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

Renal function was evaluated in 104 patients with severe chronic heart failure whom we treated with captopril or enalapril. Seventy patients showed no change or an improvement in renal function (group A), and 34 patients developed functional renal insufficiency (group B). Before converting-enzyme inhibition, group B patients received higher doses of furosemide (p less than 0.02) and had lower central venous pressures (p less than 0.05) than group A patients. After 1 to 3 months of converting-enzyme inhibition, an excessive reduction in left ventricular filling pressure (to less than 15 mm Hg) or mean arterial pressure (to less than 60 mm Hg) was noted in 28 of 34 (82%) patients in group B but in only 22 of 70 patients in group A (31%) (p less than 0.001). At the end of the study, drug-induced azotemia resolved after a reduction in the dosage of diuretics, despite unaltered treatment with captopril and enalapril. Hence, the deterioration of renal function after converting-enzyme inhibition in heart failure is not a toxic or immunologic reaction to therapy but results from specific hemodynamic events that can be ameliorated by sodium repletion.
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PMID:Functional renal insufficiency during long-term therapy with captopril and enalapril in severe chronic heart failure. 302 21

Compensatory mechanisms such as systemic vasoconstriction and sodium retention are activated to various degrees in patients with congestive heart failure (CHF). The renin-angiotensin system (RAS) mediates many of these compensatory responses. Increased angiotensin can result in net vasoconstriction and increase afterload. In addition, it contributes to the avid sodium retention that occurs in patients with CHF. The RAS promotes sodium retention by enhancing proximal tubular reabsorption of sodium and water through changes in intrarenal hemodynamics. In addition, the direct renal tubular influence of angiotensin II and aldosterone contribute to sodium retention. In experimental heart failure in the rat, angiotensin activation leads to reduction in effective plasma flow whereas the glomerular filtration rate was unchanged. In clinical CHF, activation of the RAS may also contribute to azotemia in patients with CHF. Significant correlations between serum creatinine levels and plasma renin activity have been observed. Furthermore, renal plasma flow and the glomerular filtration rate frequently improve after therapy with converting-enzyme inhibitors (CEIs). Occasionally, however, CEIs may produce an excessive fall in systemic BP and, hence, renal perfusion pressure, which may overcome autoregulatory mechanisms and contribute to a deterioration in renal function. CEIs enhance the effectiveness of furosemide in promoting natriuresis and correction of hyponatremia. Diuretic-induced hypokalemia can also be corrected by angiotensin-converting enzyme (ACE) inhibitors due to blockade of aldosterone production. On the basis of these results, we recommend titration of the ACE inhibitors' dose to minimize hypotension and the concurrent use of furosemide in patients with CHF receiving ACE inhibitors, especially for those in whom azotemia, hyponatremia, and hypokalemia complicate the course.
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PMID:Renal effects of angiotensin-converting enzyme inhibition in cardiac failure. 303 93

We use extracorporeal membrane oxygenation (ECMO) to treat respiratory and cardiac failure in children who are unresponsive to standard ventilator and pharmacologic management. All patients have cardiac and abdominal ultrasonography prior to ECMO to identify major structural anomalies and anatomically normal kidneys. Despite this, oliguric renal failure is seen in a number of patients. Acute renal failure (ARF) developed in two of the first 20 patients we placed on ECMO and both of these patients died. Six of the last 27 patients (22%) also developed ARF and were treated with continuous hemofiltration (CH) placed in-line with the extracorporeal circuit. The technique of CH removes plasma water and dissolved solutes while retaining proteins and cellular components of the intravascular space. The duration of CH ranged from 9 to 112 hours (mean 57.5 hours). Indications for CH were hypervolemia, hyperkalemia, and azotemia. The mean serum potassium prior to CH was 5.6 (range 4.3 to 7.0) compared with 4.5 after filtration. We filtered 5 to 10 mL/kg/h and replaced it with crystalloid chosen on the basis of serum and filtrate electrolytes. These six patients had a 33% mean weight gain prior to CH. We were able to remove as much as 2,200 g in the most edematous patient with significant improvement in cardiopulmonary status. Four of the patients on CH died of their primary pulmonary or cardiac disease without specific problems related to ARF. The other two patients were successfully weaned from ECMO, extubated, and have not needed further therapy for renal failure. We conclude that CH is useful in managing the complications of oliguric renal failure during ECMO.
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PMID:Experience with renal failure during extracorporeal membrane oxygenation: treatment with continuous hemofiltration. 364 94

A 37-year-old woman with longstanding systemic lupus erythematosus developed cardiac insufficiency, nephrotic syndrome, and azotemia. The findings at echocardiography and cardiac scintigraphy suggested amyloidosis, which was confirmed by rectal biopsy and fine needle biopsy of subcutaneous abdominal fat. Postmortem examination revealed systemic amyloidosis with massive deposits in the heart, spleen and kidneys. She had persistently increased concentration of serum amyloid A protein during the last 4 years of her life, and her amyloidosis was of the secondary (AA) type, as shown by immunohistochemical studies.
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PMID:AA amyloidosis in systemic lupus erythematosus. 366 91

