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Query: UMLS:C0018801 (heart failure)
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During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.
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PMID:Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. 131 66

Heart transplantation represents a widely accepted therapeutic modality for patients with end-stage myocardial failure. With increasing experience, 1-year survival rates of over 75% and 5-year survival rates of over 60% have been achieved, mainly due to patient selection, standardized surgical techniques as well as improved postoperative management. During early follow-up, particular attention should focus on diagnosis and treatment of graft rejection and infection, which require individualized immunosuppression, while in the later postoperative course coronary atherosclerosis, hypertension, chronic renal insufficiency and malignancy become more important as potential complications. The general principles in the management of these patients are discussed.
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PMID:[Heart transplantation--postoperative management]. 330 15

Captopril, an inhibitor of the conversion enzyme, is a medication with a known efficacy in the treatment of arterial hypertension and congestive cardiac insufficiency. Its side-effects are few. Among them, agranulocytosis is a severe complication, all the more severe and frequent as it occurs in patients with chronic renal insufficiency, collagen disease, or patient treated with medication having a leucopenic potential. Our case reports an agranulocytosis secondary to captopril in a patient with cardiac insufficiency presenting none of these aggravating factors. The mechanism of agranulocytosis secondary to captopril remains currently debatable, but does not seem, in the present case, to be dose related. Thus, a captopril prescription must comply with certain rules; decrease of the dosage in case of renal insufficiency, usual precautions in patients with collagene diseases. The association to a medication with leucopenic potential is to be avoided. Hematologic monitoring will be adapted to each particular case.
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PMID:[Agranulocytosis caused by captopril]. 354 68

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

The frequency and degree of circulatory insufficiency depending on the stage of the disease are analyzed in 404 patients with chronic glomerulonephritis and 145 patients with chronic pyelonephritis aged 15 to 74 years. When the renal function is still preserved different degrees of circulatory insufficiency are diagnosed in 29.4% of patients. Circulatory insufficiency complicates more often chronic glomerulonephritis than pyelonephritis and is more common in the aged. Latent cardiac insufficiency is more common. In the period of chronic renal insufficiency cardiac decompensation is seen in 78.1% of cases, its frequency is practically the same in glomerulonephritis and pyelonephritis. The mechanisms of development of cardiac insufficiency and the principles of treatment depending on the functional state of the kidneys are discussed.
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PMID:[Circulatory failure in chronic glomerulo- and pyelonephritis]. 712 Jul 48

The authors share their results from the studies on the incidence and characteristic of hypertonic syndrome in 132 patients with chronic glomerulonephritis (ChGN). In that random group, 65.1 per cent had renoparenchymal hypertension (RPH), 34.8 per cent of the patients had RPH among the patients with normal renal function, and with various degrees of chronic renal insufficiency (ChRI) - 95.4 per cent. In 69 patients, the diagnosis was confirmed by puncture biopsy, with a predomination of membranous, membranous-proliferative, IgA and endoproliferative ChGN. With the exception of IgA nephritis, RPH in the rest is found relatively often even in the absence of ChRI. The symptomatics of RPH was relatively poor--most frequently the patients complained of headache--in 48 per cent but patients with ChGN without RPH also had the same complaints--26 per cent. Complaints as dizziness, tinnitus and insomnia were rare. The hypertension was with a short duration (according to anamnestic data)--in 2/3 less than three years and 40 per cent of the patients had hypertonic crises or/and acute left cardiac insufficiency in spite of the relatively little alterations in ECG and fundus of the eye. Those were mainly patients with advanced ChRI. The authors lay stress upon the necessity of complex treatment of renal insufficiency and of hypertension with a view to the improvement of the prognosis of those patients.
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PMID:[Incidence and characteristics of the hypertension syndrome in chronic glomerulonephritis]. 716 7

A 35-year-old hypertensive man presented with chronic renal insufficiency, congestive heart failure, and refractory hypotension. He had metabolic acidosis and profound hypocalcemia. Left ventricular function and blood pressure worsened after intravenous infusion of saline and bicarbonate, but improved dramatically after intravenous calcium administration. This case illustrates that hypocalcemia is a cause of refractory hypotension and heart failure.
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PMID:Refractory hypotension associated with hypocalcemia and renal disease. 812 46

