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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

Lipid and carbohydrate metabolism variables were studied in twenty-eight patients with chronic renal failure (mean GFR 7.7 +/- 2.5 ml/min) and uraemic symptoms. 71% of the patients had hypertriglyceridaemia (greater than or equal to 2.2 mmol/l). Total serum cholesterol was normal while VLDL cholesterol was high and alpha-lipoprotein cholesterol was low. The fractional elimination rate of Intralipid was low and inversely correlated to serum triglyceride levels. Intravenous glucose tolerance was reduced with normal or slightly increased fasting blood glucose and insulin values before and during the test. Serum triglycerides were correlated to plasma insulin but not to residual renal function or serum urea levels. The cause of hypertriglyceridaemia and lowering of alpha-Lp cholesterol is not unequivocally clear. Present evidence indicate that retarded catabloism of triglyceride-rich lipoproteins is important but accentuated release of triglyceride-rich lipoproteins may have occurred in a number of cases. The commonly used treatment with beta-blocking agents for hypertension in chronic renal failure may accentuate certain of the metabolic responses in uraemia.
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PMID:Lipid and carbohydrate metabolism in uraemia. 23 60

It has been suggested that intrarenal levels of angiotensin II may preferentially control efferent arteriolar resistance or may influence the glomerular filtration coefficient (Kf). To examine these possibilities, micropuncture and clearance experiments were performed on nine anesthetized dogs evaluating renal and glomerular hemodynamics before and during the administration of an angiotensin converting enzyme inhibitor (SQ20,881). During the micropuncture measurements, renal arterial pressure was reduced to range of 85 to 90 mm Hg in order to maximize renin secretion and intrarenal formation of angiotensin II. Also, this procedure minimizes potential errors in the determination of single nephron glomerular filtration rate (SNGFR) and of glomerular pressure when estimated by techniques that require complete blockade of proximal tubule fluid flow. During the administration of SQ20,881, a converting enzyme inhibitor (CEI), renal blood flow increased significantly by 13%, but GFR was not altered. There were no significant alterations in SNGFR, proximal tubule pressure, peritubular capillary pressure or estimated glomerular pressure. By using the micropressure measurements in combination with the whole kidney hemodynamic data, it was estimated that afferent resistance was reduced 23%. Although significant decreases in efferent resistance could not be documented, there was a tendency for this variable to decrease also. Neither Kf nor effective filtration pressure were altered significantly by CEI. These results do not support the contention that intrarenal effects of angiotensin II are exerted predominantly on the efferent arteriolar resistance segments; rather, they suggest that angiotensin may exert a modest tonic effect on both pre- and postglomerular resistance elements in the anesthetized hydropenic dog.
Hypertension
PMID:Glomerular and renal hemodynamics during converting enzyme inhibition (SQ20,881) in the dog. 39 40

Morphometrical investigations (point-counting method) showed that in different inflammatory (endocapillary -- acute -- GN, mesangioproliferative GN, membranoproliferative GN) glomerulonephritides and in non-inflammatory glomerular diseases (perireticular amyloidosis), there are statistically significant correlation between serum creatine concentrations at the time of biopsy and the enlargement of the cortical interstitium by fibrosis. Similar results were obtained in investigating different grades of benign nephrosclerosis with transition into secondary malignant nephrosclerosis conditioned by hypertension and in chronic diffuse sclerosing interstitial nephritides of different etiologies. As hypothesis, we assume that a narrowing of the postglomerular vessel network by interstitial fibrosis take place. This could lead to an increase resistance of the renal cortical blood flow. In spite of an elevated effective filtration pressure, the slowing of the glomerular blood flow may lead to the reduction of GRF and to an increase of the serum creatinine concentration. Additionally, in the case of interstitial fibrosis the tubules look atrophied. This could be the consequence of the reduced GFR as a sign of inactivity. On the other hand, tubular atrophy could result from malnutrition in the case of interstitial fibrosis. The resorptive capacity of these atrophied-looking tubules could be lowered and the GFR could be diminished by the so-called Thurau mechanism.
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PMID:The role of the interstitium of the renal cortex in renal disease. 46 60

Severe segmental renal atrophy with loss of parenchymal elements in small kidneys is commonly known as segmental hypoplasia. The scars are seen as cortical depressions overlying shrunken medullary pyramids and their dilated calyces, and are characterized histologically by colloid-filled tubular microcysts and a paucity or absence of glomeruli. This lesion has been identified in 17 patients, 11 female and 6 male, between 6 and 23 years of age. Eleven patients had hypertension, which developed in six while they were under observation. Thirteen had histories of urinary tract infection, and 16 had evidence of vesicoureteric reflux. Seven patients had impaired renal function (GFR less than 40 ml/minute/1.73 m2). Abnormal metanephric differentiation (dysplasia) in two specimens, one in association with posterior urethral valves, suggested an occasional intrauterine origin of the abnormality. Twelve patients had radiographic evidence of decreasing renal size over two to five years of observation, even after surgical correction of reflux, in four of them unaccompanied by infection. We conclude that segmental "hypoplasia" is an acquired lesion, although it sometimes has intrauterine origins, and that it is commonly associated with vesicoureteric reflux, even in the absence of demonstrable infection.
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PMID:Segmental "hypoplasia" of the kidney (Ask-Upmark). 50 98

