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)

We analysed sodium excretion and its circadian variation in 70 patients with nephrotic syndrome and 19 healthy controls over 1-3 days, with a regimen of bed rest and constant sodium intake around the clock. We sampled urine and blood and took their blood pressure every 3 h. We also scored 60 renal biopsies for presence of interstitial fibrosis and tubular atrophy. Peripheral oedema was estimated in 37 patients. Fifty-nine patients excreted > 10 mmol sodium per 24 h, in equilibrium with dietary intake. In group A (n = 24), sodium excretion followed a normal circadian rhythm, with a daytime peak. In group B (n = 35), 29 had reversed circadian rhythm with a night-time peak, and 6 had no apparent rhythm. Nephrotic syndrome was more severe in group B than in A (serum albumin 19.5 vs. 24.1 g/l, p < 0.05; oedema 7.0 vs. 3.8 kg, p < 0.01). Group B also had signs of more advanced renal disease (GFR 49 vs. 99 ml/min; number of biopsies with tubulo-interstitial damage: 20/28 vs. 4/23; p < 0.001). Reversed sodium rhythm was associated with reversed circadian rhythms for GFR, effective renal plasma flow and urine flow, and blunting or reversal of the day-night differences in blood pressure and plasma renin activity. Eleven patients had urinary sodium excretion < 1 mmol/24 h. With respect to severity of nephrosis, they resembled group B, but GFR and incidence of tubulointerstitial lesions were like group A. Half of the patients with nephrotic syndrome had reversed circadian rhythm for sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary sodium excretion in patients with nephrotic syndrome, and its circadian variation. 815 87

Most of the excess mortality and morbidity in diabetic end-stage renal disease patients is ascribed to diabetes-associated cardiovascular disease, which is accelerated by uremia. We compared the interdialytic weight gain in 33 diabetic patients (group 1) undergoing maintenance hemodialysis in an ambulatory facility retrospectively over 3 months, with 25 randomly selected nondiabetic hemodialysis patients (group 2); in addition, we assessed glycemic control in the diabetic subjects using glycosylated hemoglobin (HbA1c). Interdialytic weight gain was expressed as a percentage of the immediately preceding postdialysis weight, and a mean was calculated for each subject. In all subjects, predialysis serum aldosterone, plasma renin activity, and the interdialytic change in serum sodium were measured. Both groups received an equivalent amount of dialysis using a cellulose membrane (mean +/- SD of thrice weekly dialysis: group 1 = 3.8 +/- 0.35 hours, group 2 = 3.86 +/- 0.3 hours; P < 0.5) and had similar predialysis serum creatinine, hematocrit, and serum albumin levels. Group 1 patients had a mean age of 56.5 +/- 11.4 years (age range, 30 to 71 years) and group 2 had a mean age of 55.8 +/- 15.4 years (age range, 29 to 76 years) (P < 0.84). Mean (+/- SD) duration on maintenance hemodialysis was 18.7 +/- 15.3 months (range, 2 to 84 months) for group 1 and 21 +/- 28.9 months (range, 3 to 156 months) for group 2 (P < 0.9). Interdialytic weight gain was 30% greater in group 1 (4.2% +/- 0.19%) than in group 2 (3.2% +/- 0.2%) (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interdialytic weight gain correlates with glycosylated hemoglobin in diabetic hemodialysis patients. 817 11

Dietary phosphorus restriction ameliorates renal injury in rats. This may be due to changes in renal hemodynamics, including those factors associated with protein-induced hyperfiltration. To test this, we measured inulin clearance (CIn), p-aminohippuric acid clearance (CPAH), mean arterial blood pressure, and renal vascular resistance (RVR) 1 h before and 100 min after either oral gavage of 2 g bovine serum albumin or intravenous infusion of 5% glycine in female Sprague-Dawley rats previously fed for 3-8 wk a 0.5% or a 0.1% phosphorus diet. Baseline CIn, CPAH, blood pressure, and RVR were similar. After albumin gavage, CIn rose 20% (P < 0.01) for the 0.5% phosphorus group but did not change for rats fed the 0.1% phosphorus diet. Other measured parameters, including plasma glucagon and renin activity, were not influenced by dietary phosphorus content. In contrast, during intravenous infusion of glycine, hyperfiltration was induced in phosphorus-restricted rats. Thus dietary phosphorus restriction ablates oral protein but not intravenous amino acid-induced hyperfiltration, suggesting a gut-mediated mechanism for the former. These data highlight the potential importance of dietary phosphorus as a mediator of renal hemodynamics.
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PMID:Effect of phosphorus restriction on renal response to oral and intravenous protein loads in rats. 847 79

