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

Acute renal failure, severe hypertension, and some complications of the nephrotic syndrome and chronic renal failure are the renal emergencies most frequently seen in the pediatric age group. Diagnosis of acute renal failure is based mainly upon U/P ratios of osmolality and urea as well as a negative mannitol test. Conservative medical management is useful in uncomplicated cases, whereas dialytic procedures are more effective in severe or complicated cases. The most frequent reversible complications in chronic renal failure are infections, extracellular volume changes, electrolyte imbalance and cardiovascular alterations. Intercurrent infection and vein thromboses are the most frequent complication in minimal change nephrotic syndrome and they may be a cause of death. Early diagnosis and adequate treatment are mandatory in these complications.
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PMID:Renal emergencies in children. 72 76

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
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PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

Aspirin has been shown to acutely block the natriuretic effect of spironolactone in the mineralocorticoid-treated normal rat, dog, and man. It has been suggested that aspirin is contraindicated in hypertensive patients receiving spironolactone. Five patients with low-renin essential hypertension and two with hypertension due to primary aldosteronism, all of whom have normalized their blood pressure on chronic spironolactone therapy, were cotreated in a double-blind fashion with either aspirin or aspirin-placebo during alternate six-week periods. Aspirin did not appear to alter the effect of spironolactone on blood pressure, serum electrolytes, urea nitrogen, or plasma renin activity.
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PMID:Failure of aspirin to antagonize the antihypertensive effect of spironolactone in low-renin hypertension. 78 8

Prazosin was used in combination with other antihypertensive drugs in the successful management of hypertension in seven patients with chronic renal failure and six renal transplant recipients, also with chronic renal failure. The addition of small doses of prazosin (mean 3 mg/day) to the antihypertensive regimen produced significant falls in systolic and diastolic blood pressures in both the lying and standing positions. The standing blood pressures were significantly lower than the lying blood pressures during prazosin treatment. Neither the mean blood urea concentrations nor the mean plasma creatinine concentrations changed significantly during prazosin administration. Chromium-51 edetic acid clearances did not change significantly during prazosin treatment in the seven patients in whom it was measured. Severe symptomatic postural hypotension occurred in one patient a week after starting prazosin 3 mg/day. This hypotensive episode was associated with a transient and reversible deterioration in renal function. Another patient developed a rash while on prazosin but it was probably related to propranolol rather than prazosin. Prazosin is thus an effective antihypertensive drug in patients with chronic renal failure, and it may be used with a variety of other drugs. It should be used cautiously, however, since patients with chronic renal failure may respond to small doses, and significant postural falls in blood pressure may result. There was no evidence that the use of prazosin resulted in progressive deterioration in the residual renal function of the patients with chronic renal failure.
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PMID:Use of prazosin in management of hypertension in patients with chronic renal failure and in renal transplant recipients. 81 12

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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PMID:Pathogenesis of the glomerulopathy associated with renal infarction in rats. 94 Feb 76

Twenty-six patients with radiological unilateral chronic pyelonephritis, 36 patients with bilateral chronic pyelonephritis, 14 patients with papillary necrosis and nine patients with obstructive atrophy have been followed from five to 135 months for a total of 374 patient years. Serial changes in renal function and pyelographic appearances have been correlated with bacteriuria, analgesic ingestion, blood pressure and reflux. The calculated survival rate at five years was 95 per cent for patients with bilateral pyelonephritis and 92 per cent for patients with papillary necrosis. The ten-year survival rate was 86 per cent and 56 per cent respectively. The survival rate for patients with unilateral pyelonephritis and obstructive atrophy was 100 per cent at five and ten years. Bacteriuria was not associated with deteriorating renal function determined by serial plasma creatinine estimations. Although all patients in whom there was some radiographic change had bacteriuria on later review, other factors, including excess analgesic intake, reflux and stones were recognized in most. There was a high incidence of analgesic ingestion among patients whose renal function declined and in whom there was some change in serial radiographs. The prevalence of hypertension among patients with normal renal function was 12 and 28 per cent for patients with unilateral pyelonephritis and bilateral pyelonephritis respectively. There was a significant increase in both blood urea and plasma creatinine in all patients with hypertension (diastolic pressure greater than 90 mm Hg) and a much higher prevalence of hypertension in patients whose plasma creatinine exceeded 1.3 mg/100 ml. Thrity per cent of patients with unilateral pyelonephritis and 50 per cent with bilateral pyelonephritis had vesicoureteric reflux of varying degrees. There was no evidence to suggest that major degrees of reflux (grade 3) was associated with further renal damage. These observations indicate the benign course of the majority of patients with radiological pyelonephritis. Control of blood pressure, and analgesic intake will help to preserve renal function whilst prevention of symptomatic urinary infection by long term low dose therapy will reduce morbidity.
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PMID:A prospective study of patients with radiological pyelonephritis, papillary necrosis and obstructive atrophy. 94 Sep 21

