Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with congenital cyanotic heart disease may develop a glomerulopathy with proteinuria and impaired renal function. In order to investigate this problem we conducted a study on 27 patients with uncorrected cyanotic heart disease who were between 1 day and 25 years old. As a consequence of hypoxaemia haematocrit was elevated to 57%. Proteinuria was above 150 mg/day/1.73 m2 body surface in 12 patients. Only one of 9 children under 10 years of age had pathological proteinuria presenting as isolated albuminuria. Seven out of 10 patients between 11 and 20 years had an elevated proteinuria with a glomerular pattern. Creatinine clearance was normal in these patients. All four patients above 20 years of age had a considerable glomerular proteinuria with a mean excretion of 5.7 g/24 h/1.73 m2 body surface. These patients suffered additionally from chronic cardiac failure and creatinine clearance was below the normal range. There was a clear relationship between pathological proteinuria and age of the patients and thus duration of hypoxaemia. Patients with pathological proteinuria had a significant higher erythrocyte count (7.3 +/- 1.3 vs 5.6 +/- 1.4 10(12)/l p less than 0.01) and a lower mean corpuscular haemoglobin. In summary, children with persistent congenital cyanotic heart disease have substantial risk of developing a glomerulopathy if the cyanosis remains unchanged for more than ten years.
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PMID:Renal involvement in patients with congenital cyanotic heart disease. 178 94

A 57-year-old patient presented with periorbital and lower limb edema. The physical examination revealed no signs of cardiac insufficiency or chronic liver disease. Initial laboratory values showed significant hypoproteinemia and hyperlipidemia. Renal function was normal. Urinary protein excretion was 5.5 g/d. Thus, the patient was diagnosed to have nephrotic syndrome. The patient's history, the physical examination and further laboratory work-up suggested a primary glomerulopathy. Percutaneous renal biopsy was performed. The biopsy was diagnostic of minimal change glomerulonephritis. A therapy with steroids was initiated which induced a complete remission of the nephrotic syndrome. The patient has been relapse-free for the entire follow-up period.
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PMID:[Eyelid and ankle edema]. 231 82

The objective is here to study the long and intermediate term clinical and haemodynamic effects of enalapril during chronic heart failure resistant to the classic digitalis-diuretics treatment. The study involves 16 patients (12 males and 4 females), with a mean age of 50 years. Before being given enalapril, 12 patients were at stage IV and 4 patients at stage II of the NYHA; the mean capillary pressure was quite elevated (30 +/- 6.3 mmHg), the cardiac index has collapsed (2.12 +/- 0.38 l.min.m2) and the stroke fraction (SF) is 0.28 +/- 0.08. At the 1st month control, there is a definite functional and haemodynamic improvement of the pre-charge as well as the post-charge. This improvement is still present at 6 months. The ventricular function is improved (SF = 0.38 +/- 0.13; p less than 0.001). The clinical tolerance of enalapril is excellent and the only adverse reaction is a transient deterioration of the renal function in a patient with diabetic glomerulopathy.
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PMID:[Treatment of chronic refractory cardiac insufficiency with enalapril]. 254 30

The clinical significance of lupus non-inflammatory necrotizing vasculopathy (NINV) is not well established. For example, since lupus renal NINV is usually reported to coexist with proliferative and active glomerulonephritis, it is difficult to demonstrate the role of NINV on renal pathophysiology. Here we report a 16-year-old SLE boy with renal NINV presenting as ischemic glomerulopathy and small vessels-related ischemic heart failure. The renal biopsy demonstrated mild proliferative glomerulonephritis and NINV initially, and one month later repeated renal biopsy showed NINV with ischemic glomerulopathy. These findings established that NINV, but not proliferative glomerulonephritis, was responsive for his acute renal failure (ARF). Another interesting question is about the pathophysiology of his myocardial dysfunction. This patient presented typical angina and congestive heart failure (CHF). Echocardiograms and ventriculography revealed dilatation of four chambers and low ejection fraction. Serial electrocardiograms demonstrated evolutionary ischemic changes. Coronary angiography revealed no abnormality of large vessels. These findings suggested small vascular lesions-induced myocardial ischemia was the underlying mechanism of dilated cardiomyopathy. As myocardial biopsy was not done in our case, we could only speculate, but not prove, that the NINV observed in renal biopsy may also involve in cardiac microvascular beds. Nevertheless, this interesting case emphasized the role of obliterative small vascular lesions in the pathophysiology of ARF and myocardial dysfunction. The patient was treated with high-dose corticosteroid, plasma infusion and hemodialysis. His cardiac function improved gradually, however the renal function did not recover.
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PMID:Systemic lupus erythematosus presented as non-inflammatory necrotizing vasculopathy-induced ischemic glomerulopathy and small vessels-related ischemic cardiomyopathy. 1219 89

The aim of the study was to analyze the etiology, the factors for progression of chronic renal failure to end-stage-renal disease (ESRD), and the influence of ESRD on the survival rate among a cohort of 59 heart transplant patients (HTP) referred for the management of chronic renal failure (CRF). At the time of the first nephrology consultation (6 +/- 4.25 years after cardiac transplantation) the mean creatininemia was 261.5 +/- 99 micromol/L and mean creatinine clearance (Cockcroft formula) was 32 +/- 15 mL/min. The cause of CRF were calcineurin inhibitor toxicity in 38.9% of patients, vascular events in 15.2%, hemolytic uremic syndrome in 5%, membranous glomerulopathy in 3.3%, diabetes in two patients, focal/segmental glomerulosclerosis in 3.3%, renal hypoplasia in 1.7%, and unknown in 27%. Evolution to ESRD occurred in 38.9% of patients: 17 patients started hemodialysis, three peritoneal dialysis, and two received a preemptive kidney transplantation. Creatininemia (micromol/L) at the time of nephrology referral was 229.2 +/- 72.6 versus 315.8 +/- 113.4 (P < .001) and creatinine clearance (mL/min) was 34.9 +/- 15.1 versus 27.3 +/- 13.7 (P = .049) for patients with CRF versus ESRD, respectively. Both proteinuria (g/24 hours) of 1 +/- 2.2 versus 2.3 +/- 1.8 (P = .02) and tobacco use in 35.1% versus 54.4% (P = .045) were significantly associated with progression of CRF, while age at the time of heart transplantation, cause of cardiac failure and renal failure, high blood pressure, type 2 diabetes, dyslipidemia, alcoholism, cirrhosis, and cerebral vascular accident were not. Death occurred in 18 HTP: 50% of patients with ESRD and 18.5% of patients with CRF-a 2.6 relative risk of of death in HTP patients with ESRD compared with HTP with CRF only (P < .01).
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PMID:Chronic renal failure and end-stage renal disease are associated with a high rate of mortality after heart transplantation. 1584 18

The autopsy specimens of the myocardium and kidneys from 233 patients with infective endocarditis (142 and 91 with and without a history of drug abuse, respectively) were studied by conventional microscopy and immunohistochemistry. In the drug abusers (DA), myocytolysis was a dominant form of myocardial damage and in the non-DA that was contraction degeneration. In DA, lower cardiomyocytic cl-2 expression arouses speculations on the possible role of apoptosis in the pathogenesis of heart failure in this group of patients. Membranous glomerulopathy was a hallmark of renal pathology in DA, contrasting with the predominance of mesangial lesions in non-DA. Increased CIC deposition may be regarded as a major contributing factor.
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PMID:[Myocardial and renal morphological changes in drug addicts with infective endocarditis]. 1951 56