Fosinopril is the prodrug of the active diacid ACE inhibitor fosinoprilat. In patients with heart failure, fosinopril reduces pulmonary capillary wedge pressure, mean arterial blood pressure, mean right atrial pressure and heart rate, and increases stroke volume index and cardiac index. The drug has compensatory dual elimination routes via renal and hepatic systems and accumulates to a lesser extent than enalapril and lisinopril in patients with chronic renal insufficiency with or without heart failure. Comparative studies of 3 or 6 months' duration with fosinopril 10 to 40 mg/day have demonstrated clinical efficacy significantly superior to that of placebo in patients with heart failure [mostly New York Heart Association (NYHA) functional class II or III]. Fosinopril treatment consistently increased exercise duration and improved heart failure symptoms in these patients. Significantly fewer fosinopril than placebo recipients withdrew or were hospitalised because of worsening heart failure. Additionally, significantly more fosinopril than placebo recipients showed improvement, and fewer patients had deteriorated, in terms of NYHA functional class. Fosinopril and enalapril showed similar clinical efficacy over 6 and 12 months' treatment in patients with NYHA functional class II to IV heart failure. As yet, there are no data showing a mortality benefit with fosinopril. Fosinopril was well tolerated in clinical trials in patients with heart failure. Dizziness (11.9 vs 5.4% for placebo), cough (9.7 vs 5.1%) and hypotension (4.4 vs 0.8%) were the most commonly reported adverse events. In 6- or 12-month comparative studies, fosinopril therapy was associated with a lower incidence of dizziness and hypotension, but a higher incidence of vertigo, than enalapril therapy. 0.8% of patients discontinued the drug because of cough, which occurred to a similar extent with fosinopril and enalapril. Thus, based on available clinical evidence, fosinopril is an effective and well tolerated option for the management of patients with heart failure. Although clinical data are limited, fosinopril may be especially useful in patients with renal or hepatic impairment.
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PMID:Fosinopril. A review of its pharmacology and clinical efficacy in the management of heart failure. 921 Oct 84

Essential hypertension and congestive heart failure (CHF) are examples of cardiovascular disorders that may cause renal failure, although sometimes a primary kidney defect may lead to hypertension. Renal damage in malignant and severe hypertension is dramatic, extensive, and rapidly progressive, although nephrosclerotic damage, which develops slowly and appears late in hypertension, is a rare cause of morbidity because mild to moderate hypertension is now the most common form. However, the incidence of end-stage renal failure associated with hypertension is markedly increasing, perhaps because of underdiagnosis of renal damage in hypertension, insufficient lowering of blood pressure in clinical practice, or inability of antihypertensive drugs to lower blood pressure sufficiently to preserve the kidney, a goal that may need specific drugs that act, for example, on the renin-angiotensin system (RAS). Renal vasoconstriction and reduction of renal blood flow are early companions of cardiac insufficiency and may be involved in the development of sodium and water retention. Profound reduction of cardiac output and arterial hypotension in severe CHF may lead to acute renal failure. Chronic renal insufficiency is associated with elevated cardiovascular morbidity and mortality. Renal impairment is often caused by a disease process, such as diabetes mellitus, that involves both the cardiovascular system and the kidney. When the primary disease is renal, possible reasons for an association include renal-dependent increase in blood pressure, activation of the RAS, overproduction of other vasoactive substances of renal origin, and electrolyte imbalances leading to fatal arrhythmias.
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PMID:Cardiovascular disease and the kidney: an epidemiologic overview. 1002 46

We report the case of a 70-year-old hypertensive man with a solitary kidney and chronic renal insufficiency who developed two episodes of transient anuria after losartan administration. He was hospitalized for a myocardial infarction with pulmonary edema, treated with high-dose diuretics. Due to severe systolic dysfunction losartan was prescribed. Surprisingly, the first dose of 50 mg of losartan resulted in a sudden anuria, which lasted eight hours despite high-dose furosemide and amine infusion. One week later, by mistake, losartan was prescribed again and after the second dose of 50 mg, the patient developed a second episode of transient anuria lasting 10 hours. During these two episodes, his blood pressure diminished but no severe hypotension was noted. Ultimately, an arteriography showed a 70-80% renal artery stenosis. In this patient, renal artery stenosis combined with heart failure and diuretic therapy certainly resulted in a strong activation of the renin-angiotensin system (RAS). Under such conditions, angiotensin II receptor blockade by losartan probably induced a critical fall in glomerular filtration pressure. This case report highlights the fact that the angiotensin II receptor antagonist losartan can cause serious unexpected complications in patients with renovascular disease and should be used with extreme caution in this setting.
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PMID:Repeated transient anuria following losartan administration in a patient with a solitary kidney. 1125 25


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