Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal protection is defined as an attenuation or significant slowing of the irrevocable decrease in renal function over time, which occurs subsequent to renal dysfunction. Control of systemic hypertension by whatever means exerts a renal protective effect. Evidence suggesting a specific action of individual antihypertensive agents is less certain. Calcium antagonists may exert a specific renal protective effect. Experiments in rats with reduced renal mass, desoxycorticosterone-induced hypertension, chronic angiotensin II infusion, and in spontaneously hypertensive rats support such a view. In three crossover trials, calcium antagonists reduced proteinuria in patients with type 2 diabetes mellitus. Preliminary data from a single prospective trial in patients with renal insufficiency offer additional support; however, definitive conclusions cannot be reached without further trials. In particular, comparative trials of different classes of antihypertensive agents with equal blood pressure control are needed. Thus far, only reducing systemic blood pressure per se has been shown to be of value in attenuating hypertension-induced renal dysfunction in humans.
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PMID:Are calcium antagonists of value in ameliorating the course of chronic renal disease? 161 61

We report the case of an elderly black woman with a 20-year history of insulin-independent diabetes mellitus (IDDM), chronic renal failure, hypertension, proliferative retinopathy, and classical histologic features of diabetic glomerulosclerosis on renal biopsy. Repeat determinations of urinary albumin excretion rates failed to disclose significant microalbuminuria. This presentation should remind the clinician that a small minority of patients with IDDM of long duration may have severe diabetic glomerulosclerosis and renal insufficiency without detectable microalbuminuria.
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PMID:Diabetic glomerulosclerosis and chronic renal failure with absent-to-minimal microalbuminuria. 162 84

We have presented an unusually swift progression of progressive systemic sclerosis (PSS), with death from cardiogenic shock in a 22-year-old woman who had severe hypertension and acute renal insufficiency. She arrived at our hospital with pericardial tamponade and shock. Despite initial improvement after pericardiocentesis, the patient's condition soon deteriorated and she died of cardiogenic shock. PSS was diagnosed at autopsy. Although the course of PSS is frequently indolent, it may also be fulminant, leading to death before diagnosis is determined.
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PMID:Progressive systemic sclerosis causing rapidly progressive myocardial disease and death. 163

The clinical course of 138 children who underwent unilateral nephrectomy and had a normal contralateral kidney at the time of nephrectomy was reviewed. The diagnosis leading to nephrectomy included obstructive uropathy in 46% of the cases, reflux or pyelonephritis in 30%, Wilms tumor in 15%, hypertension in 4%, dysplastic kidney in 2% and trauma in 2%. Mean age at nephrectomy was 7.3 years and median followup was 24.7 years. Of the 138 patients 121 (88%) are well and 17 died, including 14 secondary to metastatic Wilms tumor and 1 of renal failure. Survival of nonWilms tumor patients was similar to that of an age-matched control group. In 30 patients 24-hour creatinine clearance and 24-hour urinary protein excretion were measured. Proteinuria (greater than 150 mg./24 hours) was found in 8 of the 30 patients (27%) (p less than 0.001), renal insufficiency developed in 9 (30%) (p less than 0.0001) and hypertension occurred in 10% (p greater than 0.10). Children with an acquired solitary kidney are at increased risk for proteinuria and renal insufficiency.
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PMID:Prognosis of children with solitary kidney after unilateral nephrectomy. 164 May 59

