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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentrations of urea, urate, phosphate and creatinine were measured in the plasma of 30 consecutive patients admitted acutely with heart failure. On admission, 20 had a raised plasma urea, 21 had a raised plasma urate, but only 6 had a raised plasma phosphate and only 6 had a raised plasma creatinine. A further 9 of the patients developed a raised plasma urea after admission. The increase in plasma urea present on admission was greater than expected for the fall in GFR (as indicated by the increase in plasma creatinine). The results for plasma and urine taken together suggest that a major cause of the raised plasma urea was an increased urea production rather than a reduced glomerular filtration rate. There was no obvious relationship between plasma urea and clinical features, or diuretic therapy.
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PMID:The cause of the raised plasma urea of acute heart failure. 43 64

The effects of ticrynafen (250-500 mg) on salt-water and uric acid metabolism have been studied in 18 patients with no haemodinamic abnormalities or salt-water repletion (cardiac failure, oedema). The main results are: -- an effective natriuresis is observed in the first days and is attenuated thereafter. In subjects with a reduced GFR, a negative salt balance is obtained altough the volume of diuresis is not significantly increased. -- The potassium loss is variable according to dosage (maximum at 500 mg), renal function (low when reduced). -- The increase of urinary uric acid excretion and the lowering of blood uric acid concentration are rapid and prolonged. In conclusion, we confirm the effective natriuretic and uricosuric properties of ticrynafen.
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PMID:[Thienylic acid, a new drug with saluretic and uricosuric activity. Preliminary data]. 74 34

Recent studies indicate that endothelin (ET), a potent endogenous systemic and renal vasoconstrictor peptide, may mediate decreases in GFR in models of acute renal dysfunction. Moreover, in an animal model of radiocontrast-induced nephropathy (RCIN), it was recently demonstrated that early renal hemodynamic responses to radiocontrast are attenuated by intra-arterial atrial natriuretic factor (ANF), which prevents subsequent RCIN. The studies presented here were therefore designed to determine whether i.v. infusion of radiocontrast produces increases in endogenous plasma and urinary ET and whether these responses are modulated by intra-arterial ANF in an animal model of RCIN. In these studies, dogs with pacing-induced heart failure received i.v. radiocontrast in the presence and absence of an intra-aortic infusion of ANF. Significant increases in both plasma and urinary ET were observed during and after radiocontrast. Although coadministration of ANF did not prevent increases in plasma and urinary ET, ANF preserved renal function acutely in this model of RCIN by increasing GFR above baseline levels.
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PMID:Radiocontrast increases plasma and urinary endothelin. 183 65

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29

Isosorbit 5-mononitrate is useful in ischaemic heart disease and in cardiac failure because of its favourable pharmacokinetic properties, in particular the absence of the so-called first pass effect, the great biological availability and long elimination time. The authors demonstrated on the preparation Elentan long, Schwarz Monheim GFR, which contains 50 mg isosorbit 5-mononitrate the improved efficiency of the left ventricle after three months administration to 15 patients with confirmed ischaemic heart disease, by exerting a favourable effect on the diastolic, systolic and global left ventricular function. Nitrates are drugs of first choice in some forms of ischaemic heart disease and are also effective in cardiac failure because they exert a marked effect on some cardiac functions on which the efficiency of the left ventricle depends. Elentan long proved, while using simple dosage, a preparation with favourable characteristics as regards biological availability and nitrate tolerance.
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PMID:[Effectiveness of the delayed-action form of isosorbide 5-mononitrate in ischemic heart disease]. 203 13

The RAS is part of an extremely powerful feedback system for long-term control of arterial pressure and volume homeostasis as illustrated in Figure 4. Disturbances that tend to lower blood pressure such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due in large part to the combined actions of ANGII and reduced renal perfusion pressure. In response to disturbances such as high sodium intake, suppression of ANGII greatly amplifies the effectiveness of the basic pressure natriuresis and diuresis mechanism, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium-water retaining effects of ANGII necessitate increased blood pressure to maintain sodium and water balance via pressure natriuresis. The sodium retaining actions of the RAS are mediated by intrarenal as well as extrarenal mechanisms. The intrarenal actions of ANGII include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles which increases tubular reabsorption by altering peritubular capillary physical forces. The constrictor action of ANGII on efferent arterioles also plays an important role in stabilizing GFR and therefore in preventing fluctuations in excretion of metabolic waste products that depend upon a high GFR for excretion. ANGII is known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-renal effect of ANGII which influences sodium excretion is stimulation of aldosterone secretion. Current evidence, however, suggests that the various intrarenal actions of ANGII are quantitatively more important in causing sodium retention than those mediated by changes in aldosterone secretion. However, the combined intrarenal and extrarenal actions of ANGII on sodium reabsorption provide the body with one of its most potent feedback systems for long-term regulation of body fluid volumes and arterial pressure.
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PMID:Role of the renin-angiotensin system in control of sodium excretion and arterial pressure. 222 Apr 9

