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

A new system is proposed for treating the spectrum of patients with high blood pressure. It is based on studies of the renin axis using renin profiling, pharmacologic probes and our bipolar vasoconstriction-volume hypothesis. The new system does not require renin profiling, pharmacologic testing or a vasoconstriction-volume analysis for widespread application. But these procedures, whenever available, will make treatment more efficient and more certain, and at the same time provide better base line definition. In the new system, all patients, except the elderly and those with congestive heart failure, bradycardia or a history of asthma, are treated first with propranolol alone, a procedure which will diminish or normalize blood pressure in many patients with high and noraml renin levels. For nonresponders, diuretic therapy is then superimposed. Subsequently, a propranolol subtraction trial picks out the low-renin patients who will usually respond to a diuretic alone. This program is likely to be fully effective in possible up to 85 per cent of patients. For the residual smaller fraction, drugs such as hydralazine, methyl DOPA, clonidine, reserpine or guanethidine are then added in traditional trial and error fashion. The proposed system has the theoretic attraction for long-term commitment, implicit in antihypertensive therapy, of achieving blood pressure control in large fractions with one drug instead of two or with two drugs instead of three or more. Moreover, the large groups who respond to therapy with propranolol alone (most high-renin and normal-renin patients) or to diuretics alone (most low-renin patients) gain the advantage of simple, more specific, long-term (i.e., antirenin or antivolume) therapy. The use of propranolol alone has practical and theoretic advantages over diuretics. Control may be achieved with even fewer side effects and without hypokalemia and chronic dehydration with its possibly adverse consequences (hyperuricemia, azotemia, hyperlipidemia, hyperreninemia, increased blood viscosity). Also, propranolol provides more direct control of the increased peripheral resistance and of neurogenically-induced swings in blood pressure. At the same time, the new system efficiently exploits the long-term use of diuretic therapy alone in low-renin patients in whom volume excess seems a causal factor. And it tends to avoid the use of diuretics in high-renin patients and of beta-blockers in low-renin patients in whom these drug types may be contraindicated.
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PMID:Modern system for treating high blood pressure based on renin profiling and vasoconstriction-volume analysis: a primary role for beta blocking drugs such as propranolol. 1 Jul 30

Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
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PMID:Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride. 13 13

Neocarzinostatin (NCZ), an acidic polypeptide antibiotic, was given to 47 patients with cancer and leukemia, and tolerance to two schedules, a single dose given as a 2 hour infusion and a continuous infusion over 5 days was investigated. Immediate reactions, including fever, chills, rigor, hypertension and mental confusion, were dose-limiting for the 2 hour infusion schedule, occurring at 3000 U/m2 and higher. Continuous administration for 5 days eliminated the immediate reactions and then hematological toxicity--often prolonged leukopenia and thrombocytopenia--became dose-limiting. Other toxicities of NCZ at both dose schedules included anemia, fever and chills, anorexia, nausea and vomiting, hepatic dysfunction, azotemia, hypophosphatemia, aminoaciduria, stomatitis, phlebitis and/or cellulitis at the venous infusion site and pruritus. Patients with solid tumors who had received little or no prior chemotherapy and had good bone marrow reserve tolerated up to 6000 U/m2/24 hours X 5 days. One patient with previously treated acute myelocytic leukemia was induced into a good partial remission lasting 10 weeks.
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PMID:Phase I study with neocarzinostatin: tolerance to two hour infusion and continuous infusion. 15 43

A total of 150 patients with renal pathology (chronic glomerulonephritis, pyelonephritis, urolithiasis, etc.) accompanied by the development of psychoneurological disturbances were examined. In the initial stage of the renal insufficiency the authors observed neurasthenic, radicular, polyneuritic, renovisceral syndromes, in a more remote stage--encephalopathies and disturbances of the brain circulation. The important part in the above-mentioned disturbances is played by azotemia, metabolic acidosis, disturbances of fluid-electrolyte and albumine balance, as well as arterial hypertension.
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PMID:[Changes in the nervous system in kidney diseases]. 20 20