Important side effects of cyclosporin (CSA) are renal insufficiency and hypertension. They might be related to a renal vasoconstrictive effect of CSA, and this vascular response might be due to a local mechanism. CSA was injected in isolated renal artery perfused at constant flow in dogs. Changes in renal perfusion pressure reflected variations in vascular resistance. Pure CSA was dissolved in autologous blood and injected at doses of 0.5, 1, 5, and 10 mg. The infusion of 0.5 and 1 mg caused averaged renal perfusion pressure increases of 8 +/- 4 mmHg and 15 +/- 8 mmHg. Renal venous CSA levels averaged 32 +/- 3 and 49 +/- 9 nmol/l, respectively, at the end of injections. Infusion of 5 and 10 mg of CSA caused averaged renal perfusion pressure increases of 32 +/- 12 mmHg and 81 +/- 21 mmHg. Renal venous CSA levels at the end of injections averaged 142 +/- 30 and 382 +/- 82 nmol/l, respectively. A positive correlation was found between the changes in renal perfusion pressure and renal venous CSA levels. Blockade of alpha-adrenergic receptors, surgical renal sympathectomy, administration of thromboxane receptor antagonist, and endothelial-dependent vasodilation by acetylcholine infusion did not affect the renal vasoconstriction effect of CSA; renal response to CSA was prevented by blockade of the Ca channels with diltiazem, and the plasma endothelin concentration in renal venous blood increased significantly after injection of CSA. A dose-dependent increase in renal arterial resistance occurs with therapeutic blood levels of CSA. Renal vasoconstriction is induced by a local effect at the arterial wall, which is independent of neurogenic, adrenergic, and prostaglandin mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-dependent effect of cyclosporin on renal arterial resistance in dogs. 166 Oct 90

Cyclosporine is the core component of all immunosuppressive protocols. Renal insufficiency and hypertension are the two major side effects of cyclosporine use. A vascular effect of cyclosporine could explain these complications. To study the effect of cyclosporine on vessel wall, a model of isolated renal and femoral artery perfusion was used in the dog. The injection of 0.5, 1, 5 and 10 mg of cyclosporine in the renal artery caused an average increase in renal perfusion pressure of 8 +/- 4, 15 +/- 8, 32 +/- 12 and 81 +/- 21 mmHg (p less than 0.05) respectively. Blockade of alpha-adrenergic receptors and renal sympathectomy did not modify the renal vascular response to cyclosporine. The injection of 1, 5, 10 and 20 mg of cyclosporine in the femoral artery caused an average increase in perfusion pressure of 4 +/- 2, 10 +/- 4, 9 +/- 2 and 20 +/- 8 mmHg (p less than 0.05) respectively. Blockade of alpha-adrenergic receptors and lumbar sympathectomy prevented the vasoconstrictive effect of cyclosporine on the femoral artery. Therefore, cyclosporine caused a significant increase in renal perfusion pressure and a modest vasoconstriction of the femoral artery. This effect appears to be related to an adrenergic mechanism only in the femoral circulation. We conclude that other studies are needed to define the mechanism responsible for the vasoconstrictive effect of cyclosporine.
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PMID:[Effect of therapeutic doses of cyclosporine injected into the renal and femoral arteries in dogs]. 166 94

Six children presented with severe hypertension caused by Takayasu's arteritis (TA), of whom four had bilateral renal artery narrowing and two coarctation syndrome. Two presented with hypertensive encephalopathy and four with congestive cardiac failure. All had a strongly positive skin reactions to purified protein derivative of mycobacterium tuberculosis. Bilateral renal arterial bypass grafts performed in two children resulted in prolonged normalization of their blood pressures, but the grafts clotted 12-18 months later. Primary renal autotransplantation was unsuccessful in two children, one with bilateral renal arterial narrowing and iliac vessel involvement and one with a long coarctation. Secondary renal autotransplantation was successful in a third child with localized aortitis. A successful aortic patch graft was performed in one child with coarctation of the aorta. Angiotensin-converting-enzyme inhibitors should be used with caution in treating the hypertension caused by TA, since bilateral renal arterial narrowing is common and their administration may result in renal insufficiency. The long-term prognosis is guarded in severely hypertensive children with extensive vascular disease due to TA.
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PMID:Management of severe hypertension in childhood Takayasu's arteritis. 167 62

