Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dopamine (DA) was infused in a dose of 2 micrograms/kg/min in 12 children and adolescents with chronic renal failure to test the vasodilatory reserve capacity of the kidney. Mean basal GFR and ERPF were 17.8 and 93.1 ml/min/1.73 m2, respectively. DA infusion had no significant influence on GFR but effective renal plasma flow (ERPF) increased by 14% (p less than 0.05). After DA, GFR did not correlate with ERPF. There was a significant increase in urinary sodium excretion (+22%). Sodium excretion correlated with osmotic clearance and urine flow rate with free water clearance. Plasma prolactin concentration was decreased (p less than 0.01), whereas noradrenaline, adrenaline and free dopamine increased significantly after DA. Plasma renin activity, aldosterone, arginine vasopressin and atrial natriuretic peptide levels remained unchanged. The data indicate that in pediatric patients with advanced renal failure DA fails to increase filtration capacity, whereas effective renal plasma flow and sodium excretion are stimulated. It is speculated that in this situation preglomerular and tubular renal functions regulated by dopamine receptors are better conserved than those affecting glomerular microcirculation.
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PMID:Effect of low-dose dopamine on kidney function and vasoactive hormones in pediatric patients with advanced renal failure. 362 87

Status epilepticus can lead to impaired renal function, which has been attributed to complications of myoglobinuria. We confirmed changes in renal function in the absence of myoglobinuria by measuring renal hemodynamics, fluid and electrolyte excretions, and plasma levels of renin and atrial natriuretic peptide (ANP) before and after a 30-min period of recurrent generalized seizures in anesthetized, paralyzed rats. Renal plasma flow (RPF), renal blood flow (RBF) and glomerular filtration rate (GFR) decreased by approximately 60% after seizures. In contrast, urinary sodium excretion, urine flow, and plasma ANP levels increased approximately threefold. Urinary potassium excretion and plasma renin levels were unchanged. Renal function is profoundly altered after 30 min of seizures, primarily due to intense renal vasoconstriction precipitating a dramatic reduction in GFR. The concomitant increases in sodium and urine excretion may be mediated by the marked increase in plasma ANP levels. The decreases in GFR and RBF might contribute to the renal failure observed in some patients after status epilepticus.
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PMID:Recurrent seizures alter renal function and plasma atrial natriuretic peptide levels in rats. 755 80

The ability of a 13 amino-acid analog of atrial natriuretic peptide (ANP), A68828, to prevent development of cisplatin toxicity was evaluated in a rat model. ANP (1 microgram/kg/min), A68828 (10 micrograms/kg/min), A68828 (50 micrograms/kg/min), or peptide buffer was given as an intravenous infusion over 1 h beginning 15 min prior to an infusion of 5 mg/kg cisplatin. Animals receiving cisplatin plus peptide buffer vehicle developed predictable renal failure, with mean plasma creatinine and blood urea nitrogen concentrations of 1.09 +/- 0.09 mg/dL and 50.13 +/- 5.96 mg/dL, 72 h after treatment. ANP and A68828 (10 micrograms/kg/min) attenuated the increase in these indices of nephrotoxicity (mean plasma creatinine 0.86 +/- .06 mg/dL and 0.76 +/- 0.11 mg/dL, respectively). Surprisingly, the higher dose of A68828 (50 micrograms/kg/min) did not reduce cisplatin nephrotoxicity (72-h plasma creatinine 1.61 +/- 0.34 mg/dL). These results indicate that a short-term infusion of ANP or the analog A68828 can reduce the severity of cisplatin toxicity. At high doses of A68828 the beneficial effects of treatment may be lost.
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PMID:Protection from cisplatin nephrotoxicity by A68828, an atrial natriuretic peptide. 764 62

Nephropathia epidemica (NE) with renal syndrome, caused by the Puumala-virus, is manifested clinically by the triad of fever, hemorrhage and renal failure. We observed raised plasma concentrations of endothelin-1 (ET-1) and atrial natriuretic peptide (ANP) in 23 patients during the acute phase of NE. They all developed transient renal failure and all displayed characteristics of NE, also verified by a rapid IgG antibody test. Blood pressure was normal or low in all subjects during the acute phase of the disease. Plasma ET-1 and ANP levels returned to normal following recovery one month later. The cause of increased ET-1 synthesis in NE remains unknown. It may be related to vascular damage or extravasation of blood. ET-1 may participate in the pathogenesis of acute renal failure of NE. Raised plasma ANP levels were most likely caused by fluid retention during the acute phase of NE. However, high levels of circulating ET-1 might have contributed to increased release of ANP.
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PMID:Raised plasma endothelin-1 concentration in patients with nephropathia epidemica. 790 Sep 44