Twenty-five years after the discoveries of the existence of atrial granules and of volume receptors in the heart atria the search for natriuretic hormones has led to the isolation and identification of the atrial natriuretic factors (ANF) now considered as a hormonal system. These peptides are probably synthesized and stored in the Golgi apparatus of cardiac myocytes and are released in response to atrial wall stretch following acute plasma volume expansion and increased central blood volume, e.g., during head-out water immersion, in arterial hypertension, or increased left and/or right atrial pressure in cardiac failure, but also possibly in response to increased frequency of myocardial contractions, e.g. in paroxysmal tachycardia. The mechanisms of the renal action of these potent natriuretic hormones are not yet precisely known. Increased GFR may contribute to the initial rise in urinary sodium excretion and increased renal medullary blood flow to the later phase of natriuresis. The proximal tubule, the thin descending and the ascending limb of Henle's loop and especially the medullary collecting tubule were so far incriminated as tubular sites of action of ANF. Finally, recycling of sodium in medullary tissue and secretion of sodium via back-flux from the interstitium into the medullary collecting tubule are postulated to result in the hypernatric urine observed after ANF administration. Direct suppression of the secretion of renin, aldosterone, vasopressin, and vasopressin-stimulated cAMP synthesis may also contribute to its diuretic, natriuretic, and antihypertensive effects. The renal hemodynamic and tubular as well as the adrenal and systemic vascular effects are related to enhanced cGMP synthesis in medium-sized arterial vessels, in glomeruli and specific tubular segments, and in adrenal tissue, and may be calcium dependent. Specific ANF-binding sites were detected in these target organs. Although increased ANF release was observed in response to atrial distension in various disease states, which may contribute to renal sodium elimination in human hypertension and congestive heart failure, further studies are needed to identify its precise physiological and pathophysiological significance.
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PMID:Atrial natriuretic hormones--thirty years after the discovery of atrial volume receptors. 294 41

The dopamine alpha- and beta-adrenoceptor dose-response curves are investigated in four patients who are exempt from cardiovascular disease. A dose-related increase in CO, HR and SV is observed with infusion rates of up to 3 micrograms kg-1 min-1. With concentrations greater than 10 micrograms kg-1 min-1, both BP and SVR increase. Low-dose dopamine infusion less than 3 micrograms kg-1 min-1 is investigated in ten other patients. With this infusion rate, a selective renal vasodilation is induced without peripheral or cardiac beta-adrenoceptor activation. Dopamine is responsible for an increase in diuresis FENa, GFR and RBF. These properties are indicated in renal failure, and when haemodynamic support is required in cardiac failure, if an infusion rate of up to 10 micrograms kg-1 min-1 is able to reverse cardiac insufficiency.
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PMID:The use of low doses of dopamine in intensive care medicine. 608 36

Fractional dextran clearances (theta D) were used to ascertain whether the albuminuria accompanying cardiac failure (CF) has a hemodynamic basis. In 17 patients with grade-IV CF in whom GFR and effective renal plasma flow (ERPF) were depressed to 58 +/- 7 and 215 +/- 20 ml/min/1.73 m2, respectively, theta D was elevated relative to normal control subjects over the Stokes-Einstein radius (r) interval of 28 to 46 Angstrom. For dextran of equivalent size to albumin (r = 36 Angstrom), the rate of urinary excretion (UD36V) was not increased because elevated theta D36 was offset by the depressed GFR. In contrast, urinary albumin excretion (UalbV) was increased to 82 +/- 35 microgram/min. Thus, for albuminuria in CF to have the hemodynamic basis suggested by elevation of theta D requires that (I) the fractional clearance for anionic albumin be disproportionately enhanced relative to uncharged dextran by reduced glomerular plasma flow and/or (2) that glomerular electrostatic barrier function be impaired in CF. In seven patients with minimal change nephropathy, UD36V was similar to that in CF, but UalbV was 40 times greater than that in CF. Thus, if glomerular electrostatic barrier function is impaired in CF, such dysfunction is trivial by comparison with minimal change nephropathy.
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PMID:Albuminuria and the permselective properties of the glomerulus in cardiac failure. 739 24

We investigated the rate of decline in GFR and the changing prevalences of micro- and macrovascular complications in 20 type II diabetic patients [mean age 58 (46-71) years, female:male = 7:13, duration of diabetes 16 (12-30) years] from the stage of macroproteinuria with GFRs which were still normal until the beginning of dialysis or the time of death. Controls of renal function, proteinuria, HbAlc, serum lipids, and blood pressure were performed every 6 months at the beginning of the study and later on at 3-month intervals. Fundoscopy, electrocardiogram at rest and in case of need a symptom-limited treadmill ECG, a Duplex ultrasound examination of the carotid vessels, and a Doppler sonographic examination of the femoral arteries were repeated each year. The creatinine clearance (mean +/- SD) of the patients was 81 +/- 6 mL/min/1.73 m2 at the beginning of the study. The rate of decline in creatinine clearance was 1.01 +/- 0.38 mL/min/month during the whole period of observation. Twelve patients (group A) required dialysis after a mean time of 74 (40-119) months; their creatinine clearance was 7 +/- 2 mL/min/month at the beginning of renal replacement therapy. Eight patients (group B) died a short time before the beginning of dialysis treatment; their creatinine clearance was 13 +/- 5 mL/min/1.73 m2. The causes of death were sudden death (n = 4), cardiac failure (n = 1), and stroke (n = 2); in one case it was unknown. The two patient groups did not differ in respect to the mean age, duration of diabetes, HbAlc values, serum cholesterol levels, and blood pressure. The decline in the creatinine clearance was also similar in both patient groups, with 1.07 +/- 0.35 versus 0.98 +/- 0.41 mL/min/month. Only the mean serum triglyceride concentration was significantly higher in the patients who died before dialysis. At the start of the study, cerebrovascular disturbances (including plaques in the carotid vessels) were found in 30%, cardiovascular disturbances (including pathologic ECG findings) in 45%, a peripheral vascular disease in 15%, and diabetic retinopathy (grade I and II) in 75%. At the beginning of dialysis treatment or the time of death, respectively, the prevalence of cerebrovascular diseases was increased to 70% and the prevalence of cardiovascular diseases to 90%; peripheral vascular disease was present in 50% and diabetic retinopathy in all of the cases. We conclude that type II diabetic patients show high mortality (40%) and poor quality of life, not only when they require dialysis treatment, but also in the predialysis phase.
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PMID:High mortality and poor quality of life during predialysis period in type II diabetic patients with diabetic nephropathy. 804 65


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