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

Conservative management of chronic renal failure in children is essentially based on dietary prescription including recommendations for high caloric intake and a certain limitation of protein intake according to GFR in order to avoid any extra loading with nitrogen wastes. Prescriptions for sodium potassium and water have to be adjusted on their residual output. Prevention of osteodystrophy needs supplement of calcium, chelation of phosphorus with aluminium hydroxide and the prescription of vitamin D or its active derivatives. High blood pressure when present must be carefully controlled. Drugs, when necessary, have to be given with a dosage taking into account the level of renal failure. Finally, the mode of life of the uremic child should be as close to normal as possible.
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PMID:Conservative treatment of chronic renal insufficiency in children. 4 67

Low renin essential hypertension and the syndrome of mineralocorticoid excess have two features in common, low plasma renin activity and volume-sensitive hypertension. The proposal that both disorders share a common mechanism--because of the ability of agents that inhibit or antagonize the adrenocortical secretion to lower blood pressure in the low renin hypertensive group--appears to be based on a circular argument. The beneficial effect of removal or neutralization of the adrenocortical contribution only constitutes evidence for volume-dependency or sensitivity, which is how the low renin group is defined. Any measure that blocks a component of the normal homeostatic chain for the maintenance of extracellular and intravascular volume including the adrenal cortex would be expected to have a beneficial effect in volume-sensitive hypertension. Evidence for an adrenal factor in low renin hypertension must rest on the isolation of an active substance that reproduces the effect when readministered. 18-Hydroxy-11-deoxycorticosterone (18-OH-DOC) does not meet these criteria. It is not significantly increased in experimental hypertension and, although its overproduction in unselected low renin essential hypertensive patients remains controversial, the magnitude of the reported elevations is insufficient in relation to the low biologic activity of the steroid to account for a significant effect. Apart from its increase in the 17alpha-hydroxylase defect, 18-OH-DOC is increased in primary aldosteronism and may also be an indicator of a histologic variant of the aldosteronoma. On the basis of a large body of evidence showing parallelism between the 11beta- and 18-hydroxylase functions of the fasciculata zone, we have proposed that both enzymic functions are functionally related and may involve the same enzyme protein and catalytic site. According to this view, the secretion of 18-OH-DOC would have no special significance of its own but would be an obligatory consequence of the secretion of fasciculata zone corticosterone.
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PMID:Adrenocortical factors in hypertension. I. Significance of 18-hydroxy-11-deoxycorticosterone. 18 51

The prevalence of clinical and sub-clinical occlusive arterial disease and of risk factors implicated in the pathogenesis of arteriosclerosis was assessed in 21 patients with chronic renal failure, 27 on maintenance haemodialysis and 51 renal allograft recipients. Clinical occlusive arterial disease was present in 27 patients, and sub-clinical arterial disease in 34. Myocardial infarction, cerebral thrombosis and lower limb arterial thrombosis had occurred only in the transplant recipients; these patients had, however, been followed for a longer period of time than the other two groups. In the allograft recipients, the cumulative incidence of any occlusive arterial disease was 416 per 1000, and that of coronary heart disease was 267 per 1000 at six years. Hypertension was present in 76 per cent of patients prior to renal replacement therapy. Following institution of definitive therapy, hypertension was of shorter duration and less common in haemodialysis patients than in renal transplant recipients. Uraemic and haemodialysis patients with occlusive arterial disease had required antihypertensive medication for significantly longer than those free of arterial disease. Transplant recipients with hypertension had a greater mean serum creatinine, were receiving a larger maintenance dosage of corticosteroids and less frequently had undergone prior bilateral nephrectomy than those transplant patients without hypertension. Serum lipid levels were elevated in 62 per cent of patients. In the uraemic and haemodialysis patients hypertriglyceridaemia was the predominant abnormality while in the transplant recipients combined hypertriglyceridaemia/hypercholesterolaemia was more frequent. Despite regular aluminium hydroxide therapy 81 per cent of uraemic and haemodialysis patients had a calcium X phosphate product higher than normal. Arterial and/or soft tissue calcification as demonstrable in 20-38 per cent of patients within each group, but could not be related to the calcium X phosphate product of radiographic evidence of hyperparathyroidism. Glucose intolerance was present in 71 per cent of the uraemic and haemodialysis patients and 33 per cent of the transplant recipients. Hyperuricaemia, cigarette smoking, obesity and a sedentary existence were also prevalent. The majority of patients had several risk factors implicated in the pathogenesis of arteriosclerosis. Occlusive arterial disease is a major problem in patients with end stage renal disease, being no less common after transplantation than with long-term maintenance dialysis. The aetiology is multifactorial.
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PMID:Occlusive arterial disease in uraemic and haemodialysis patients and renal transplant recipients. A study of the incidence of arterial disease and of the prevalence of risk factors implicated in the pathogenesis of arteriosclerosis. 32 93