Adrenomedullin is a potent hypotensive peptide newly discovered in pheochromocytoma tissue by monitoring its elevating activity on platelet cAMP. We measured plasma concentration of adrenomedullin in patients with essential hypertension and chronic renal failure. As compared with normal subjects, plasma adrenomedullin was increased by 26% (P < 0.05) in hypertensives without organ damage and by 45% (P < 0.005) in those with organ damage. The increase in plasma adrenomedullin was more prominent in renal failure than in hypertension. Renal failure patients with plasma creatinine of 1.5-3, 3-6, and > 6 mg/dl had higher plasma adrenomedullin levels than healthy subjects by 78% (P < 0.05), 131% (P < 0.001), and 214% (P < 0.001), respectively. Moreover, adrenomedullin showed intimate correlations with norepinephrine, atrial natriuretic peptide, and cAMP in plasma (r = 0.625, P < 0.001; r = 0.656, P < 0.001; and r = 0.462, P < 0.001; respectively). Thus, plasma adrenomedullin is supposed to increase in association with changes in sympathetic nervous activity and body fluid volume in hypertension and renal failure. Considering its potent vasodilator effect, adrenomedullin may be involved in the defense mechanism preserving the integrity of the cardiovascular system in these disorders.
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PMID:Plasma levels of adrenomedullin, a newly identified hypotensive peptide, in patients with hypertension and renal failure. 796 64

The vasoconstrictor peptide endothelin-1 (ET1) has only recently been characterized and its effects are at present largely speculative. It has been hypothesized that ET1 acts on mesangial cells to cause vasoactive changes which might ultimately contribute to the development of glomerulosclerosis. Opposite to ET1, nitric oxide (NO) inhibits mesangial cell contraction and proliferation. NO activates soluble guanylic acid cyclase and the final product, cyclic GMP (cGMP), has been recently used as a marker of NO action. Urinary levels of ET1 and cGMP were detected in 58 patients with biopsy-proven glomerulonephritis (GN), including 36 IgA nephropathy (IgAGN), 30 with normal and 6 with impaired renal function, 10 patients with non-IgA mesangial GN and 12 pts with membranous GN (MGN) with normal renal function. Compared to normal controls (0.019 +/- 0.006 ng/min), urine ET1 levels were significantly higher in patients with normal renal function having IgAGN (0.035 +/- 0.017, p < 0.01), MGN (0.028 +/- 0.013, p < 0.05), non-IgA mesangial GN (0.027 +/- 0.012, p < 0.05) and those with IgAGN and renal failure (0.032 +/- 0.011, p < 0.01). However no difference was found between MGN patients and normals by deleting MGN cases with mild to moderate mesangial proliferation. The mean value of urinary cGMP in IgAGN patients with renal failure (0.186 +/- 0.117 nmol/min) was lower (p < 0.05) than that of each group with normal renal function (IgAGN: 0.378 +/- 0.010 nM/min; MGN: 0.338 +/- 0.064 nmol/min, non-IgAGN: 0.436 +/- 0.168 nmol/min). The same significant differences were obtained by correcting cGMP values for creatinine urinary excretion. Urinary ET/cGMP ratio (assumed as an index of the relative balance between vasoconstrictor and vasorelaxing factors) was found to be higher than normal (0.570 +/- 0.010 ng/nmol) both in IgAGN patients with normal renal function (0.103 +/- 0.064 ng/mol, p < 0.05), and in those with renal failure (0.203 +/- 0.108 ng/nmol, p < 0.02). Urinary cGMP values were not related to plasma levels of atrial natriuretic peptide (ANP). These data show that hyperexcretion of ET1 occurs in a number of patients with mesangial proliferative GN. In some of them, mainly those with established glomerular damage, the local production of ET1 is not counter-balanced by adequate cGMP biosynthesis.
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PMID:Urinary endothelin in glomerulonephritis patients with normal renal function. 807 34

The present study aimed to investigate whether brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), cortisol and thyroid hormone concentrations change during hemodialysis in patients with chronic renal failure. Blood samples were withdrawn in 30 patients with chronic renal failure before hemodialysis, 2 hours after the beginning and at the end of hemodialysis. ANP and BNP concentrations were determined by radioimmunoassay after Sep Pak C18 extraction. Cortisol, T3, T4, FT4 and TSH serum concentrations were measured by enzyme immunoassay. BNP and ANP plasma levels were strongly elevated in patients with renal failure (BNP 22.4 fold, ANP 4.7 fold versus controls [n = 20]) and decreased significantly (p < 0.001) during hemodialysis (BNP [pg/ml]: 192.1 +/- 24.9, 178.6 +/- 23.0, 167.2 +/- 21.8; ANP [pg/ml]: 240.2 +/- 28.7, 166.7 +/- 21.3, 133.0 +/- 15.5). BNP plasma concentrations showed a stronger elevation than ANP plasma levels and a less pronounced decrease during hemodialysis (BNP: 13.5 +/- 1.8%, ANP: 40.2 +/- 3.5%, p < 0.001) which might in part be due to the longer half-life of BNP. Cortisol and TSH levels did not change significantly whereas T3, T4 and FT4 levels increased significantly (p < 0.001) during hemodialysis. Since corticosteroids and thyroid hormones stimulate natriuretic peptide release, these data suggest that the dialysis-induced decrease of ANP and BNP plasma concentrations is not augmented by a loss of cortisol or thyroid hormones during hemodialysis. The present data provide support that BNP and ANP plasma concentrations are sensitive indicators of the extracellular fluid volume status.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in brain natriuretic peptide and atrial natriuretic peptide plasma concentrations during hemodialysis in patients with chronic renal failure. 807 9