A new method for concentrated ascitic fluid reinfusion using a double ultrafiltration device is reported as 22 procedures in 20 cirrhotic patients (6 females, 14 males; median age 55 years, range 33-69) with tense, refractory ascites. Eight of the 20 patients had elevated creatinine levels. The mean time for each procedure was 189 +/- 82 min, during which a mean of 7.7 liters (1.3-13.3) of ultrafiltered ascitic fluid was removed and 613 ml (140-1700) of concentrated ascitic fluid rich in albumin (mean: 60 g, range 14-175) was reinfused. The procedure resulted in a mean weight loss of 8.1 kg (2.2-14.0) and a mean increase of 163 ml in urine output (24 hr). A reduction in the serum creatinine level (P < 0.05) and an increase in the plasma atrial natriuretic factor level (P < 0.02) 24 hr after reinfusion, while no changes in serum albumin, plasma and urinary electrolytes, plasma renin activity, aldosterone, and antidiuretic hormone levels were noted. Although minor evidence for a disturbance in coagulation was observed, there were no episodes of clinical bleeding. Four patients (20%) had transient chills or fever. Based upon this experience, it can be concluded that reinfusion of cascade filtered and concentrated ascitic fluid is a rapid, safe, and effective treatment for patients with tense ascites; it appears to have less side effects than more traditional methods and importantly does not require administration of heterologous plasma derivatives.
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PMID:Concentrated ascitic fluid reinfusion after cascade filtration in tense ascites. 848 89

Post-transplant erythrocytosis (PTE) has been increasingly recognized as a complication of kidney transplantation, and several risk factors have been defined. Recent evidence suggests renal function may also play a role in hematological recovery after transplantation and risk of PTE. In this study of kidney transplant recipients (n = 123), simultaneous Tc99m DTPA GFR (n = 710) and hemoglobin levels were compared with possible clinical determinants. The frequency histogram of post-transplant hemoglobin was bell-shaped and continuously distributed above and below the arbitrary definition of PTE, suggesting that PTE is not a separate disease entity. Hemoglobin reached a plateau at 12 months after transplantation and was correlated with isotopic GFR (r = 0.46, p < 0.001). This consistent and statistically independent relationship became prominent 3 months after transplantation. Hemoglobin was independently predicted by multivariate analysis by time after transplantation, presence of polycystic renal disease, greater serum albumin and reduced serum urea (which in turn were reflected by number of infective and rejection episodes), shorter kidney anastomosis time and a higher GFR, but not by immunosuppressive therapy. Rejection or infection episodes impaired hematological recovery. The independent determinants of GFR included hematological recovery. The independent determinants of GFR included hemoglobin level, kidneys from young, male donors, fewer HLA-DR mismatches and rejection episodes, shorter time on dialysis and greater azathioprine dose. Renal function was not altered by therapeutic phlebotomy. Determination of hemoglobin level by both donor and recipient variables supports the relevance of tubular and glomerular function in control of erythrocystosis after renal transplantation. A role for renin-angiotensin mediation in the alteration of intraglomerular hemodynamics and erythropoietin secretion is postulated.
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PMID:Erythrocytosis after renal transplantation: risk factors and relationship with GFR. 854 30

Renin can be detected in cardiovascular and other tissues but it disappears after bilateral nephrectomy indicating that tissues can take up or bind renal renin from the circulation. If renin uptake is the result of specific binding, plasma prorenin may be a natural antagonist of tissue directed renin-angiotensin systems. To investigate if specific prorenin/renin uptake occurs in rat tissues, binding studies were performed, with rat microsomal membrane preparations using recombinant rat prorenin metabolically labeled with 35S-methionine as a probe. A high affinity binding site for both renin and prorenin was identified. Affinities for prorenin and renin were approximately 200 and 900 pmol/L, respectively. Binding was reversible, saturable, and pH and temperature dependent. The relative binding capacities of membranes from various rat tissues were as follows (fmol/mg): renal cortex (55), liver (54), testis (63), lung (31), brain (18), renal medulla (15), adrenal (17), aorta (7), heart (4), and skeletal muscle (1). Bound prorenin was displaced by rat and human renin or prorenin but not by the prosequence of rat prorenin, angiotensin I or II, rat or human angiotensinogen, the renin inhibitor SQ30697, atrial natriuretic factor, amylase, insulin, bovine serum albumin, hemoglobin, heparin, lysozyme, ovalbumin, cytochrome C, pepsin, pepsinogen, ribonuclease A, mannose-6-phosphate, alpha-methyl mannoside, gonadotropin releasing hormone, or an antibody to hog renin binding protein. these results demonstrate specific binding of prorenin to a site in rat tissues, herein named ProBP, that also binds renin. It is possible that differences in prorenin/renin binding capacity determine the activity of tissue-directed renin-angiotensin systems and that prorenin is a natural antagonist. Alternatively, a prorenin/renin receptor may have been identified that may function by transducing an intracellular signal.
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PMID:Specific prorenin/renin binding (ProBP). Identification and characterization of a novel membrane site. 873 81