To delineate the worth of chronic HF in end stage renal failure, since 1976 we have treated 9 patients with dialysis-resistant hypertension, 6 patients with dialysis intolerance, 7 patients with hypertriglyceridaemia and 7 patients with polyneuropathy. We found an improvement of polyneuropathy and volume-sodium dependent hypertension and symptoms of dialysis discomfort markedly diminished. No amelioration was detected in anaemia, hypertriglyceridaemia and volume-independent hypertension. Hyperphosphataemia was poorly controlled despite increased amounts of aluminium hydroxide. PTH values increased and renal osteopathy seemed to deteriorate.
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PMID:Haemofiltration - critical evaluation of clinical benefits. 54 84

Adrenal vein catheterizations were done in rats made hypertensive by administration of methylandrostenediol (MAD; 17alpha-methyl-5-androstene-3beta,-17beta-diol), and in control rats at intervals during treatment. All MAD-treated rats were hypertensive by 7 weeks. Secretion of corticosterone was consistently decreased at all times in MAD-treated rats. 18-Hydroxy-11-deoxycorticosterone secretion and 11-deoxycorticosterone (DOC) secretion decreased and increased, respectively, compared to controls at 2, 4, and 6 weeks. Aldosterone secretion was decreased at 2 and 4 weeks. This study shows an in vivo block of adrenal 11- and 18-hydroxylation. Transient DOC accumulation by treatment with MAD produced hypertension, though DOC oversecretion and other changes in steroidogenesis were waning by the time hypertension developed.
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PMID:Adrenal steroidogenesis in methylandrostenediol-induced hypertension. 74 61

Cooperation between the family physician and the kidney-center begins with the recognition of a renal disease and pre-dialysis treatment. Our patients usually are sent for the preparation of an arterio-venous shunt operation (Cimino or modifications) when serum creatinin levels amount to 8 to 10 mg/100 ml. Peripheral veins on both forearms should be reserved for these procedures early in the course of renal disease and vascular punctures should be avoided. Dialysis treatment is performed either at the kidney-center, at one of our partner-centers, at the central self-care facility operating under the care and supervision of the kidney-center or as home-dialysis-treatment. Each patients continues to receive technical and medical services of the center. Central self-care dialysis as well as home-dialysis are organized by the Kuratorium for Heimdialyse e.V. in this area. This organization also provides an on-cell-service of technicians. Nurses and physicians take regular rotations to staff the dialysis- and the self-care-units. The family physician takes care of the hemodialysis patinet in cooperation with the hospital. In case of medical problems the patient is transferred to the kidney-center. The patient must be well instructued on problems and complications which might occur during hemodialysis, either due to the basic disease or in connexion with hemodialysis. In some cases of complications patients must be admitted to the center without delay. Emergency situations usually can be avoided as technical standard of dialysis equipment and standard of training of patients or their parners is high. Medications, such as phosphate binders (aluminium hydroxide), iron vitamins and allopurinol are provided if necessary. Patients are advised to limit intake of fluids and potassium containing foods. The sodium intake depends on blood pressure-values. In case of hypertension there will be salt restriction, in case of hypotension the salt intake is increased. Chronic intermittent hemodialysis treatment can result in successful rehabilitation. Further improvement concerning personal and medical problems can only be expected from kidney transplantation.
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PMID:[Care of the hemodialysis patients by the family physician]. 84 54

A boy with functional abnormalities of the gastro-intestinal tract, hyponatraemia, hypokalaemia and hypertension is described. All symptoms developed within the first 2 months of life. Increased aldosterone levels were associated with suppressed values in the renin-angiotensin system. The diagnosis of idiopathic hyperaldosteronism was made because of adrenal hyperplasia and the failure to suppress aldosterone to undetectable levels with glucocorticoids. Treatment with spironolactone alone, or in combination with either intravenous dopamine or ibopamine orally, amiloride, enalapril, hydralazine or clonidine corrected serum potassium values but failed to normalize blood pressure and to correct plasma renin activity and plasma aldosterone. However, the combination of spironolactone with nifedipine decreased blood pressure. Abnormal gastro-intestinal motility was corrected by low doses of oral magnesium hydroxide. To assess intracellular calcium homeostasis, the patient's peripheral blood mononuclear cells were incubated with increasing concentrations of calcium. As these cells failed to maintain physiological calcium concentration, a defect in intracellular calcium homeostasis was suspected.
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PMID:A neonate with idiopathic hyperaldosteronism. 176 77

