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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severity of renal injury and recovery of function in acute renal failure (ARF) are strongly related not only to the magnitude and nature of ARF insult but also to numerous factors in the host which govern renal susceptibility to the insult and repair of renal lesion. Prior ARF affords resistance to a rechallenge with the same or different ARF insult. The mechanisms for this acquired resistance to ARF have not been well established, but suggested mechanisms include (a) increased resistance of regenerated tubular epithelial cells to a rechallenge, (b) glomerular refractoriness to vasoactive substances, (c) failure of damaged kidney to concentrate the toxic substance, (d) enhanced antioxidant enzyme activity in glomeruli, and (e) increased Na(+)-K(+)-ATPase activity in regenerated tubular epithelial cells. Controversy still exists regarding roles of these factors in the resistance to renal failure. Functional and morphologic recovery of postischemic kidney is enhanced by antecedent unilateral nephrectomy but delayed in the presence of the contralateral kidney. The mechanisms for the effect of uninephrectomy remain unsettled. Recent studies suggest contributions of changes in preglomerular vascular resistance; alterations in the environment which follow ischemia to all functioning excretory renal tissues; and altered production and release of vasoactive substances such as angiotensin, endothelin, thromboxane, and atrial natriuretic peptide.
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PMID:Factors affecting severity of renal injury and recovery of function in acute renal failure. 132 11

The natriuretic peptide system consists of at least three endogenous ligands: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), and three receptors, ANP-A receptor (guanylate cyclase A), ANP-B receptor (guanylate cyclase B) and clearance receptor (C receptor). ANP, the prototype of natriuretic peptides, is mainly produced in the atrium and secreted into the circulation as a cardiac hormone. ANP is also produced in the ventricle and in the central nervous system. BNP, first isolated from the porcine brain, has a marked divergence in its molecular size and sequence among species. In humans and rats, the major site of production of BNP is the ventricle of the heart. BNP is also secreted into the circulation as a cardiac hormone. The plasma BNP level in normal subjects is approximately one sixths of the plasma ANP level; however, the plasma BNP level markedly increases in heart failure, renal failure and hypertension and the augmentation of the BNP secretion is much larger than that of the ANP secretion. In addition, clearance of BNP from the circulation is slower than that of ANP. Furthermore, BNP is secreted more urgently than ANP in acute heart failure. CNP distributes mainly in the central nervous system and pituitary gland. No significant amount of CNP is detectable in the heart and plasma. Thus, CNP is a local regulator rather than a cardiac hormone. Three natriuretic receptors have ligand selectivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Natriuretic peptide family]. 134 67

The negative effect of artificial ventilation with positive pressure on renal function, expresses itself as a decrease of water and sodium excretion, being directly related with the raise of intrathoracic pressure. Factors participating in this process are: lowering in cardiac output, arousal of sympathic nervous system, increase in vasopressin action, activation of renin-angiotensin-aldosterone system and decrease of atrial natriuretic peptide release. This disorder of hydromineral metabolism produces: Impairment of hemodynamic equilibrium, favors the increase of hypoxia and renal failure. The effects of mechanical ventilation on renal function can be attenuated with the adoption of the following measures: a) techniques (use of low levels of PEEP and early disconnection of respirator); b) therapeutic (dopamine 2-3 mcg/kg/min, rational use of diuretics and fluids); y c) monitoring of renal function and hydro-mineral equilibrium.
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PMID:[The kidney in mechanical ventilation]. 148 39

Plasma levels of brain natriuretic peptide, a recently identified cardiac hormone with natriuretic activity, were measured in 11 healthy subjects, 13 cirrhotic patients without ascites, 18 nonazotemic cirrhotic patients with ascites and 6 patients with cirrhosis, ascites and functional kidney failure. Plasma levels of brain natriuretic peptide were similar in healthy subjects and cirrhotic patients without ascites (5.56 +/- 0.65 and 7.66 +/- 0.68 fmol/ml, respectively). In contrast, cirrhotic patients with ascites, with and without functional kidney failure, had significantly higher plasma concentrations of brain natriuretic peptide (19.56 +/- 1.37 and 16.00 +/- 1.91 fmol/ml, respectively) than did healthy subjects and patients without ascites (p less than 0.01); no significant difference was found between the two groups of cirrhotic patients with ascites with respect to this parameter. In the whole group of cirrhotic patients included in the study, brain natriuretic peptide level was directly correlated with the degree of impairment of liver and kidney function, plasma renin activity and plasma levels of aldosterone and atrial natriuretic peptide. The results of this study indicate that brain natriuretic peptide is increased in cirrhotic patients with ascites and suggest that sodium retention in cirrhosis is not due to deficiency of this novel cardiac hormone.
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PMID:Plasma levels of brain natriuretic peptide in patients with cirrhosis. 161 67

