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

Plasma and urinary catecholamines (norepinephrine and epinephrine) and urinary dopamine excretion were studied in 45 essential hypertensive patients subdivided into borderline (labile) and stable hypertension. Borderline hypertensive patients had a higher mean fractional renal clearance of catecholamines (the clearance of catecholamines relative to creatinine clearance) than both control subjects and stable hypertensive patients. A significantly positive correlation between the renal clearance of catecholamines and urinary dopamine excretion was also found in those with borderline hypertension, but not in control subjects or those with stable hypertension. These data indicate that patients with borderline hypertension have a relatively exaggerated renal catecholamine release. They probably reflect an increased sympathetic discharge to the kidney in "borderline" hypertension, occuring to a lesser degree in stable hypertension and control subjects. Thus, urinary catecholamine measurements do not specifically reflect the level of circulating catecholamines, particularly in borderline hypertension.
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PMID:An increase in urinary catecholamines of renal origin in patients with "borderline" hypertension. 101 11

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

1. A group of patients with essential hypertension was divided into three categories on the basis of the plasma renin activity. 2. There was no correlation between the plasma renin activity categorized as high, normal or low and the duration of hypertension, the incidence of left ventricular enlargement, the blood urea nitrogen, serum creatinine, cholesterol or uric acid respectively. 3. Analysis of data showed that the incidence of cardiovascular events in the hypertensive population correlated with the plasma renin activity only in combination with known risk factors.
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PMID:Plasma renin activity and cardiovascular disease. 107 64

Available clinical evidence indicates a high prevalence of hyperuricemia in patients with essential hypertension; this becomes accentuated with diuretic therapy. Since there is an association of hyperlipidemia with hyperuricuria and hypertension and since hyperuricemia is a feature of diuretic therapy, we explored whether these relationships might be provoked by prolonged diuretic therapy. Eighteen male patients with uncomplicated essential hypertension of mild severity were treated for 9 months with hydrochlorothiazide and supplemental potassium chloride, 100 mg and 45 mEq/day, respectively. Arterial pressure, renal function, and serum electrolyte, uric acid, blood glucose, and lipid concentrations were measured several times before and during therapy. Arterial pressure remained significantly reduced during therapy (P less than 0.001); this was associated with reduced serum potassium (P less than 0.01) and increased blood glucose and serum uric acid concentrations (P less than 0.005, P less than .025, respectively). Blood urea nitrogen, serum creatinine, sodium, cholesterol and triglyceride levels did not significantly change with treatment. Thus, although diuretics increase serum uric acid and blood glucose, their effect on serum lipid concentration is negligible.
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PMID:Effects of diuretics on lipid metabolism in patients with essential hypertension. 107 5

Although many investigators have felt that humoral antibody was responsible for chronic rejection, attempts to detect it in the sera of recipients in the presence of functioning renal allografts have been largely unsuccessful. A modification of the mixed antiglobulin reaction has increased its sensitivity so that the development of low titers of immunoglobulin (IgG) antibody antibody specific for donor kidney cells can be detected in renal allograft recipients while renal function is still good. Donor-specific antibody was detected in the sera of 11 of 13 patients whose transplants had ceased to function from 5 to 43 months after transplantation. In five recipients the antibody was present prior to as well as after transplantation and in six recipients antibody developed after transplantation from 3 to 25 months prior to the cessation of function. In the patients with antibody, chronic rejection was characterized by hypertension which required treatment with multiple drugs, by proteinuria of greater than one gram per day, by a gradual, progressively rising serum creatinine, and by an absence of acute ologuric rejection episodes. Pathologically there was extensive intimal proliferation and occlusion of the intrarenal arteris. There also was significant glomerulonephritis which consisted of thickening of the basement membranes, mesangial cell proliferation, simplification of the capillary loops, and in some patients fibroepithelial crescent formation. These findings suggest that IgG antibodies directed against cell-surface antigens of the donor are the chief cause of chronic renal allograft rejection.
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PMID:Donor-specific IgG antibody and the chronic rejection of human renal allografts. 109 75

A 28-year old patient with malignant hypertension developed endstage renal failure necessitating chronic maintenance hemodialysis for seven months and transplantation of a renal allograft that was rejected within a month. After this, with continued control of the hypertension, the patient's own kidneys gradually resumed function and achieved anendogenous creatinine clearance of 30 ml/min. She has not required further dialysis for more than nine months. Recovery of sufficient renal function to maintain homeostasis, one year after onset of uremia, indicates the prolonged antihypertensive treatment period that may be necessary to reverse the renal arteriolar changes associated with malignant hypertension. This experience further underlines the necessity of moderation in the use of nephrectomy in the management of severe hypertension.
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PMID:Malignant hypertension. Recovery of kidney function after renal allograft failure. 109 41

