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)

This study was designed to evaluate the role of aldosterone, glomerular filtration and blood pressure on sodium excretion in renal disease. Sodium clearance (CNa), plasma aldosterone (PA), plasma renin activity (PRA), glomerular filtration rate (GF), paraaminohippurate clearance (CPAH) and blood pressure were measured simultaneously in 19 normal subjects, 38 patients with benign essential hypertension, 3 with renal artery stenosis, 48 with chronic glomerulonephritis, 20 with the nephrotic syndrome, 24 with tubulo-interstitial disease and 21 with a renal homograft. CNa was significantly depressed in patients with the nephrotic syndrome. Mean PA and PRA were increased in renal artery stenosis but within the normal range in other groups. CNa correlated inversely with PA in all groups but one (tubulo-interstitial disease). CNa correlated directly with GF in the nephrotic syndrome and with the mean blood pressure (mBP) in chronic glomerulonephritis and tubulo-interstitial disease. PA correlated directly with PRA and inversely with GF or CPAH in most groups. It is concluded that PA is an important determinant of the basal natriuresis in renal disease with the exception of tubulo-interstitial nephropathies. In the nephrotic syndrome sodium retention is largely determined by the interaction of PA and GF. In chronic nephropathies, but not in benign essential hypertension, the fractional sodium excretion is partly blood pressure-dependent. Impairment of renal function is often accompanied by a rise in PA.
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PMID:Interrelationships between sodium clearance, plasma aldosterone, plasma renin activity, renal hemodynamics and blood pressure in renal disease. 39 72

The effect of a 4 hr upright posture on serum potassium (SK) levels was investigated in a certain group of hospitalized renal patients with selective hypoaldosteronism and in healthy subjects. Significant (p less than 0.001) postural increase in SK (0.4 MMol/L) was found only in the 3 young patients with chronic glomerulonephritis and hypoaldosteronism who presented with hyperkalemia (5.84 +/- 0.13 mMol/L) as outpatients, but showed a marked improvement toward normokalemia (4.95 +/- 0.13 mMol/L; p less than 0.001) within the hospital without any specific treatment. In healthy persons in the fastqng condition the influence of the upright position of short duration (45 min) was also studied on SK and a very small but significant increase (0.15 mMol/L) was found. It was concluded: 1. the postural SK INCREASE MAY OFFER AN--AT LEAST PARTIAL--EXPLANTATION FOR THE "OUTPATIENT HYPERKALEMIA", 2. The normal activity of renin-angiotensinaldosterone system may play a role in the counteraction of the trend for SK rise in the upright posture.
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PMID:Increase of serum potassium in the upright posture in selective hypoaldosteronism. 42 8

In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. During sodium restriction despite a marked increase in PRA and PA levels poor correlations were found between these variables indicating disorganisation within the RAAS and probably a diminished role for renin-angiotensin in the regulation of aldosterone production in three hyperkalemic patients with chronic glomerulonephritis. On the other hand, in the same patients significant correlations were found between fluctuations of SK and PA on constant normal and low sodium diets supporting the concept of an (at least) equal role of potassium and RAAS in the acute regulation of PA. A prominent role for SK was found in an unusual hyperkalemic patient with interstitial nephritis when PRA was suppressed and the elevated SK showed a definite postural rise inducing dramatic increases in PA in the upright posture. Reversion of the postural SK rise masked again the governing role of SK.
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PMID:Regulations of plasma aldosterone in young hyperkalemic patients with stable chronic renal failure. 46 73

Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.
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PMID:Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. 49 1

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.
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PMID:Clinical evaluation of angiotensin II antagonist in advanced hypertension. 88 41

Patients with chronic glomerulonephritis and mild hypertension show a consistent behaviour in their renin-aldosterone-system. There is a close correlation between the elevation of mean blood pressure and destruction of glomeruli. No correlation has been found between renin values and the degree of hypertension. Thus the cuase of mild hypertension occurring in the early stages of chronic GN remains to be elucidated. Normal PRA values in spite of hypertension and expansion of ECFV accompaning progression of chronic glomerulonephritis could be a sign of "relative hyperreninemia". Apparently various mechanisms are involved in the pathogenesis of renal hypertension. These include sodium retention, increased cardiac output. anemia, renin, aldosterone, prostaglandins, expanded plasma volume and peripheral vasoconstriction. These factors are more or less active in the different stages of hypertension and renal failure.
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PMID:Plasma renin activity (PRA) and aldosterone (PA) in patients with chronic glomerulonephritis (GN) and hypertension. 94 54

Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline-depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and 11 patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion ("low renin hypertension"). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.
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PMID:[Plasma aldosterone and plasma renin activity in patients with essential and renal hypertension under acute stimulation with saline depletion and acute suppression with saline infusion]. 115 49

A study was made of the structural rearrangement of renal tissues in intravital nephrobiopsy specimens and of the functioning of the renin-angiotensin-aldosterone system and kallikrein-synthetic function in patients with mesangioproliferative (MSPGN) and membranous proliferative glomerulonephritis (MPGN). The morphological changes were revealed. The patients with associated MSPGN and secondary hypertension (SH) mostly demonstrated emptying and hyalinosis of arteries, whereas those with associated MPGN and SH manifested for the most part the derangement of the tubulointerstitial structures. In patients with MPGN, the levels of total renin (TR) and inactive renin (IR) were significantly higher than in those suffering from MSPGN. This can be regarded as risk factor of earlier development of SH. In MPGN patients, the content of TR and IR as well as that of active renin (AR) did not depend on the clinical pattern of chronic glomerulonephritis. As compared to MSPGN patients with isolated urinary syndrome, those with associated MSPGN and SH had a higher AR level, which agreed well with systolic and mean arterial pressure. Apparently, the latter one is implicated in the mechanism of SH in MSPGN. In associated MPGN and SH, kallikreinuria was found to be lowest, which may be the consequence of tubulointerstitial lesions. Discoordination of the renin-angiotensin and kallikrein systems is likely to be one of the causes of earlier formation and severe course of SH in the morphological pattern under consideration.
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PMID:[The morphofunctional parallels in arterial hypertension in patients with chronic glomerulonephritis]. 144 Mar 15

The restructure of renal tissue in intravital nephric biopsy specimens, renin-angiotensin-aldosterone together with kallikrein synthetic functions were studied and compared in patients with mesangioproliferative and membranoproliferative glomerulonephritis (MsPGN and MPGN). The characteristics of the morphological changes were defined. In MsPGN with secondary hypertension (SH), nephronic wasting and hyalinosis of arteries were mostly detectable whereas MPGN with SH was primarily marked by the derangement of the tubulointerstitial structures. In MPGN, the levels of total and inactive renin (TR and IR) were significantly higher than in MsPGN. This can be regarded as risk factor of early development of SH. The content of TR and IR and in addition that of active renin (AR) in MRGN did not depend on the clinical form of chronic glomerulonephritis. As compared to MsPGN with an isolated urinary syndrome, in MsPGN with SH, AR was prevalent, while its level correlated well with systolic and the mean arterial pressure. AR may be implicated in the mechanism of SH in MsPGN. In MPGN with SH, kallikreinuria was found to be extremely low, which may be consequent to tubulointerstitial injuries. The discoordination of the renin-angiotensin and kallikrein system may be one of the causes of earlier formation and the grave course of SH in the morphological pattern under consideration.
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PMID:[The morphofunctional parallels in arterial hypertension in patients with chronic glomerulonephritis]. 144 Mar 31

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.
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PMID:Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release. 183 31


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