We compared the efficacy and safety of apheresis and reinfusion of concentrated ascites (ARCA) versus total paracentesis plus intravenous albumin (PARA) in a prospective trial on cirrhotic patients with tense ascites. Twenty-four patients were randomized to either ARCA (N = 12) or PARA (N = 12), and followed for two years. Sex, age, Child's class, and renal and liver function were similar in the two groups. The times the procedures were 2.7 +/- 1.0 (ARCA) vs 2.2 +/- 1.1 (PARA) hr, with removal of 8.8 +/- 3.5 (ARCA) and 6.9 +/- 3.4 (PARA) liters of ascites and intravenous infusion of 59.8 +/- 35.2 (ARCA) and 42.5 +/- 20.5 (PARA) g of albumin. Both procedures were safe. Biochemical signs of coagulative disturbances having no clinical relevance were observed after ARCA, with an increase in prothrombin time (P = 0.005) and serum FSP (P = 0.02). No significant changes in renal function, serum albumin, or plasma and urinary electrocytes were shown. Plasma renin activity increased after PARA (P = 0.02) and plasma atrial natriuretic factor increased after ARCA (P = 0.008), although no differences were observed in diuresis in the immediate follow-up. During the long-term follow-up, patient survival and recurrence of tense ascites were the same in both groups. We conclude that apheresis and reinfusion of concentrated ascites are as safe and effective as total paracentesis with albumin infusion for the treatment of tense ascites in cirrhotic patients.
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PMID:Reinfusion of concentrated ascitic fluid versus total paracentesis. A randomized prospective trial. 928 38

Nitrosated proteins exhibit actions characteristic of free NO. As the vasorelaxation effect of nitrosated albumin is rapidly inactivated in plasma, we postulated that a protease could remove or modify the NO attached to albumin. We found that the ability of plasma to inactivate the vasorelaxing action of NO-bovine serum albumin (NO-BSA) is restricted to a plasma fraction containing macromolecules. We also found that a crude preparation of renal renin also inactivated the vasorelaxation action of NO-BSA and UV-spectrophotometric analysis showed that the 335-nm signal of NO-BSA was significantly decreased by renin. This decrease could be prevented by a renin inhibitor or by immunodepleting the renin preparation with a monoclonal antibody to renin. The data suggest that renin accelerates the uncoupling of NO to albumin. Such a function may be important in the control of vascular tone and blood pressure.
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PMID:Renin inhibits the vasorelaxation induced by nitroso albumin. 973 38

We rapidly infused 234 +/- 3 mL of 5% human serum albumin in eight men while measuring haematocrit, haemoglobin concentration, plasma volume (PV), albumin concentration, total protein concentration, osmolality, sodium concentration, renin activity, aldosterone concentration, and atrial natriuretic peptide concentration to test the hypotheses that plasma volume expansion and plasma albumin content expansion will not persist for 24 h. Plasma volume and albumin content were expanded for the first 6 h after infusion (44.3 +/- 1.9-47.2 +/- 2.0 mL kg-1 and 1.9 +/- 0.1-2.1 +/- 0.1 g kg-1 at pre-infusion and 1 h, respectively, P < 0.05), but by 24 h plasma volume and albumin content decreased significantly from 1 h post-infusion and were not different from pre-infusion (44.8 +/- 1.9 mL kg-1 and 1.9 +/- 0.1 g kg-1, respectively). Plasma aldosterone concentration showed a significant effect of time over the 24 h after infusion (P < 0.05), and showed a trend to decrease at 2 h after infusion (167.6 +/- 32.5(-1) 06.2 +/- 13.4 pg mL-1, P = 0.07). These data demonstrate that a 6.8% expansion of plasma volume and 10.5% expansion of plasma albumin content by infusion does not remain in the vascular space for 24 h and suggest a redistribution occurs between the intravascular space and interstitial fluid space.
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PMID:Albumin infusion in humans does not model exercise induced hypervolaemia after 24 hours. 985 15

Angiotensin-I-converting enzyme (ACE) has been classically associated with the renin-angiotensin system which regulates peripheral blood pressure. Peptides derived from the major whey proteins, i.e. alpha-lactalbumin (alpha-la) and beta-lactoglobulin (beta-lg) in addition to bovine serum albumin (BSA), inhibit ACE. Some of these inhibitory peptides, i.e. alpha-lactorphin (alpha-la f(50-53)), beta-lactorphin (beta-lg f(102-105)), beta-lactotensin (beta-lg f(146-149) and albutensin A (BSA f(208-216)), have other bioactivities. The most potent lactokinin reported to date, (beta-lg f(142-148)), has an ACE IC50 of 42.6 mumol/l. While they do not have the inhibitory potency of synthetic drugs commonly used in the treatment of hypertension, these naturally occurring peptides may represent nutraceutical/functional food ingredients for the prevention/treatment of high blood pressure. Studies with gastric and pancreatic proteinase digests of whey proteins indicate that enzyme specificity rather than extent of hydrolysis dictates the ACE inhibitory potency of whey hydrolysates.
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PMID:Lactokinins: whey protein-derived ACE inhibitory peptides. 1039 49


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