We have retrospectively examined 324 patients with chronic renal failure and evaluated the probable underlying causes of neurologic complications, laboratory data and therapeutic interventions. The common neurologic problems in our patients were alterations in consciousness (40.7%) and convulsions (35.1%). When BUN concentration was above 135 mg/dl and creatinine clearance was below 8 m/min/1.73 m2, alteration of consciousness was observed and when BUN concentration was 200 mg/dl and creatinine clearance was below 7 m/min/1.73 m2, abnormal convulsives appeared. Changes in deep tendon reflexes and pathologic reflexes were associated with hypertension. All of the patients with cortical atrophy using computerized cranial tomography aluminum hydroxide at least for 18 months, and six of them had hemodialysis. Fourteen patients who underwent dialysis developed convulsions and were thought to have disequilibrium syndrome. These findings are consistent with the suggestion that the metabolic and biochemical derangements associated with CRF may be particularly detrimental to the still developing CNS of the child.
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PMID:Neurologic complications in chronic renal failure: a retrospective study. 224 42

We examined the photodynamic effects of porphyrins, known photosensitizers, on proteins of cytosol and plasma that bind them and are implicated in their transport. Their susceptibility to photodecomposition by porphyrins was found to be higher than that of proteins with low or no affinity for tetrapyrroles. Inhibition of porphyrin binding by the addition of equimolar amounts of heme had no effect, indicating that protein photodecomposition may be induced, in part, by free or nonspecifically bound porphyrins. HBP, a heme-binding Z protein of liver cytosol, exhibited the highest susceptibility of all proteins tested, including glutathione S-transferases, albumin, hemopexin, and apotransferrin. HBP was extensively photo-oxidized, as evidenced by a decrease in its antigenicity and electrophoretic mobility, and it was cross-linked by naturally occurring porphyrins as well as by the synthetic tin-protoporphyrin and hematoporphyrin derivative. The water-soluble singlet oxygen scavengers L-histidine (50 mmol/L) and sodium azide (100 mmol/L) completely prevented the photodynamic effects of uroporphyrin (100 mumol/L) on HBP. Hydroxyl radical scavengers such as manitol and benzoate were partially effective, whereas water-insoluble singlet oxygen scavengers such as beta-carotene were totally ineffective. Preferential inhibition of cross-linking over other photodynamic effects of uroporphyrin was consistent with previous reports that cross-linking occurs subsequently to amino acid oxidation.
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PMID:Effects of porphyrins on proteins of cytosol and plasma. In vitro photo-oxidation and cross-linking of proteins by naturally occurring and synthetic porphyrins. 244 89

19-Nor-deoxycorticosterone (19-nor-DOC) is a mineralocorticoid present in both rat and human urine, and it is elevated in some forms of experimental and human hypertension. Although the exact steps in the biosynthesis of 19-nor-DOC are uncertain, it is probably produced from a 19-oxygenated derivative of DOC, which undergoes 19-desmolation in the kidney. Since DOC biosynthesis is partly due to renal 21-hydroxylation of progesterone (Prog), we sought to determine whether a parallel pathway could exist for the biosynthesis of 19-hydroxy-DOC, a precursor to 19-nor-DOC. In order to test this hypothesis, authentic 19-hydroxy-progesterone was incubated with homogenized renal tissues from either rat or human sources. Formation of 19-hydroxy-DOC was found to be the major metabolite in both rat and human incubations, as demonstrated by an HPLC retention time identical to authentic 19-hydroxy-DOC. 19-Hydroxy-DOC formation was further verified by GC/MS analysis with highly sensitive selected ion recording. Since it has been demonstrated that the placenta can convert progesterone to 19-hydroxy-progesterone, the renal 21-hydroxylation of 19-hydroxy-progesterone to 19-hydroxy-DOC could be an alternate pathway of 19-nor-DOC production especially during pregnancy.
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PMID:Renal 21-hydroxylation of 19-hydroxy-progesterone to 19-hydroxy-deoxycorticosterone. 260 34


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