The pharmacokinetics of iloprost were studied in 12 hospitalized patients suffering from severe peripheral arterial occlusive disease (PAOD) stages III or IV according to Fontaine. The patients were 8 males and 4 females aged from 49 to 83 years. Apart from PAOD, several other concomitant diseases were present, e.g. myocardial and/or renal insufficiency, diabetes and hypertension. Patients were treated daily with i.v. infusions of iloprost at dosages of 1.0-3.3 ng/kg/min over a period of 4 to 6 h. Dose-normalized steady-state plasma levels ranged from 39 to 100 pg/ml (65 +/- 20 pg/ml). The total clearance accounted for 16 +/- 5 ml/min/kg. Post-infusion disposition in the plasma was biphasic with half-lives of 4 +/- 2 min and 37 +/- 8 min. The plasma level profiles obtained on days 4 and 14 of treatment in 3 patients were similar. Sex specific kinetic differences were not observed. In comparison to healthy volunteers, studied in an earlier trial, total clearance was slightly lower and consequently steady state levels were increased (p less than 0.05) in PAOD patients. Half-lives in the plasma were not significantly different.
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PMID:Pharmacokinetics of iloprost in patients with severe peripheral arterial occlusive disease. 170 Jul 23

Hemorheological therapy through hemodilution has been gaining importance for several years and been applied to an ever increasing degree in stationary as well as in ambulant treatment. While renal insufficiency without previously established nephropathy is known to be a side effect of dextrans, cases of HES-induced nephropathy have so far not been reported. Two cases are presented in which in the course of stationary hemodilution therapy with HES an acute deterioration of an already exiting nephropathy was noted. Possible pathophysiological causes for such a deterioration are most likely to be found in an increased permeability of the glomerular basal lamina. Hydroxyethyl starch molecules are filtered above the physiological renal threshold which increases the viscosity of the primary urine. This can be counteracted by increasing diuresis. This conclusion can be drawn from our own observations which proved that renal insufficiency can be avoided through sufficient fluid intake (approx. 3 liters/day). In patients with creatinine values above 1.5/dl and arterial hypertension the indication for hemodilution therapy must be analysed carefully. If hemodilution therapy proves to be necessary, sufficient fluid intake must be guaranteed. Retention parameters must be controlled every other day in the course of the therapy. As an alternative, the administration of gelatin preparations should be considered as it does not cause cumulation.
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PMID:[Hydroxyethyl starch-induced transient renal failure in preexisting glomerular damage]. 171 32

Hypertension is a risk factor for the development of atherosclerosis and its complications, which are among the major causes of morbidity and mortality. Although recent clinical trials indicate that antihypertensive treatment reduces morbidity and mortality associated with stroke, congestive heart failure, and renal insufficiency, questions remain as to whether such treatment also prevents coronary heart disease (CHD) mortality. The observed reduction in CHD mortality from pooled clinical trial data was 10-14% and was much less than the expected 20-25% reduction for a 5-6 mm Hg reduction in diastolic pressure. One explanation may be that subtle adverse metabolic effects of treatment may have blunted the beneficial effects. Isradipine, a dihydropyridine calcium antagonist, is a potent antihypertensive drug with antiatherogenic properties in animal models. Therefore, we hypothesized that isradipine may be appropriate for testing the efficacy of antihypertensive treatment in retarding the progression of atherosclerosis in humans. The Multicenter Isradipine/Diuretic Atherosclerosis Study (MIDAS) is a clinical trial designed to compare the efficacy of isradipine (2.5 or 5 mg b.i.d.) with hydrochlorothiazide (12.5 or 25 mg b.i.d.) in retarding the progression of early carotid atherosclerosis as monitored by high-resolution B-mode ultrasonography.
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PMID:The Multicenter Isradipine/Diuretic Atherosclerosis Study: a study of the antiatherogenic properties of isradipine in hypertensive patients. MIDAS Research Group. 172 Apr 79


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