In five patients with chronic renal failure, rapid correction by dialysis of hypertension and/or high blood urea levels provoked acute neurological disorders, followed by slowly reversible neuropsychiatric disturbances. Focal EEG alterations were noted in three patients with normal carotid angiograms. Our cases differed from those usually described as suffering from the dialysis disequilibrium syndrome because of their duration, the severity of mental disturbances, and the asymmetrical pattern of EEG abnormalities. We propose that the symptoms observed could be due to cerebral ischemia. This possibility emphasizes the importance of limiting the duration and efficiency of the first dialyses in patients with severe hypertension and high nitrogen retention, especially if high performance dialyzers are used.
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PMID:Unusual aspects of the dialysis disequilibrium syndrome. 95 37

The annual increase in plasma urea was measured in 253 hypertensive patients. On average there was a significant increase in plasma urea with time which did not depend on the sex of the patient or the type of hypertension. It did, however, depend on the initial level of plasma urea. A table giving the upper limits for expected annual increment may prove useful in clinical assessment. The relation between plasma urea and presenting blood pressure and age was examined in 1217 patients seen at the Hammersmith Hospital hypertension clinic from 1952 to 1967. The plasma urea was significantly related to both age and diastolic and systolic blood pressure. It was higher in men than in women up to 60 years of age, but not above that age, and it increased with presenting mean blood pressure in both sexes, but the increase was greater in men. There was a quadratic relation between age and plasma urea in both men and women. In both sexes the plasma urea increased between the ages of 60 and 80.
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PMID:Plasma urea in hypertensive patients. 97 92

While hemodialysis therapy in its present form is capable of sustaining life, dialysis patients are not metabolically normal and we are unable to say what technical factors contribute adequate therapy. Recent efforts to resolve these problems have led to the assumption that substances in the molecular weight range of 800 to 3000 daltons may be pathogenic in uremia and these may not be effectively removed by dialysis. Accordingly, four groups of patients (ten each) underwent changes in their routine which were theoretically designed to alter independently the concentration of small (urea) and "middle" molecules in the blood. In two groups, the concentration of urea was theoretically increased or decreased while the concentration of so-called middle molecules was maintained unchanged. In the remaining two groups, middle molecule concentration was theoretically increased or decreased while small molecule concentration was unchanged. Patients were evaluated prior to and after completing altered dialysis therapy. The results suggest three related conclusions. First, the uremic syndrome may be viewed as a constellation of abnormalities which can be subgrouped by association so that azotemia may be correlated with neuropathic disease and hypertension with weight gain or body size, for example. Second, those physiologic variables which changed after altered dialysis tended to deteriorate with increasing concentration of small molecules in the blood and remained independent of theoretical changes in middle molecules. Finally, when patients are relatively under-dialyzed, they may spontaneously modulate the reduced removal of metabolites such as urea by decreasing the dietary intake of nutrients.
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PMID:Factors in the dialysis regimen which contribute to alterations in the abnormalities of uremia. 100 30


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