Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The review discusses the pathophysiology of the renal mechanisms of blood-pressure control. The physiology of the renin-angiotensin system is described and the mineralo-corticoid function has also been considered. The implications of alterations of these systems in various nephropathies are briefly summarized (renal artery stenosis, infarction, Page's syndrome, acute glomerulonephritis, essential hypertension a.o.).
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PMID:[Pathophysiology of renal hypertension (author's transl)]. 110 Dec 91

Transient hyperkalemia has been reported to occur in patients with acute glomerulonephritis, but the pathogenetic mechanism has not been investigated systematically. We studied the mechanism of hyperkalemia (5.7 to 6.7 mmol/liter) in four men with post-infectious glomerulonephritis. All four patients had clinical findings consistent with acute glomerulonephritis (edema, hypertension, proteinuria, hematuria, and an elevated ASO titer) and a renal biopsy performed in three of the patients confirmed the diagnosis. In comparison to normal subjects (N = 18), plasma aldosterone (5.4 +/- 1.6 vs. 22.8 +/- 2.6 ng/dl, P less than 0.005) and plasma renin activity (0.3 +/- 0.2 vs. 4.3 +/- 0.6 ng/ml/hr, P less than 0.005) were reduced. Hyperkalemia resolved within one to two weeks in two patients as the nephritis resolved and diuresis ensued, and aldosterone and renin levels obtained at follow-up visits were normal. Hyperkalemia persisted despite furosemide-induced diuresis in the other two patients, but resolved with fludrocortisone treatment. Thus, hyperkalemia in patients with acute glomerulonephritis is a manifestation, in part, of hyporeninemic hypoaldosteronism. It is ameliorated by mineralocorticoid therapy and improves spontaneously with resolution of the glomerulonephritis.
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PMID:Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism. 207 57

Because the role of systemic hormones in the pathophysiology of edema in acute renal disease remains incompletely understood, we compared the levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA) in patients with acute glomerulonephritis (AGN), nephrotic syndrome (NS), and normal individuals during salt deprivation and salt loading. Sixteen patients with AGN (10 males) and nine patients with NS and hypoalbuminemia (7 males) were studied on admission, and after recovery (12 AGN patients) or remission (4 NS patients). Eighteen normal controls were each studied after five days on a low (20 mEq Na/day), regular (120 mEq Na/day) and high (300 mEq Na/day) dietary salt intake. Patients with AGN and NS had comparable edema (AGN 2.8 +/- 0.53 kg; NS 3.36 +/- 0.47 kg; SE) and urinary Na excretion (mean +/- SEM: AGN 0.97 +/- 0.11 mEq/hr; NS 1.06 +/- 0.16 mEq/hr), but AGN patients had five times higher ANF (AGN 27.2 +/- 4.06 fmol/ml; NS 5.51 +/- 1.02 fmol/ml; P less than 0.001) and six times lower PRA ng/liter.sec levels (AGN 0.187 +/- 0.047; NS 1.144 +/- 0.222; P less than 0.001) than NS patients. The degree of edema was correlated with ANF levels in AGN patients (P less than 0.001) but not in NS patients. There was a strong exponential negative correlation (r = -0.773, P less than 0.0001) between ANF and PRA, in which AGN patients and Na-restricted controls were located in the opposite ends of the volume sensing-response, and NS patients in the middle, alongside controls with regular Na intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in the acute nephritic and nephrotic syndromes. 214 29

The clinical features, pathogenesis, and pharmacologic management of hypertensive crises are reviewed, with emphasis on newer therapies. Hypertensive crises may be divided into hypertensive emergencies and hypertensive urgencies. Hypertensive emergencies, in which acute organ damage exists, require blood pressure reduction within one hour. In hypertensive urgencies no acute end-organ damage has yet occurred; however, blood pressure should be controlled within 24 hours. Factors that may precipitate a hypertensive crisis include renovascular hypertension, acute glomerulonephritis, head injuries, renin- or catecholamine-secreting tumors, antihypertensive-therapy withdrawal syndromes, eclampsia, and ingestion of tyramine by patients receiving monoamine oxidase inhibitors. The traditional drug of choice for therapy of hypertensive emergencies is sodium nitroprusside. Intravenous labetalol produces a prompt, controlled reduction in blood pressure and is a promising alternative. Other agents used are diazoxide, trimethaphan camsylate, hydralazine, nitroglycerin, and phentolamine. However, all these agents have disadvantages, including unpredictable antihypertensive effects, difficult blood pressure titration, and serious potential adverse effects such as profound hypotension, reduced renal blood flow, and increased myocardial workload. Most patients with hypertensive urgencies can be effectively treated with orally or sublingually administered agents. Older regimens of reserpine, methyldopa, or guanethidine, with their slow onsets and long durations of action, have been largely replaced by clonidine and nifedipine. Captopril and minoxidil have also been used with some success. Despite the lack of comparative trials with traditional agents, demonstrated efficacy and desirable pharmacologic characteristics have made several new agents acceptable for therapy of hypertensive crises.
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PMID:Drug therapy of hypertensive crises. 304 49