The possibility has been explored of using a specific angiotensin ii antagonist, saralasin (P-113, 1-sar-8-ala-angiotensin ii) to recognize patients whose hypertension depends upon excessive angiotensin ii activity. Among 60 hypertensive patients, saralasin infusion reduced blood pressure in 16 "responders," but not in 44 "nonresponders." The "responders" had the following findings: elevated plasma renin activity in renal vein (or veins) or peripheral veins or both (16 of 16); reduced renal blood flow, shown by arteriography, isotopic studies or pyelography (15 or 16), or progressive azotemia (one of 16); and reduction in blood. These findings indicated that angiotensin ii probably caused hypertension in the "responders," One "nonresponder" had renal vein levels of plasma renin activity suggestive of angiotensinogenic hypertension. Since hypertension was invariably angiotensinogenic when it was reduced by saralasin and, with one possible exception, was never angiotensinogenic in "nonresponders," the antagonist appears to provide an efpressure to or toward normal after corrective operation (four of four) or propranolol therapy (eight of eight). fective means of recognizing angiotensinogenic hypertension.
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PMID:Use of an angiotensin II antagonist (saralasin) in the recognition of "angiotensinogenic" hypertension;. 23 90

92 cases of extramembranous glomerulitis (EMG) documented by histology and immunofluorescence have been studied. At the time of renal biopsy the clinical and biologic picture was as follows: no proteinuria in 2%, isolated proteinuria in 18%, nephrotic syndrome without hypertension or azotemia in 41%, and hypertension and/or azotemia associated with proteinuria or nephrotic syndrome in 39%. A possible cause of the EMG was found in 27 cases: it was drug-induced or toxic in 10 instances, paraneoplastic in 7, lupus in 5 and parasitic (loasis) in 5.65 cases are regarded as idiopathic. The evolution is known in 66 cases and varies with the etiology: it is usually benign in secondary forms except the paraneoplastic cases. In the idiopathic forms it results in hypertension or more or less severe chronic renal failure in 62% of cases. The prognosis cannot be established on the basis of the initial histology. No treatment has proved effective.
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PMID:[Extramembranous glomerulitis. Apropos of 92 cases]. 32 37

In patients with severe atherosclerosis of the abdominal aorta or previous operations on the abdominal aorta, right renal revascularization may be difficult to achieve using aortorenal bypass. An experimental study was performed demonstrating the efficacy of hepatorenal bypass as an alternative operative procedure in this regard. Follow-up studies in these dogs demonstrated no adverse postoperative effects on hepatic function or morphology. In addition, two patients underwent hepatorenal bypass with a saphenous vein graft as surgical treatment for azotemia and hypertension caused by atherosclerotic right renal artery stenosis. Postoperatively, the blood pressure diminished and renal function improved in both patients. No evidence of persistent hepatic dysfunction was observed.
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PMID:Experimental and clinical hepatorenal bypass as a means of revascularization of the right renal artery. 43 70

In some patients successful renal revascularization can be done after complete renal artery occlusion. We report on a patient with atherosclerotic occlusion of the renal artery and its branches in whom an aortorenal bypass with a branched saphenous vein graft was performed in situ, with cure of hypertension and reversal of azotemia. This is a useful and versatile technique for replacing the renal artery and its major branches.
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PMID:Atherosclerotic renal artery occlusion extending into branches: successful revascularization in situ with a branched saphenous vein graft. 45 24

A 56-year-old Samoan man with a documented history of hypertension, who presented with atrial fibrillation and hypotension, quickly developed renal failure with a serum urea nitrogen of 1.370 g/L and a serum creatinine of 92 mg/L. After hydration of the patient, the creatinine value became normal in two days, the urea nitrogen in four days. The urinary creatinine output during the first 24 h of hospitalization was 3.7 g. This case illustrates the rapidity with which unusually large amounts of creatinine (more commonly seen in chronic renal failure) can accumulate and be excreted in pre-renal failure. It also reaffirms the usefulness of the urea nitrogen/creatnine ratio in evaluating the causes of azotemia.
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PMID:Pre-renal azotemia mimicking chronic renal failure in a hypotensive patient. 49 10

A 4-year-old boy had hemolytic uremic syndrome (HUS) associated with depression of serum C3 level, a B-hemolytic streptococcal throat infection, and an elevated level of antistreptolysin O titer. In addition to the characteristic histologic changes associated with this syndrome, substantial infiltration of polymorphonuclear leukocytes and nodular deposits of C3 globulin were seen in the glomeruli of the first biopsy specimen. Two months after clinical remission, he had a recurrence of hemolytic anemia, thrombocytopenia, and acute renal failure. The serum C3 concentration had decreased again, and serum C3NeF was detected in the serum. The typical changes associated with HUS were still present on electron microscopy. Bilateral nephrectomy and renal transplantation were done because of the development of uncontrollable severe hypertension and increasing azotemia. This patient had three manifestations of HUS, but because of several differences, such as hypocomplementemia, serum C3NeF, a recurrence, and persistent glomerular deposits of C3 globulin, he appears to have had a different form of the syndrome.
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PMID:Hemolytic uremic syndrome with hypocomplementemia, serum C3NeF, and glomerular deposits of C3. 57 89


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