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)

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

The theoretical background for a conservative therapeutic treatment of uremia is described, with illustrative results from preliminary clinical trials in 10 patients and 10 normal reference subjects. The proposed treatment focuses upon the patient's gastrointestinal tract--the normal site for metabolism of both exogenous (dietary) and endogenous (recycled) protein--enabling it to behave like the rumen of the cow. The objective is to induce the uremic's organism to utilize its own "waste" substances. The patient swallows enterosoluble capsules containing specifically adapted enzymes (immobilized or free) from apathogenic soil microorganisms. These are pre-adapted to convert urea, creatinine, uric acid, guanidino derivatives, and other nonprotein nitrogen compounds (NPN). The enzymes utilize many other substances, in particular ammonia, potassium, phosphorus, and several other factors potentially dangerous for the uremic. The enzymes apparently cleave vasoconstrictatory peptides in the intestines. In the course of the therapy, renoparenchymal hypertension decreased significantly, and increased again when the regimen was interrupted. The results from the present studies are in full accord with the information published in the relevant fields. The time appears ripe for large-scale trials of the therapeutic regimen outlined, especially as many commercial microbial enzymes already have a long history of safe use in food processing.
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PMID:Bacterial enzymes in uremia management. 27 91

Progressive uremia is the hallmark of many renal diseases, some reversible. The signs and symptoms tend to parallel the declining glomerular filtration rate. With an understanding of the usual progression, the physician is equipped to plan therapy. Hypertension must be treated. Phosphorus binding, protein limitation and fluid and electrolyte control can be started at appropriate times and managed fairly easily. There are several cycles of deterioration that can be reversed if recognized promptly.
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PMID:The management of uremia. 33 23

1. Total-body neutron-activation analysis in vivo was carried out in 11 hypertensive subjects to measure simultaneously the total body content of sodium, chlorine, calcium, phosphorus and nitrogen. 2. There was a highly significant correlation between total body sodium measured by activation analysis and total exchangeable sodium measured by a standard isotope-dilution technique (r = 0.92, P less than 0.001). Exchangeable sodium averaged 80.3% of total body sodium. 3. The measured values of chlorine, calcium, phosphorus and nitrogen were similar to those for healthy subjects reported by others. 4. Activation analysis in vivo appears promising as an additional tool for investigating sodium metabolism in hypertension, as it is the only method available for determining the total body content of this element. The radiation dose (1 rem) is sufficiently low to permit repeated measurements in the same subject.
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PMID:Concurrent estimation of total body and exchangeable body sodium in hypertension. 41 89

Analysis of data of 10 practically healthy subjects and 43 patients with hypertensive disease has indicated that there are circadian rhythms of urine volume and excretion of calcium, potassium, sodium, magnesium and phosphorus in healthy subjects. In the earlier stages of hypertensive disease significant rhythms of sodium and magnesium excretion are not revealed. However, in patients in the IIA stage of hypertension, circadian rhythms of sodium and magnesium excretion are significant. Such a phenomenon shows that the regulation of sodium and magnesium rhythmostasis has been reestablished. But in the later stages of hypertensive disease breakdown of compensatory mechanisms and dysrhythmostasis are again observed, which are expressed by absence of significant rhythms of cations and urine excretion in patients in the IIB and IIIA stages of hypertensive disease.
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PMID:Circadian rhythms of electrolyte excretion in hypertensive patients and healthy subjects. 72 Jan 73

A strain of genetically selected White Carneau pigeons (WC-2) with increased atherosclerosis at similar plasma cholesterol concentrations as randomly bred (RBWC) pigeons was studied to evaluate the commonly known risk factors for atherosclerosis. Indicators for the presence of hypertension, diabetes mellitus, "stress", hyperuricemia and hypothyroidism were determined. In pigeons fed the atherogenic diet, major differences in atherosclerosis were seen between WC-2 and RBWC. WC-2 pigeons had more aortic surface covered with plaque and greater concentrations of aortic nonesterified cholesterol, esterified cholesterol, uronic acid, and hydroxyproline, as well as a greater prevalence and severity of coronary artery atherosclerosis. For WC-2 and RBWC pigeons we found similar levels of hypercholesterolemia, mean blood pressure, plasma triglyceride and glucose concentrations. In addition, several other physiological variables such as plasma uric acid, calcium and phosphorus concentrations, adrenal and thyroid weights which have been implicated in the pathogenesis of atherosclerosis were similar. The findings indicate that the differences in extent and severity of atherosclerosis between WC-2 and RBWC cannot be explained by differences in the risk factors studied. Possible genetic regulation of atherosclerosis by mechanisms operable in the arterial wall of WC-2 pigeons is suggested.
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PMID:Risk factors in pigeons genetically selected for increased atherosclerosis susceptibility. 72 42