We report that the inhibition of the angiotensin converting enzyme is an effective short-term treatment of low-renin hypertension in acute glomerulonephritis (AGN). We treated 9 patients who had AGN with moderate to severe hypertension and suppressed plasma renin activity with 25-50 mg of captopril per os every 6-8 hours. Control of blood pressure was achieved in 1-2 hours and maintained thereafter. Captopril therapy was associated with an increase in plasma renin activity, a decrease in plasma aldosterone and an increase in the urinary excretion of prostaglandin E2 and kallikrein, independent of changes in urine output. Creatinine clearance increased 39.6 +/- SE 15.2% with captopril and decreased in the postcaptopril period, suggesting that captopril exerted a reversible effect on glomerular filtration rate, possibly modifying intrarenal vasoconstriction. Our study shows that rapid control of hypertension in AGN may be obtained with oral inhibition of the angiotension converting enzyme. Stimulation of PGE2 and kinins, as well as angiotensin II blockade appear to contribute to the hypotensive effect of the drug; by inference, the suppressed activity of vasodilator systems seems to play a significant role in the hypertension of AGN.
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PMID:Short-term treatment with captopril in hypertension due to acute glomerulonephritis. 328 29

A boy of two years has an hematuria which was first related with an hypertensive acute glomerulonephritis. However because of recurrency of the hematuria radiological investigations were performed and a solid tumor of the right kidney was discovered. The arterial hypertension regressed after the right nephrectomy. Pathology demonstrated a tumor of Grawitz which is rare in children and which is seldom associated with an arterial hypertension. We found only five similar cases in the literature. Arterial hypertension can be related either with a compression of the renal artery of with an inadequate secretion of renin by the tumor.
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PMID:[Grawitz's tumor with arterial hypertension in children. Apropos of a case]. 380 80

A 9 year old Mexican boy presented with severe hypertension, hypokalaemia and features suggesting acute glomerulonephritis. Nephrosclerosis was present on renal biopsy. Aldosterone levels were unresponsive to variations in dietary salt intake and plasma renin activity was suppressed. Following oral dexamethasone therapy (2 mg/day), plasma aldosterone decreased to undetectable levels, serum potassium normalized and plasma renin activity gradually increased. Dexamethasone also restored the normal responsiveness of the renin-aldosterone system to postural stimuli. The patient exhibited a marked response to a single dose of ACTH with a rise in plasma aldosterone. Long-term blood pressure control and normal potassium levels have been achieved with oral prednisone therapy (5 mg/day) for a period of one year. This case of dexamethasone suppressible hyperaldosteronism (DSH) illustrates that the degree of hypertension in this syndrome may produce severe renal microvascular lesions. DSH should be considered in all children who present with low renin hypertension.
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PMID:Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis. 627 30

After a brief presentation of the pathogenetic scheme of renoparenchymal hypertension (RPH) in acute glomerulonephritis, of the pathogenesis of not controlled by dialysis and renin-dependent RPH, as well as of the more important causes for origination of arterial hypertension in patients with transplanted kidney, the author suggests the hypothesis, that the RPH in patients with ChRI , prior to the inclusion of the chroniodialysis treatment, originates, is maintained and becomes more frequent and graver , very likely, due to the gradual and progressive accumulation of factors within the patient's organism, elevating the arterial pressure, either by their reduced excretion through the affected kidneys or due to their increased production. In the development of the hypothesis, the author is based on some well known facts from literature and on his own studies, as elevated level of catecholamines in myocardium of patients that died with uremia, decreased elimination of catecholamines in patients with ChRI , elevated level of plasma cortisol in patients with chronic glomerular nephritis and ChRI , elevated levels of somatotropic and of thyreotropic hormone in patients with ChRI , elevated levels of angiotension 2 and of plasma aldosterone in some of the patients with RPH and ChRI , enhanced tendency to sodium and water retention in patients with ChRI , a tendency to increased volume of circulating plasma, increased stroke volume, increased general peripheral resistance, tendency to acidosis and to elevation of the serum level of potassium in advanced ChRI .
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PMID:[Hypothesis of the pathogenesis of renoparenchymal hypertension in chronic kidney failure patients before starting treatment with periodic hemodialysis]. 673 Apr 48

The blood pressure is the resultant of the relationship of three different factors: cardiac output, peripheral vascular resistance and blood volume. The etiology of hypertension in children is variable; however increased peripheral vascular resistance (renin dependent) and increased blood volume (sodium dependent), play a role in a variable degree in most cases of hypertension. Increased blood volume is the predominant factor in some cases of (acute glomerulonephritis), whereas vasoconstriction is the most important mechanism in others (renal segmental hypoplasia). Therefore, it becomes important to evaluate each individual case in order to approach therapy. Diuretics are indicated in patients with hypertension secondary to hypervolemia, while antihypertensives are more useful in cases with vasoconstriction. The scheme of treatment for acute hypertensive crises followed in the Department of Nephrology of the Hospital Infantil de Mexico is presented by the authors. A review of the most commonly antihypertensives used in Pediatrics is made, regarding mainly mechanisms of action, indications, recommended doses and side effects.
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PMID:[Treatment of arterial hypertension in children]. 747 Feb 63

Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
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PMID:[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]. 892 9


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