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

Two cases of scleroderma are presented in which malignant hypertension developed abruptly, accompanied by rapidly progressive renal failure. The malignant hypertension was associated with high plasma renin levels and like other forms of hyperrenninemic hypertension and uremia, was refractory to both antihypertensive medication and extracellular fluid volume control with hemodialysis. Blood pressures became controllable only after bilateral nephrectomy was performed, and in each case resulted in a reversal of a rapidly progressive downhill course. Though both patients had multisystem involvement at the onset of renal failure, the non-renal manifestations of scleroderma have not progressed rapidly. Consequently, when patients with scleroderma develop malignant hypertension and uremia, aggressive therapy with dialysis and nephrectomy may significantly prolong survival.
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PMID:Malignant hypertension and uremia in scleroderma: efficacy of nephrectomy and hemodialysis. 88 14

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.
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PMID:Nephronophthisis. Renal function and histologic studies in a family. 88 91

In 46 patients of the chronic hemodialysis program blood pressure regulation was studied according to variations of sodium and fluid balance. A strong relationship was observed between blood pressure and the amount of exchangeable sodium. In the hypertensive patients exchangeable sodium was increased depite fulfilled clinical signs of sufficient dehydration. The blood volume was found to be small and the plasma renin activity increased in those hypertensive patients, in which sufficient fluid depletion was inhibited by extreme fluctuations of the blood pressure during dialysis. A diminution of the sodium concentration keeping the fluid balance constant induced an increase of blood pressure and deteriorated the subjective feeling of the patients. By an increase of the sodium concentration up to 155 mEq/l severe blood pressure fluctuations during during dialysis could be prevented, although further fluid was taken off by ultrafiltration. This effect seemed to be mediated--at least partly--by an increase of the low blood volume and a suppression of plasma renin activity. After the patients became normotensive, dialysis procedure could be continued with normal sodium concentration. By a temporary high sodium regimen of the dialysis procedure some patients with renal failure and 'uncontrollable hypertension' can be preserved from bilateral nephrectomy.
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PMID:Role of sodium and water in hypertensive patients on maintenance hemodialysis. 89 Dec 7

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.
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PMID:[Dr. Atkins' dietetic revolution: a critique]. 89 45

We describe here a family with hemolytic-uremic syndrome culminating in renal failure and severe hypertension in the involved male adults. Members of this family developed a microangiopathic hemolytic anemia, progressive renal failure, the onset of elevation of blood pressure, and an untimely death in young adulthood. One affected family member has survived the initial crisis. The family history presents further evidence for an autosomal dominant pattern of inheritance of hemolytic-uremic syndrome with presentation in adulthood.
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PMID:Adult hemolytic-uremic syndrome. Familial variant. 90 Oct 83

An early diastolic murmur thought to indicate functional aortic regurgitation was heard in 7 of 74 consecutive patients with end-stage renal failure assessed for chronic intermittent haemodialysis and transplantation. In all 7 cases the murmur was transient and related to episodes of hypertension and fluid overload and disappeared on correction of these factors. In a further 2 patients aortic regurgitation resulted from a structural abnormality of the aortic valve. Thus, an early diastolic murmur is not uncommon in this situation and does not necessarily indicate organic aortic valve disease which might preclude selection for haemodialysis and transplantation.
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PMID:Early diastolic murmurs in end-stage renal failure. 90 86

A six year-old girl presented with acute oliguric renal failure, secondary to acute, non-obstructive pyelonephritis. Evidence for pyelonephritis as the cause of renal failure included: the evolution of typical changes on serial intravenous pyelograms, an acute interstitial inflammatory exudate on percutaneous renal biopsy, and gram-positive cocci on gram stain of the biopsy tissue. Although a specific causative organism was not conclusively identified, enterococcus was isolated from the initial catheterized urine specimen. The patient recovered from the acute illness but was left with impaired renal function, hypertension, and cortical scarring. Acute, non-obstructive pyelonephritis can produce acute renal failure in children and must be considered in the differential diagnosis of this syndrome.
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PMID:Acute renal failure secondary to acute pyelonephritis. 91 54

The pathologic lesions of the kidney in scleroderma in many respects resemble those of malignant hypertension, perhaps even in the absence of comparable blood pressure elevation. Because the malignant vascular changes have been related to hyperreninemia, we measured plasma renin activity in 23 patients with scleroderma with or without hypertension and/or renal failure. We found that high renin levels in most cases shortly preceded or coincided with a phase of sudden deterioration of the disease, characterized by a rapidly progressive renal failure. The outcome of this phase was invariably fatal, except for two patients in whom bilateral nephrectomy successfully arrested the rapid downhill course. These findings suggest that an unexplained increase in circulating renin levels in an otherwise stable patient with scleroderma may be taken as a possible marker of imminent deterioration requiring close monitoring and immediate therapeutic intervention.
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PMID:Is elevated plasma renin activity of prognostic importance in progressive systemic sclerosis? 92 42

Hypertensive patients with various renal lesions and a mean plasma creatinine of 2mg/100ml showed increases (p is less than 0.05) in mean exchangeable sodium and plasma renin activity, while blood volume was not altered significantly. Patients with mild renal failure and normal blood pressure demonstrated no consistent abnormalities in these parameters. Blood pressure correlated significantly with exchangeable sodium and with the 'sodium-renin' and 'blood volume-renin' products; but not with circulating renin or volume individually. This suggests that subtle abnormalities in the physiological sodium/volume-renin feedback mechanism may occur already in the earliest stages of renal disease and may contribute to the hypertension in such patients.
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PMID:Blood pressure, circulating renin and the body sodium/volume state in patients with mild renal failure. 93 20

Patients with chronic glomerulonephritis and mild hypertension show a consistent behaviour in their renin-aldosterone-system. There is a close correlation between the elevation of mean blood pressure and destruction of glomeruli. No correlation has been found between renin values and the degree of hypertension. Thus the cuase of mild hypertension occurring in the early stages of chronic GN remains to be elucidated. Normal PRA values in spite of hypertension and expansion of ECFV accompaning progression of chronic glomerulonephritis could be a sign of "relative hyperreninemia". Apparently various mechanisms are involved in the pathogenesis of renal hypertension. These include sodium retention, increased cardiac output. anemia, renin, aldosterone, prostaglandins, expanded plasma volume and peripheral vasoconstriction. These factors are more or less active in the different stages of hypertension and renal failure.
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PMID:Plasma renin activity (PRA) and aldosterone (PA) in patients with chronic glomerulonephritis (GN) and hypertension. 94 54


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