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)

Anuria complicated the malignant phase of hypertension in twelve patients (ten males and two females). Five were black; five had primary hypertension; one had HBs virus angiitis; the six remaining cases suffered from previously documented renal disease, including two with Berger's disease. Renal angiography showed interruption of renal blood flow as far as the main branches of the renal artery and/or a false impression of 'cortical necrosis' and of 'renal infarcts'. In contrast, renal biopsy did not show irreversible vascular damage. Thus, anuria was mainly functional and due to active renal vasoconstriction. This was confirmed by the subsequent course; diuresis resumed after 1 week to 24 months of dialysis. Repeat angiography in six cases showed recovery of renal circulation and disappearance of 'cortical infarcts', even when plasma renin activity remained elevated and hypertension was not controlled. In one case captopril induced a new reversible episode of anuria. These observations suggest that active vasoconstriction with prolonged anuria might be due to some vasoconstrictive substance other than angiotensin II.
Nephrol Dial Transplant 1990
PMID:Protracted anuria due to active vasoconstriction in primary or secondary malignant hypertension. 211 43

Renal haemodynamics, sodium excretion, and free-water clearance were evaluated at baseline and after acute frusemide administration in nine moderately volume-expanded healthy volunteers receiving a single administration of either 750 mg lithium carbonate or placebo. Lithium plasma concentration under 0.29 mmol/l exerted no significant effect on renal haemodynamics, on absolute, fractional, or cumulative sodium excretion, or on free-water and chloride clearances at baseline or after frusemide administration. Despite previous volume expansion and presumably depressed proximal reabsorption, frusemide decreased the fractional reabsorption of lithium significantly, suggesting that a small but significant part of lithium may be reabsorbed in the thick ascending limb of Henle's loop. By contrast, frusemide did not change renal haemodynamics or plasma renin activity. Using combined free-water and lithium clearances at baseline and after frusemide administration, fractional reabsorption of sodium in the (FRTAL) was calculated as delta CH2O/CLi, where delta CH2O, the difference in free water clearance before minus after frusemide, is taken as an index of sodium reabsorption in the thick ascending limb, and lithium clearance as an estimation of sodium delivery to the thick ascending limb. FRTAL was calculated in these volume-expanded subjects to lie from 11% to 20% depending on whether some lithium is assumed to be in the thick ascending limb.
Nephrol Dial Transplant 1990
PMID:Does lithium affect renal sodium handling and renal haemodynamics in normal man? 212 49

Hypertension is frequently present in glomerulonephritis without renal insufficiency but its pathogenesis is poorly understood. Eighty-five patients with glomerulonephritis and normal renal function, including 55 hypertensive patients, and 24 normal subjects were studied to obtain data on the mechanisms responsible for hypertension. Plasma renin activity (PRA), plasma noradrenaline, total exchangeable sodium, and urinary prostaglandin E (PGE) were determined. Moreover, the autonomic nervous system was explored with the following tests: tilt test, diving reflex, lying down, and deep-breathing tests. In 15 of the 30 normotensive patients with glomerulonephritis, PRA was measured after the administration of propranolol and then indomethacin. No significant differences were found in the mean values of PRA, plasma noradrenaline, total exchangeable sodium, urinary PGE, and autonomic nervous system behaviour between glomerulonephritis patients with and without hypertension or between hypertensive glomerulonephritis patients and control subjects. In many of the normotensive glomerulonephritis patients we found an elevated PRA that was normalised by propranolol but not by indomethacin. In summary, hypertension in glomerulonephritis is not associated with abnormalities in the sodium balance, with renin-angiotensin or with autonomic nervous system abnormalities. A renin hypersecretion seems to be present only in some normotensive patients with glomerulonephritis.
Nephrol Dial Transplant 1989
PMID:Hypertension in primary glomerulonephritis without renal insufficiency. 251 57