The effect of subcutaneous and intraperitoneal administration of recombinant human erythropoietin (rHuEPO) on blood pressure was evaluated in 20 patients with renal failure on continuous ambulatory peritoneal dialysis. The two groups of patients were commenced on a 16-week course of twice weekly rHuEPO by either the subcutaneous (10 patients) or the intraperitoneal route (10 patients). One patient in the latter group was subsequently excluded because of operation and transfusion. The hemoglobulin increased significantly from 6.9 +/- 0.3 g/dl to 9.8 +/- 0.6 g/dl after subcutaneous rHuEPO treatment (p less than 0.01) at an average dose of 84 +/- 9 U/kg body weight/week. For the intraperitoneal group, despite a higher average rHuEPO dosage (133 +/- 7 U/kg body weight/week), the hemoglobin level was not significantly altered (7.0 +/- 0.4 g/dl to 8.0 +/- 0.4 g/dl, p less than 0.05). During the 16-week period of rHuEPO therapy, an increase in antihypertensive therapy was required more frequently in patients in the intraperitoneal group but the difference between groups failed to reach statistical significance. There was no conclusive evidence that the rise in hematocrit was an independent precipitant of hypertension. Patients who were hypertensive prior to rHuEPO therapy appeared most susceptible to the pressor effects in that 8 of 11 treated hypertensive patients required more intensive antihypertensive treatment during EPO administration whereas none of the untreated patients developed hypertension during the study (Fisher's exact test, p = 0.007). Plasma levels of the vasoactive hormones, atrial natriuretic peptide (ANP), plasma renin activity (PRA), and endothelin (ET) remained unchanged during both subcutaneous and intraperitoneal rHuEPO therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of subcutaneous and intraperitoneal administration of recombinant human erythropoietin on blood pressure and vasoactive hormones in patients on continuous ambulatory peritoneal dialysis. 182 43

The newborn infant is in a state of renal insufficiency with a glomerular filtration rate (GFR) as low as 20 ml/min per 1.73 m2 at term, and 10 ml/min per 1.73 m2 at 28 weeks of gestation. While the immature "insufficient" kidney can cope with most of the normal demands, its reserve is limited, and often overwhelmed by commonly occurring neonatal stresses. Various vasoactive systems such as the renin-angiotensin system, intrarenal adenosine, the prostaglandins and the atrial natriuretic peptide, are hyperactive in the neonatal period. Some of these systems appear crucial for the maintenance of GFR. Overstimulation of both angiotensin II and adenosine by an hypoxaemic stress can further impair the GFR, eventually leading to established renal failure. Inhibition of angiotensin II formation by the administration of angiotensin converting enzyme inhibitors can, on the other hand, also lead to renal failure. Prevention of these renal risks requires a precise knowledge of the newborn kidney physiology, physiopathology and pharmacology.
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PMID:Vasoactive factors in the immature kidney. 183 25

Plasma atrial natriuretic peptide (ANP) levels were measured in non-dialyzed and dialyzed chronic renal failure (CRF) patients and in normal subjects. Changes in plasma ANP in response to hemodialysis (HD) and to isolated ultrafiltration (UF) were also investigated in dialyzed CRF patients. Plasma ANP levels were significantly higher in 28 non-dialyzed CRF patients than in 27 normal subjects (mean +/- SEM, 174.0 +/- 25.9 vs 25.0 +/- 1.9 pg/ml, p less than 0.001). Plasma ANP levels did not correlate with blood urea nitrogen or serum creatinine, however patients with advanced renal failure (creatinine clearance less than 10 ml/min) with cardiomegaly (cardiothoracic ratio greater than 50%) or hypertension (BP greater than 140/90 mmHg) had significantly higher plasma ANP levels than those who were not. A 6-hour HD significantly decreased the plasma ANP level (423.4 +/- 71.3 to 220.6 +/- 40.0 pg/ml, p less than 0.001) and body weight in 21 dialyzed CRF patients, and the decrement in plasma ANP showed a positive correlation with the decrement in body weight (r = 0.425, p = 0.056). In 8 dialyzed CRF patients, we further performed a 1-hour isolated UF for removal of isoosmotic intravascular fluid without changes in the solute concentrations, followed by a subsequent 5-hour HD. The decrease in plasma ANP during the 1-hour UF period was 68% of the total ANP decrement for the whole 6-hour study. The average plasma ANP level was decreased with 94.6 +/- 42.5 pg/ml/kg/h in the UF period compared to 3.5 +/- 1.4 pg/ml/kg/h in the HD period (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma atrial natriuretic peptide in patients with chronic renal failure. 198 Dec 24