The effects of chlorthalidone, spironolactone and propranolol in reducing blood pressure were compared in the same 11 normoreninemic hypertensive patients. All three drugs decreased the blood pressure significantly and no agent had a superior blood pressure-lowering effect. The blood pressure did not normalize. The data suggest that no one variable--volume factors, relative hyperactivity of the renin-aldosterone system or beta-adrenergic hyperactivity--is the prime mover in normoreninemic hypertension. Long-term treatment with chlorthalidone resulted in slight hyperreninism (26.3 +/- 4.9 ng-ml-1-3 hours-1) (mean +/- standard error) with concomitant changes in plasma aldosterone (23.0 +/- 3.2 ng-100 ml-1). The body weight decreased significantly (--1.8 kg, P less than 0.005). Plasma potassium concentrations were low (3.2 +/- 0.1 mEq-liter -1). Creatinine clearance was unimpaired (117 +/- 6 ml-min-1). Treatment with spironolactone resulted in more marked hyperreninism (47.0 +/- 14.3 ng-ml-1-3 hours-1) and hyperaldosteronism (61.9 +/-11.8 ng-100 ml-1). The body weight decreased significantly (--1.9 kg, P less than 0.004). Significant hyperkalemia occurred (4.4 +/- 0.1 mEq-liter-1). The glomerular filtration rate decreased significantly to 93 +/- 3 ml-min-1 (P less than 0.004). Treatment with propranolol resulted in marked suppression of the plasma renin activity (1.8 +/- 0.2 ng-ml-1-3 hours-1) and plasma aldosterone levels (8.9 +/- 1.3 ng-100 ml-1). A significant increase in body weight occurred (+2.3 kg, P less than 0.013). The plasma potassium concentration increased to a level not significantly different from the value found after treatment with spironolactone (4.2 +/- 0.1 mEq-liter-1). The creatinine clearance decreased significantly to 99 +/- 5 ml-min-1 (P less than 0.008). Hyperreninemia (by spironolactone and chlorthalidone), effective hyperaldosteronism (by chlorthalidone) and volume retention (by propranolol) are considered to represent expressions of mechanisms counteracting the depressor effects of these different pharmacologic maneuvers, leading to the maintenance of supranormal blood pressure.
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PMID:Intrapatient comparison of treatment with chlorthalidone, spironolactone and propranolol in normoreninemic essential hypertension. 110 6

Thirty-four renal transplant recipients received drip infusion urograms from 2-24 days post-transplantation. Twenty-two patients exhibited changes in renal function within 1-4 days of the urogram that were indistinguishable from allograft rejection: a tender, swollen kidney, elevation of serum creatinine, oliguria, decreased urine sodium concentration, weight gain, and hypertension. Two patients developed acute tubular necrosis and required hemodialysis, but renal function in the remaining 20 patients improved after therapy for "graft rejection" with i.v. methyprednisolone sodium succinnate. Kidneys from older-age donors that were functioning suboptimally and kidneys which exhibited subsequent clinical allograft rejection were more at risk for contrast media toxicity. This suggests that occult vascular lesions may have been present in the allograft which were exacerbated when exposed to the irritant vascular effects of contrast media, producing a mild, reversible toxic nephritis. However, several kidneys with normal function and several kidneys which never exhibited rejection activity were also adversely affected by exposure to contrast media. It appears these agents should be used cautiously, if at all, in the early post-transplant period.
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PMID:Adverse effects of meglumine diatrizoate on renal function in the early post-transplant period. 110 14

Three patients with right renal tumors extending into the inferior vena cava underwent ligation of the left renal vein coincident with right nephrectomy and en bloc resection of the vena cava. Two patients exhibited no postoperative renal dysfunction while the third demonstrated renal dysfunction which cleared by 9 days postoperatively. Features of the temporary renal dysfunction included proteinuria, elevated serum creatinine levels, oliguria, hypertension, elevated peripheral venous renin level, as well as radiographic evidence of swelling the kidney. The collateral venous drainage of the left kidney makes it possible to ligate the main vein of a solitary kidney with survival of the patient. However, postoperative temporary renal dysfunction may occur and a plan to deal with this problem should be fromulated.
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PMID:Ligation of the renal vein in the solitary kidney: effects on renal function. 111 94

Renal function was studied in 145 asymptomatic male heroin addicts admitted to a methadone detoxification program. The mean duration of addiction was ten years. Three patients had protein excretion greater than 150 mg/24 hr; in one of these, membranous glomerulonephritis was found. All except one had normal creatinine clearance. Hypertension was present in 2.7%. This study does not support the concept that heroin addiction is associated with a high prevalence of renal disease.
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PMID:Prevalence of renal disease in asymptomatic heroin addicts. 113 67


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