hypertension and perhaps to diabetic nephropathy independent of diabetes, even if Na+ retention can further deteriorate this susceptibility to hypertension. With regard to this issue, it has recently been suggested that the risk of kidney disease in patients with IDDM is associated with a genetic predisposition to hypertension. Furthermore, diabetic nephropathy occurs in familial clusters, because diabetic siblings of nephropathic diabetic patients show a higher frequency of diabetic nephropathy than the diabetic siblings of nonnephropathic diabetic patients. One of the possible genetic markers that could be useful to identify the diabetic patients with susceptibility to hypertension and diabetic nephropathy is the Na+(-)Li+ countertransport activity in erythrocytes.
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PMID:Insulin-dependent diabetes mellitus and hypertension. 204 36

Diabetic nephropathy is the main cause of the increased morbidity and mortality in insulin-dependent diabetes mellitus (IDDM) patients. Elevated blood pressure accelerates and effective blood pressure reduction with beta-blockers and/or angiotensin-converting enzyme (ACE) inhibitors delays the progression of nephropathy and reduces albuminuria. All previous reports dealing with the natural history of diabetic nephropathy demonstrated a cumulative death rate between 50 and 77% 10 yr after onset of nephropathy. Effective antihypertensive treatment reduced the cumulative death rate to 15-20% 10 yr after onset of nephropathy. Recent randomized control studies indicate that ACE inhibition may delay and even prevent the development of diabetic nephropathy in normotensive IDDM patients with persistent microalbuminuria. Several cross-sectional and prospective studies suggest an association between elevated blood pressure and the development and progression of diabetic retinopathy. Furthermore, carotid insufficiency or other causes of unilaterally or bilaterally reduced retinal blood flow (pressure) diminish the development of diabetic retinopathy. Diabetic retinopathy is characterized by abnormal leakage of fluorescein through the blood-retinal barrier, an abnormality that can be reversed during antihypertensive treatment. It is well documented that elevated blood pressure, poor metabolic control, and diabetic microangiopathy independently enhance the endothelial leakage of plasma proteins in diabetes mellitus. A link between capillary hypertension, increased extravasation of plasma proteins, and the development and progression of diabetic microangiopathy has been suggested. Blood pressure reduction diminishes the extravasation of plasma proteins. The above results strongly support the case for early and effective treatment of arterial blood pressure elevation in diabetes.
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PMID:Impact of blood pressure and antihypertensive treatment on incipient and overt nephropathy, retinopathy, and endothelial permeability in diabetes mellitus. 204 41

The effects of inhibiting angiotensin converting enzyme with perindopril and aldosterone with spironolactone were tested in hypertensive patients over fifty. Accordingly, 75 patients with mild hypertension aged 50 to 70 were randomly divided into three groups for a double-blind 8 week comparison of the actions of placebo, 4 to 8 mg/day perindopril, and 37.5 to 75 mg/day spironolactone. Side-effects caused one patient to withdraw from placebo and one from spironolactone treatment. Mean blood pressure rose by 2.4 mm Hg after placebo but dropped by 7.4 and 8.6 after perindopril and spironolactone (P less than .01). Placebo, perindopril, and spironolactone did not alter blood glucose or plasma potassium, but induced, respectively, variations of -0.09, 0, and +0.34 mmol/L in cholesterol (P = .04), and -0.02, -0.05, and +0.27 mmol/L in triglycerides (P less than .01). After the three treatments, changes in angiotensin converting enzyme activity averaged -1, -6, and -1 mU/mL (P less than .01), in active renin -2, +18, and +28 pg/mL (P less than .01), and in aldosterone, +15, +8, and +95 pg/mL (P less than .01). Placebo, perindopril, and spironolactone did not alter microalbuminuria, but reduced urinary kallikrein activity by 0.9, 1.8, and 5.4 mU/mmol creatinine (P = .04). Although short-term administration of spironolactone raised renin and aldosterone markedly and lipids moderately (possibly because of volume contraction), the present results show that perindopril and spironolactone are both safe and effective for treating hypertension at the age of 50 or older.
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PMID:Are angiotensin converting enzyme inhibition and aldosterone antagonism equivalent in hypertensive patients over fifty? 205 95

This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. The nephron hyperfiltration increases the movement of plasmatic proteins across the glomerular capillary wall with subsequent mesangial hyperactivity and sclerosis. Antihypertensive treatment in diabetes follows general guidelines and it should be instituted even in the case of microhypertension being facilitated in this setting the appearance of microalbuminuria i.e. the starting point of nephropathy. Even if experimental studies are to favor ACE inhibitors as the first-line drugs for abating glomerular hypertension by mitigation of the direct effect of angiotensin II on the efferent arteriolar tone, clinical observations suggest that, regardless of type of treatment, the normalization of systemic arterial pressure, by reversing glomerular hypertension may be effective in preventing diabetic nephropathy.
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PMID:[The pathogenesis of arterial hypertension in diabetes mellitus and its role in nephropathy]. 207 80