The common underlying heart diseases were ischemic heart disease (39%), valvular heart disease (27%), hypertensive heart disease (10%) in 104 patients (mean age 79 yrs) with congestive heart failure (CHF). Cardiomyopathy (5%) and congenital heart disease (2%) such as atrial septal defect were less common. In addition, many extracardiac diseases including anemia, hypothyroidism, renal failure and pulmonary disease contributed to the etiology of CHF in the elderly. Cardiac amyloidosis should be considered as an uncommon cause of refractory CHF. While the precipitating factor was not found in half of the 104 patients with CHF, the most common factors were respiratory infection, myocardial ischemia and arrhythmia. In addition, inappropriate drug usage including poor drug compliance, the use of beta-blockers and excessive intake of sodium and fluid precipitated or exacerbated heart failure. Renal failure was a most important complication and predisposed to refractory CHF. Aged patients with mild CHF (NYHA class II) showed an insufficient production of cyclic AMP and GMP in proportion to the increases of norepinephrine and atrial natriuretic peptide in comparison with health aged subjects after the submaximal treadmill exercise test. This finding may suggest that an inadequate compensation of neurohumoral factors is prone to cause CHF in the elderly. Appropriate management of acute CHF in the elderly begins with recognition of the underlying heart disease, complications and the severity of cardiac function. In addition to medical management including loop diuretics, vasodilator, beta-receptor agonist and phosphodiesterase inhibitor, cases associated with respiratory and renal failure require mechanical ventilation and continuous hemofiltration.
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PMID:[The etiology and management of congestive heart failure in the elderly]. 820 67

The major stimulus for atrial natriuretic peptide (ANP) release is atrial stretch and increased values are observed in volume overload states such as chronic renal failure. Since successful kidney transplantation restores volume homeostasis, we compared the effects of human cadaveric kidney transplantation on time course and changes of plasma ANP in the early postoperative period in 4 patients with successful and 4 patients with failed transplantation. ANP concentrations were elevated before transplantation in both groups (91 +/- 16 and 70 +/- 32 pmol/l) and decreased after successful (50 +/- 27 pmol/l, day 16) but increased after failed transplantation (146 +/- 45 pmol/l, day 16). Moreover, there was a close correlation between changes of body weight and ANP concentrations. Plasma renin activity decreased and plasma noradrenaline increased non-significantly in both groups, the latter more so after failed transplantation (116 +/- 42 to 194 +/- 156 vs 156 +/- 157 to 425 +/- 287 ng/l). No correlation was found between changes of renin activity or plasma catecholamines and ANP concentrations. The results indicate that the mechanisms governing release of atrial natriuretic peptide are operative in patients with chronic end-stage renal failure and after successful kidney transplantation with a return of atrial natriuretic peptide concentrations towards normal in the latter.
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PMID:Atrial natriuretic peptide release and volume regulation following kidney transplantation. 822 78

The changes in blood volume (BV), atrial natriuretic peptide (ANP), plasma renin activity (PRA), aldosterone (Aldo), norepinephrine (NE), epinephrine (Epi), parathyroid hormone (PTH), arginine vasopressin (AVP) and the cyclic nucleotides cAMP and cGMP were measured during a fluctuating BV cycle in 15 patients with end-stage renal failure maintained on chronic hemodialysis (HD). HD consisted of 4 periods of about 60 min each. The first half of each HD period consisted of ultrafiltration (UF) greater than 1,000 ml/h, and the second half consisted of no UF. Changes in relative BV were measured using continuous hemoglobinometry. Total BV at the end of treatment was 74.3 +/- 6.9% of the pretreatment volume. A significant positive correlation between BV and the levels of ANP, PTH, Epi and cGMP and an inverse correlation between BV and PRA, Aldo, AVP and NE were demonstrated. While mean values of NE and AVP levels were directly related to actual changes in BV, individual values did not homogeneously reflect this relationship. The cyclic nucleotides cGMP and cAMP did not follow immediate BV changes, but showed a significant decrease correlated with diminished BV. Based on a pre-postdialysis analysis, significant changes in PRA and Aldo were missing. It seems possible that vascular stability in dialysis patients may be maintained by the response of NE and AVP, and not by the renin-aldosterone system. The changes in ANP and cGMP values correlated most significantly (r = 0.38 and r = 0.51, p < 0.005) with the changes in BV, but no single variable could explain the blood pressure regulation during HD with intermittent rapid UF.
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PMID:Response of vasoactive substances to intermittent ultrafiltration in normotensive hemodialysis patients. 824 91


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