Studies in normal man have demonstrated an acute increase in glomerular filtration rate (GFR) and renal blood flow (RBF) after a mixed protein meal, but the hormonal mechanisms underlying this response are not well defined. Thirteen adult men were starved for 24 h, then fed a test meal containing 1.5 g/kg bodyweight of animal protein. Renal haemodynamics and plasma and urinary hormones were measured before and at 2 h and 4 h after the meal. GFR and RBF increased by 27% and 23% respectively at 2 h. Electrolyte excretion did not parallel and was independent of the haemodynamic changes. Plasma noradrenaline (median 350 versus 573 pg/ml), renin (0.64 versus 1.09 nmol AngI/l per h), and urinary prostaglandin E (PGE) (66.4 versus 238 pmol/min) were all significantly elevated at 2 h. In further experiments, nine of the subjects were given indomethacin 50 mg before and after the meal using the same protocol as before. In comparison with control data, GFR and RBF after indomethacin did not increase after the meal and plasma noradrenaline and renin and urinary PGE remained at baseline values. Electrolyte excretion was not affected. These results suggest that the renal response to protein feeding is partly mediated by intrarenal prostaglandins but is also part of a more complex interaction with the sympathetic nervous system.
Nephrol Dial Transplant 1989
PMID:Renal haemodynamic and hormonal responses to a mixed high-protein meal in normal men. 251 75

The urinary excretion rate and plasma concentration of angiotensin I (UAI, PAI) and angiotensin II (UAII, PAII), and plasma renin activity (PRA) were measured in seven healthy volunteers in the supine and upright position both on free and restricted sodium intakes. The same variables were measured before and after intravenous injection of furosemide, as well as before and during intravenous infusion of chlorothiazide. Assumption of the upright posture as well as sodium restriction increased PAI, PAII, and PRA, but UAI and UAII excretion were not altered by these manoeuvres. Furosemide injection resulted in increases of all variables, albeit that PAI and PAII were elevated to a lesser extent then PRA. Chlorothiazide infusion caused a reduction in PAI, PAII, and PRA, whereas UAI and UAII excretion increased modestly. The discrepancies between changes in plasma and urinary AI and AII may indicate that urinary angiotensin excretion provides information which is supplementary to that of plasma angiotensins.
Nephrol Dial Transplant 1989
PMID:Urinary angiotensin excretion during sodium restriction and diuretics. 251 79

The effects of 4 h haemodialysis (15 patients) or 4 h haemofiltration (five patients) on plasma concentrations of atrial natriuretic peptide (ANP) were compared by means of a sensitive radioreceptor binding assay, and related to accompanying changes in body weight, blood pressure and plasma renin activity. Before dialysis, plasma ANP concentrations were considerably elevated: haemodialysis group 10-484 pmol/l (mean 156 pmol/l); haemofiltration group 72-320 pmol/l (mean 170 pmol/l). Although plasma concentrations of ANP fell markedly with treatment in both groups: post-haemodialysis 2-187 pmol/l (mean 67 pmol/l); post-haemofiltration 47-135 pmol/l (mean 79 pmol/l), after treatment it remained above the normal range in 14 of the 20 patients. Pretreatment plasma ANP was related to systolic blood pressure (r = 0.459; P less than 0.05) but bore no relationship to mean or diastolic blood pressure, or plasma renin activity. The fall in plasma ANP concentration during treatment correlated with the postural blood pressure drop after dialysis (r = 0.505; P less than 0.05), but was unrelated to changes in weight or plasma renin activity with haemodialysis or haemofiltration. Plasma ANP concentrations rose rapidly again in the 60 min after dialysis treatment, without change in body weight. These results show that high levels of biologically active ANP circulate in end-stage renal disease. The fact that these are not reduced to normal by haemodialysis or haemofiltration, despite restoration to normovolaemic or hypovolaemic state, suggests that the increased levels of ANP in end-stage renal failure are due to both hypervolaemia and other factors, which may include occult cardiac dysfunction and loss of renal clearance.
Nephrol Dial Transplant 1989
PMID:Comparative effects of haemodialysis and haemofiltration on plasma atrial natriuretic peptide. 252 56

To assess a possible role for endogenous renal dopamine in sodium excretion, the dopa decarboxylase inhibitor carbidopa was given during intravenous salt loading. In addition, the effect of lithium on tubular sodium handling was separately determined. Nine males were studied randomly on three occasions, receiving placebo, lithium carbonate (1000 mg, 11 h prior to study) or carbidopa (100 mg x 2). On each day a baseline period was followed by infusion of isotonic saline (20 ml/kg per hour) over 3 h, and 6 h recovery. With placebo, sodium excretion increased markedly to a peak in the hour after infusion (0.15 +/- 0.03 to 0.73 +/- 0.12 mmol/min, P less than 0.01). Urine dopamine excretion increased modestly (1.33 +/- 0.12 to 1.67 +/- 0.13 mmol/min, P less than 0.01). Carbidopa effectively blocked dopamine output during the study. However, the natriuretic response was comparable to values on placebo at all time points. Fractional lithium clearance, a proposed measure of proximal tubular fluid rejection, increased significantly during saline infusion. However, baseline sodium excretion was greater in the presence of lithium, and plasma renin activity (PRA) was significantly elevated. In addition, the peak natriuretic response was smaller and cumulative sodium excretion reduced by 40% (P less than 0.01) compared to placebo. This study provides no evidence for a facilitatory role for dopamine in the natriuretic response to intravenous salt loading. Lithium, at subtherapeutic levels, cannot be presumed to be an inert marker, and clearance data must be interpreted with caution.
Nephrol Dial Transplant 1989
PMID:The effect of carbidopa and lithium on the systemic and renal response to acute intravenous saline loading in normal man. 252 33