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the 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 sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would 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 of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Clinically apparent proteinuria in essential hypertension is associated with increased cardiovascular and total mortality and is an independent risk factor for cardiovascular and cerebrovascular disease. Subclinical elevation of urinary albumin excretion is seen more frequently than clinical proteinuria in essential hypertension and the levels of microalbuminuria (excretions of 30 to 300 mg/24 h) correlate with blood pressure. The increased urinary albumin excretion in hypertension may be explained by several factors such as renal hemodynamic changes, permselectivity changes of the glomerular filter, and structural arteriolar and glomerular changes due to nephrosclerosis. It has been clearly demonstrated that microalbuminuria is a risk factor for the development of clinical proteinuria, renal failure and increased cardiovascular mortality in insulin-dependent diabetes mellitus. It is still not known whether microalbuminuria also predicts development of proteinuria and decline in renal function in hypertension but there is some evidence indicating that microalbuminuria may be a marker of increased cardiovascular risk in hypertensives.
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PMID:Microalbuminuria in essential hypertension. 208 Oct 17

Diabetic nephropathy continues to be a common complication and has an unfavorable prognosis. Metabolic and hemodynamic factors determine the natural history of the condition. Of importance for the prognosis is the detection of nephropathy at an early stage. Such early diagnosis is not possible through the detection of microalbuminuria (incipient nephropathy stage). At this stage, further progress can be reversed by optimizing the metabolic situation and initiating early treatment of increasing blood pressure. For this reason, all diabetics should be submitted to early screening for microalbuminuria. When proteinuria persists (clinically manifest nephropathy stage), renal function usually declines progressively. Vigorous treatment of hypertension, optimal metabolic management, and normalization of protein intake can slow down the rate of continued loss of renal function.
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PMID:[Diagnosis and therapy of diabetic nephropathy]. 208 27

The prevalence of various diabetic complications, their association with each other and with many risk factors, has been assessed in 2,337 newly diagnosed Type 2 diabetic patients. The patients entered into the UK Prospective Diabetes Study were aged between 25 and 65 (mean age 52 yr) and 33% had either an abnormal ECG or retinopathy. Different macrovascular complications such as strokes, heart attacks or abnormal ECG, and peripheral vascular disease showed little association one with another, and each was associated predominantly with different risk factors, e.g., strokes with hypertension, heart attacks with hypertriglyceridaemia and peripheral vascular disease with smoking and a low HDL cholesterol. Retinopathy was associated with reduced vibration perception but not with other complications. Reduced vibration perception and absent reflexes were associated with absent foot pulses and ischaemic skin changes, raising the possibility of a macrovascular, as well as microvascular, contribution to peripheral neuropathy. Microalbuminuria was associated with hypertension, which might be a factor predisposing to renal microvascular disease or be a consequence of it. Microalbuminuria was also associated with an abnormal ECG. Retinopathy, with exudates and or haemorrhages rather than just microaneurysms, was associated with hyperglycaemia. The occurrence of a particular complication in a diabetic patient is probably dependent on a combination of specific risk factors, many of which are related to, and probably affected by, potentially avoidable factors such as hyperglycaemia, obesity, smoking and hypertension.
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PMID:UK Prospective Diabetes Study 6. Complications in newly diagnosed type 2 diabetic patients and their association with different clinical and biochemical risk factors. 209 90

The renal selectivity properties towards albumin were evaluated in ten diabetic patients with arterial hypertension before and after the pharmacological normalisation of blood pressure, and were compared to 12 subjects with essential hypertension. While all patients of the control group were normoalbuminuric during hypertension, six of the diabetic group were microalbuminuric when hypertensive and became almost normoalbuminuric after blood pressure pharmacological control. All microalbuminuric diabetic patients presented altered properties of renal selectivity as epitomised by a non-preferential urinary excretion of glycosyl albumin (GA) (urinary GA/serum GA less than or equal to 1). At variance the selectivity properties were normal in normoalbuminuric diabetic patients and in essential hypertension. It was concluded that in diabetes mellitus arterial hypertension is associated with microalbuminuria when the renal properties of selectivity are altered, but does not implicate any proteinuric effect in those cases where the GBM function is preserved.
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PMID:Hypertension and renal selectivity properties in diabetic microalbuminuria. 212 64


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