Since it remains unclear how the regulatory mechanism of blood pressure and volume is associated with the renin-angiotensin system, the sympathetic nervous system, and atrial natriuretic peptide (ANP), we examined the changes in blood pressure and vasoactive hormones occurring in 12 patients with end-stage renal failure. They were divided into two groups, those who were anuric (group A, n = 7), and those who had a daily urine volume of more than 700 ml (group B, n = 5). The changes in the mean blood pressure (MBP) and these vasoactive hormones were observed during hemodialysis with water removal in group A and without water removal in group B, and during blood pressure reduction with sodium nitroprusside in group A. The basal levels of ANP in groups A and B were twice as high as those of normotensive subjects. During hemodialysis, MBP did not reveal any changes in both groups. In group A, ANP and body weight (BW) decreased, whereas the plasma renin activity (PRA) and norepinephrine (NE) increased. In group B, ANP remained stable during the first 3 hr and decreased at the end of hemodialysis. However, BW, PRA, and NE were unchanged. In group A, significant correlations were observed between the changes in BW and those in ANP (r = 0.52, p less than 0.05), PRA (r = -0.57, p less than 0.01), and NE (r = -0.76, p less than 0.01). During blood pressure reduction, MBP decreased with accompanying increases in NE and PRA. However, ANP did not show any change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interrelationships among the renin-angiotensin system, sympathetic nervous system and atrial natriuretic peptide in end-stage renal failure. 214 72

We have developed and validated a two-site liquid-phase immunoradiometric assay (IRMA) of atrial natriuretic peptide (ANP) in unextracted human plasma. Both radiolabeled rabbit anti-ANP IgG and polyclonal mouse anti-ANP must bind to ANP for detection, and the assay is specific for peptides with both an intact C-terminus and a disulfide bridge. The assay sensitivity (detection limit) is 0.96 pmol/L, and the working range is 2.3-300 pmol/L, with the hook effect occurring above 500 pmol/L. Results for diluted plasma from normal subjects and from patients with renal failure paralleled the standard curve; analytical recovery of ANP added to such samples averaged 94%. The between- and within-assay CVs at 8 pmol/L were 10% and 5%, respectively. The assay is sufficiently sensitive and precise to detect the postural change in ANP concentrations in normal subjects.
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PMID:Immunoradiometric assay of atrial natriuretic peptide in unextracted plasma. 214 57

The aim of the study was the search for the correlation between the degree of impairment renal function (measured by creatinine clearance) and plasma concentration of atrial natriuretic peptide (ANP) and urinary fractional sodium excretion (FENa) in patients with chronic renal diseases. Forty seven patients were studied: 10 with diminished renal reserve (group I), 10 with renal insufficiency (group II), 27 with renal failure (group III) and 10 chronically haemodialysed before dialysis (group IV). Control group consisted of 27 healthy persons. All patients and controls were on the diet containing 100-120 mmol sodium daily. Plasma ANP levels were significantly higher in all groups of patients (I--16.5 +/- 5.7; II--40.7 +/- 18.6; III--86.2 +/- 49.9; IV--196.1 +/- 51.3 pmol/l, respectively) than in controls (10.8 +/- 6.0 pmol/l). A significant correlation (r = 0.85; p less than 0.01) between plasma ANP concentration and FENa was found when the patients from all groups were pooled together. The results confirm the important role of ANP in the adaptation of reduced kidney mass to the excretion of sodium load.
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PMID:[Plasma atrial natriuretic peptide level and urinary fractional sodium excretion (FENa) in patients with chronic renal failure]. 215 Nov 49


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