A 20-year-old woman presented with malignant hypertension, pulmonary edema, anemia, and azotemia. Blood pressure was adequately controlled only after progressively more intensive drug regimens, finally including minoxidil, nadolol, and furosemide. On these drugs, the patient developed progressive left and right heart failure, anasarca, and malnutrition. The control of hypertension, heart failure, and fluid retention, was accomplished by administration of captopril and furosemide. Captopril is a logical alternative to vasodilators in refractory hypertension complicated by congestive heart failure.
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PMID:Efficacy of captopril in relieving congestive heart failure developing during management of hypertension. Case report. 634 Dec 22

In most normal subjects, the fractional excretion of sodium is usually less than 1 percent but may be raised with an increase in salt intake. In acutely azotemic patients, a low fractional excretion of sodium usually indicates a prerenal process that is responsive to volume repletion. However, such a low fractional excretion of sodium also can be seen with azotemia due to hepatic or cardiac failure, as well as acute glomerulonephritis, pigment nephropathy, contrast nephrotoxicity, polyuric renal failure associated with burns, acute obstruction, renal transplant rejection, and occasionally non-oliguric acute renal failure, none of which is a volume-responsive process. A fractional excretion greater than 1 percent in acutely azotemic patients usually indicates intrinsic renal injury, but is consistent with volume depletion in patients receiving diuretics or in some patients with chronic renal insufficiency. Similarly, a low quotient in acute renal parenchymal injury is usually interpreted to indicate widespread tubular integrity, but is consistent with several different pathophysiologic processes. The fractional excretion of sodium must be interpreted in light of the specific clinical setting and other laboratory data to be useful in patient management.
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PMID:Interpreting the fractional excretion of sodium. 648 45

Captopril, furosemide, and a sodium-restricted diet were administered to 6 normal dogs and 10 dogs with congestive heart failure. Serum electrolyte concentrations and renal function were monitored in both groups. In the normal dogs, no clinically meaningful changes in serum electrolyte, urea nitrogen, or creatinine concentrations developed during therapy with a sodium-restricted diet and 4 weeks each of furosemide alone, captopril alone, or furosemide plus captopril. Three of 6 normal dogs on furosemide and a sodium-restricted diet had at least one serum potassium concentration above the reference range during the 4 weeks of observation. One normal dog on captopril, furosemide, and a sodium-restricted diet developed azotemia, and 2 dogs had serum potassium concentrations above the reference range during the 4 weeks of observation. Ten dogs with congestive heart failure were treated with captopril, furosemide, a sodium-restricted diet, and digoxin. Etiopathogenesis of the heart failure included valvular insufficiency (n = 6), dilated cardiomyopathy (n = 3), and dilated cardiomyopathy and dirofilariasis (n = 1). Serum electrolyte concentrations and renal function were monitored for 5 consecutive weeks in 7 of the 10 dogs and for 17 weeks or longer in 6. Two dogs were euthanized after 4 weeks because of acute decompensation of heart failure, and one dog developed severe azotemia and uremia. Six of 10 dogs with congestive heart failure had at least one serum potassium concentration above the reference range sometime during the 5 weeks of observation, although the changes in the mean serum potassium concentrations were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of combined therapy with captopril, furosemide, and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure. 783 9

Since only oral preparations of captopril are clinically available, intravenous captopril was studied in 10 patients with mild heart failure and in 20 severe. The results showed that intravenous captopril may rapidly reduce cardiac preload and afterload, increase cardiac output, inhibit renin-angiotensin-aldosterone system, and depress plasma levels of catecholamine. After captopril infusion, a rapid symptomatic improvement occurred and the infusion could be well tolerated in patients with acute or severe heart failure. In addition, reversing hyponatremia and hypokalemia or improving azotemia may benefit the patients with acute or severe heart failure.
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PMID:Symptomatic hemodynamic and hormonal effects of intravenous captopril in patients with heart failure. 792 73

Systolic dysfunction of the heart represents a state of "prerenal" azotemia, in which the excess of total body salt and water is redistributed to venous and interstitial fluid compartments. This results in a diminished effective circulating blood volume and thereby decreases tissue perfusion. The kidneys perceive the ineffective circulating volume and employ a complex series of interconnected hemodynamic and neurohumoral effector mechanisms to restore "adequate" perfusion. This is done by reclaiming a greater fraction of filtered sodium and water and elevating systemic vascular resistance to keep perfusion pressure to vital organs constant despite diminished cardiac output. Knowledge of the physiologic compensatory responses that occur in the kidneys of heart failure patients allows clinicians to develop a logical treatment plan. This knowledge should also help avoid a therapeutic misadventure by making it possible to exclude drugs known to adversely affect renal function in patients with a failing heart and poorly compensating kidneys.
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PMID:Renal adaptation to the failing heart. Avoiding a 'therapeutic misadventure'. 820 20

Management of congestive heart failure in the past has focused on sodium and fluid restriction, rest, and digitalis glycosides. Now, significant new evidence justifies early and aggressive ACE inhibitor therapy in patients with asymptomatic or mildly symptomatic LV dysfunction. ACE inhibitors reduce the likelihood of symptomatic heart failure in asymptomatic patients with reduced ejection fraction. Patients with reduced LV function following acute MI who receive ACE inhibitors have a decreased risk of death, a lower probability of developing systematic heart failure, and fewer MI recurrences. Hypotension and azotemia can be avoided by reducing the concomitant dose of diuretics and carefully titrating the ACE inhibitor dosage to target levels.
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PMID:Mild heart failure: why the switch to ACE inhibitors? 822 26


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