Forty-three patients suffering from hypertension of different origin (chronic renal failure, gout, or idiopathic) were treated with propranolol (121 +/- 12 mg q.d.) plus hydrochlorothiazide (50 mg q.d.) for 75 +/- 9 days. Blood pressure did not return to normal limits in 15 patients, who were continued on the same protocol plus 10 to 50 mg oxdralazine q.d. After an average of 68 +/- 35 days blood pressure fell from 180/110 mm Hg to 145/90 mm Hg without orthostatism, significant side effects, or changes in GFR. This combination seems particularly successful since propranolol will prevent the undesired rise in cardiac output due to oxdralazine as well as the activation of the renin-angiotensin axis due to diuretics. Thus, the antihypertensive properties of each agent will be enhanced by a reduction in side effects by the associated drug, resulting in optimal blood pressure control.
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PMID:Oxdralazine, a new peripheral vasodilator, combined with propranolol and hydrochlorothiazide: a rational approach to antihypertensive treatment. 53 72

The spontaneous changes in renal plasma flow (RPF) were determined by sodium paraamino hippurate clearance (CPAH) in the individual kidneys of 71 patients with essential and secondary hypertension. These changes were expressed as changes in CPAH and as changes in CPAH per 100 ml Glomerular Filtration Rate (GFR = inulin clearance) for every individual kidney. Sixteen normal subjects were used as control. The RPF changes were measured between two consecutive 10 minute clearance periods during separated kidney function tests. In all the hypertensive groups studied, when RPF variability was expressed per 100 ml GFR, the variability was found to be two to five times greater than in normals. This findings suggests that in the hypertensive state the blood flow changes in the kidney are more labile than in normals. The high lability of renal blood flow could reflect and abnormality in renal vascular tone. This abnormality could be an important factor in the pathogenesis and maintenance of high blood pressure.
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PMID:High renal plasma flow lability in the kidneys of hypertensive patients. 68 55

32 patients with different histologically proven forms of glomerulonephritis were treated with heparin for an average of 31 days. A dosage of heparin was chosen, which allowed an increase in thrombin time to 20-40 seconds. Histological findings alone do not allow any prediction concerning the therapeutic success of heparin treatment in glomerulonephritis. According to our results and comparable information given in the literature, the following therapeutic scheme can be recommended: Best results are seen in patients with a slow decrease of GFR (i.e. less than 30 ml/min) during the year preceding the beginning of the treatment. In rapid progredient glomerulonephritis, however, as in patients without any changes of GFR during this time, predictions as to the course of illness cannot be made. A high level of fibrin split products in serum may be expected to be the most valuable sign of therapeutic effect, as could be documented in 7 out of 8 successfully treated patients. Hypertension and proteinuria were not influenced by the treatment. Because of severe side effects the heparin treatment of glomerulonephritis should not be initiated in patients with severe hypertension.
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PMID:[Treatment of glomerulonephritis with heparin (author's transl)]. 87 75

Hypervolemia with hypertension often occurs 36-72 hours following massive blood and fluid replacement for hypovolemic shock. This syndrome of "fluid overload" has been attributed to the rapid intravascular flux of previously sequestered fluid in patients with impaired diuresis. This hypothesis was tested in 35 injured patients who received a mean of 9.3 L of blood and 17.4 L of salt during resucitation. The renal parameters measured soon after resuscitation included: 1) renal clearance of inulin (GFR), para-amino hippurate (ERPF), milliosmoles, sodium, and free water; 2) inulin space, renal vascular resistance (RVR), O2 consumption, renin, renal blood flow (RBF), and response to furosemide. Eighteen patients developed hypertension, hypervolemia, and respiratory insufficiency. When compared to the 17 normovolemic, non-hypertensive patients, the 18 hypervolemic patients had significantly increased RVR, with a significant decrease in RBF despite an increase in plasma volume and cardiac output. Furosemide produced less diuresis and natriuresis in the hypertensive patients. The balance between hypovolemia and "fluid overload" seemed percarious in the hypertensive patients. Peripheral renin and catecholamine levels were normal in both groups. Patients with post-traumatic "fluid overload" appear to have a combination of hypervolemia, respiratory insufficiency, hypertension, increased cardiac output, decreased extracellular fluid space, and decreased renal perfusion. These findings suggest that decreased interstitial fluid space compliance rather than "fluid overload" is the underlying factor leading to respiratory insufficiency. The therapeutic aspects of these findings are discussed.
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PMID:The renal factor in the post-traumatic "fluid overload" syndrome. 89 57

Clinical states with portal venous hypertension are frequently associated with impairment in renal hemodynamics and water excretion, as well as increased renin secretion. In the present investigation, portal venous pressure (PVP) was increased in anesthetized dogs undergoing a water diuresis. Renal arterial pressure was maintained constant in all studies. As PVP was increased from 6 to 20 mm Hg, decreases in cardiac output (2.5-2.0 liter/min, P less than 0.05) and mean arterial pressure (140-131 mm Hg, P less than 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P less than 0.001), renal blood flow (RBF, 276-193 ml/min, P less than 0.001), and increases in renin secretion (232-939 U/min, P less than 0.025) in innervated kidneys. No significant change in either GFR or RBF and a decrease in renin secretion occurred with increases in PVP in denervated kidneys. To dissociate the changes in cardiac output and mean arterial pressure induced by increase PVP from the observed decreases in GFR and RBF, studies were performed on animals undergoing constriction of the thoracic inferior vena cava. In these studies, similar decreases in cardiac output and mean arterial pressure were not associated with significant changes in GFR or RBF. Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H2O (P less than 0.001). This antidiuresis was significantly blunted but not abolished by acute hypophysectomy. In hypophysectomized animals, changes in free water clearance and urine flow were linearly correlated as PVP was increased. These studies indicate that increases in PVP result in decreases in GFR and RBF and increases in renin secretion mediated by increased renal adrenergic tone. Increased PVP is also associated with antidiuresis; this antidiuresis is mediated both by vasopressin release and by diminished tubular fluid delivery to the distal nephron.
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PMID:Mechanisms of portal hypertension-induced alterations in renal hemodynamics, renal water excretion, and renin secretion. 96 99


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