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

Eight normotensive white middle-aged men were given low, moderate, and high salt diets with constant potassium intakes each for periods of at least 4 weeks. There was a tendency for body weight, serum sodium, exchangeable sodium, and inulin space to increase. Indirect blood pressure measurements revealed no change in blood pressure, either supine or upright measurements, during the 3 study intervals. Inulin clearance (and presumably glomerular filtration rate) rose with increase in dietary salt. Urinary potassium excretion rose progressively as salt intake increased. Total body potassium tended to decrease with increase in dietary salt. There was no changes in the excretion of calcium, magnesium, phosphorus, nor were there changes in the blood level of potassium. There was no change in total body water. The serum cholesterol and triglyceride levels were not appreciably affected by the different dietary sodium intakes. Plasma renin activity and urinary aldosterone excretion rose progressively with the two levels of sodium restriction. These studies indicate that normal man is able to compensate for large differences in sodium intake with minor metabolic changes. These changes do not necessarily lead to hypertension over a one-month period. Nevertheless, many hemodynamic and hormonal compensatory mechanisms come into play. It is evident that hypertension might result should the sodium load not be excreted, the circulating volume become too great for the excretory capacity, or if neural or endocrine adjustments be inadequate.
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PMID:The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man. 124 73

Although there is impressive documentation linking severe hypertension to renal insufficiency, corresponding data for mild-to-moderate hypertension are only now starting to emerge. As a result, it is only now becoming evident that a much larger portion of the hypertensive population could be susceptible to drug accumulation owing to renal insufficiency. Angiotensin-converting enzyme (ACE) inhibitor therapy routinely requires dosage adjustment in the instance of renal insufficiency, as all currently marketed ACE inhibitors are renally eliminated. Such dosage adjustments are usually considered a way to minimize side effects and to limit the duration of any induced hypotension. Dosage adjustment is usually considered at creatinine clearance levels between 30 and 60 ml/min. This is somewhat problematic, as physicians generally rely on serum creatinine determinations to assess renal function, and serum creatinine values are notoriously poor predictors of actual creatinine clearance. This is particularly true in the elderly population, where a greater disparity between the serum creatinine and creatinine clearance commonly exists, with moderate renal insufficiency frequently going unrecognized. Thus, the development of other ACE inhibitors eliminated via renal/hepatic routes may prove to be advantageous in that dosage adjustments might not be required in the setting of declining renal function, whether age-related or not. Fosinopril, a new phosphorus-containing ACE inhibitor, is administered as a prodrug and is hydrolyzed to the pharmacologically active diacid, fosinoprilat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of angiotensin-converting enzyme inhibitors in renal failure. 128 26

Fosinopril, the first agent in a new chemical class of phosphorus-containing angiotensin-converting enzyme (ACE) inhibitors, has unique pharmacologic properties. Fosinopril administration leads to complete inhibition of plasma ACE activity for 12-24 h. In patients with normal renal function, approximately equal amounts of the drug are eliminated via the hepatic and renal routes. With worsening renal function, increasing amounts of fosinopril are eliminated hepatically. This dual elimination allows for the administration of fosinopril using the same starting dosage to any patient, regardless of renal function. Fosinopril may provide end-organ protection against the effects of hypertension and antihypertensive therapy; this drug potentially protects the kidney by increasing renal functional reserve, while maintaining cardiac left ventricular performance. Moreover, despite marked blood reductions, cerebral blood flow is maintained. Controlled trials show that fosinopril in single daily doses of 10-40 mg is efficacious and safe for the long-term treatment of hypertension. At these doses, favorable responses were seen in up to 80% of patients. Fosinopril is equally effective in elderly as well as younger patients and works in black as well as in nonblack patients. The incidence of adverse events does not differ significantly between fosinopril- and placebo-treated patients. Fosinopril represents a clinically useful agent for the treatment of hypertension.
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PMID:Fosinopril: a new generation of angiotensin-converting enzyme inhibitors. 128 29


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