We studied renal, hormonal and cardiovascular effects of ANF 102-126 (WY 47987) in seven patients with chronic renal failure (serum creatinine 25-68 mg/l) and in four normal volunteers. ANF or placebo bolus injections were given at 1, 2, and 3 micrograms/kg i.v. (each dose on separate days). As compared to placebo, ANF did not induce changes of renal excretory parameters, of plasma renin and aldosterone or of blood pressure and heart rate in patients. In healthy volunteers, however, the same dose of ANF increased urinary excretion of sodium, potassium, calcium, chloride and phosphorus as well as water, and creatinine clearances, and decreased plasma aldosterone. The data suggest blunted effectiveness of ANF bolus injections in patients with renal insufficiency.
Nephrol Dial Transplant 1989
PMID:Effects of WY 47987 (atrial natriuretic factor 102-126) in patients with renal insufficiency: a placebo-controlled, randomised study. 253 73

The radio- and chemoprotective agent, S-2 (3-aminopropylamino) ethyl-phosphorothioic acid (WR-2721) has been reported to lower hypercalcaemia in patients with cancer, probably by increased renal calcium excretion and decreased parathyroid hormone (PTH) secretion and bone calcium resorption. The present study reports the first clinical use of WR-2721 in an anuric haemodialysis patient with severe secondary hyperparathyroidism. The drug was administered intravenously at different doses, i.e. 150, 300, and 500 mg/m2. The infusion was followed by a striking decrease of plasma immunoreactive (i) PTH within 30 min. The nadir of the iPTH decrease was reached at 60 min and was followed by a steady return to previous values. Serum ionised calcium decreased more progressively from 1.55 mmol/l initially to 1.30 mmol/l at 4 h after the 300-mg dose, remained at that level at 24 h, but rose again to pre-infusion values after 48 h. The extent and duration of the decrease in plasma iPTH and ionised calcium were dose-dependent. The circulating iPTH at 24 h was inversely related to the corresponding plasma ionised calcium concentration and had risen above preinfusion values at that time. Plasma concentrations of three other hormones, i.e. renin, insulin, and prolactin, were not affected by the administration of WR-2721. In conclusion, WR-2721 can induce a decrease in serum ionised calcium in the absence of any excretory kidney function. The rapid effect of the drug on circulating iPTH supports the notion of an interference with PTH secretion or catabolism.
Nephrol Dial Transplant 1987
PMID:Hypocalcaemic effect of WR-2721, S-2 (3-aminopropylamino) ethyl-phosphorothioic acid in an anuric haemodialysis patient. 303 48

The effects of intravenous acetylsalicylic acid (1.0 g bolus) on renal function and prostaglandin synthesis were evaluated in a prospective, controlled study in eight patients in an intensive care unit. Four of these patients had congestive heart failure. Administration of acetylsalicylic acid caused significant antidiuresis (-56%), antinatriuresis (-82%), renin suppression (-26%) and decreased GFR (-41%). All of these changes were completely reversible within 1-2 hours and tended to be more pronounced in the patients with congestive heart failure. Urinary excretion of prostaglandin E2 was depressed profoundly (-93%) and did not return to more than 45% of control 6 h after the administration of acetylsalicylic acid. We conclude that intravenous acetylsalicylic acid affects kidney function in a manner similar to other prostaglandin synthesis inhibitors. Its effects are, however, short-lived. The inhibition of urinary PGE2 excretion outlasts GFR depression, antidiuresis, antinatriuresis and renin suppression by several hours.
Nephrol Dial Transplant 1986
PMID:Effects of intravenous aspirin on prostaglandin synthesis and kidney function in intensive care patients. 311 Jun 70


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