Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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PMID:Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. 295 52

A 17-year-old male underwent the division of the double accessory pathways under the diagnosis of Wolff-Parkinson-White (WPW) syndrome. At this time, we perceived that Ebstein's anomaly was combined with WPW syndrome, but we didn't treat Ebstein's anomaly, because it was slight. After this operation he relieved from the tachycardia attack completely. Ten months later, he was re-admitted to our hospital because of cardiomegaly and systemic edema. Hypoproteinemia was pointed out. On the basis of the intracardiac catheterization and 131I-RISA test, it was made to be sure that hypoproteinemia was caused by the protein-losing gastroenteropathy due to the tricuspid valve regurgitation of Ebstein's anomaly. After the tricuspid valve replacement with Hancock valve, protein-losing into the gastrointestinal tract disappeared. The aggravation of the tricuspid regurgitation was unrelated to the division of the accessory pathways, and was caused by the natural course of Ebstein's anomaly.
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PMID:[A successfully treated case of Wolff-Parkinson-White syndrome with Ebstein's anomaly complicated with protein-losing gastroenteropathy]. 649 87

A case of tricuspid regurgitation (TR) complicated by severe hypoproteinemia is presented herein. A 68-year-old man who had undergone coronary artery bypass grafting (CABG) for postinfarction angina suffered repeated inferior myocardial infarction due to obstruction of the proximal right coronary artery, 3 years after which he developed systemic edema. Investigations revealed TR associated with hypoproteinemia; however, treatment consisting of aggressive diuretic therapy and albumin administration proved ineffective. The hypoproteinemia manifested as protein-losing enteropathy clinically, and the tricuspid valve was replaced to eliminate high venous pressure. The serum protein levels became normalized after the operation. Although TR is generally well tolerated in the absence of pulmonary hypertension, surgical management is recommended for patients with severe protein deficiency resistant to medical treatment.
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PMID:Hypoproteinemia caused by tricuspid regurgitation: report of a case. 987 51

Protein-losing enteropathy (PLE) with hypoproteinemia is an uncommon but serious complication of congestive heart failure. Reports of patients with PLE resulting from severe tricuspid regurgitation (TR) caused by trauma are rare. A 66-year-old male diabetic patient had a chest contusion as a result of a road traffic accident, and one year later suffered from progressively generalized edema. Examination revealed severe TR with a high central venous pressure and PLE with serum protein deficiency. Treatment with albumin administration and diuretic therapy proved ineffective, and consequently the TR was corrected by valve replacement. Postoperatively, the serum protein level gradually returned to normal. Surgical intervention successfully improved this patient with severe TR and PLE resistant to medical treatment.
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PMID:Traumatic tricuspid regurgitation resulting in protein-losing enteropathy: a case report. 1635 69

Hypoalbuminemia is considered an independent predictor of mortality, especially in elderly patients. It is common in patients with congestive heart failure, when is due to several mechanisms: increased volume of distribution, significant stasis in the mesenteric circulation and altered protein metabolism in the liver. These alterations are even more pregnant when tricuspid regurgitation is associated or aggravated by different risk factors (recent infections, anemia, hyperthyroidism). We present the case of an elderly patient with severe hypoproteinemia and important hypoalbuminemia associated with congestive heart failure and aggravation of tricuspid regurgitation. The differential diagnosis concluded that hypoalbuminemia was influenced by tricuspid regurgitation as it enhanced liver dysfunction and enteral protein absorption due to increased stasis in mesenteric system. On the other hand, hypoalbuminemia contributed to the progression of heart failure by favoring myocardial edema, volume overload, and diuretic resistance. This is why correct management of this situation should include removal of subclinical excess of fluid and renutrition. A multidisciplinary approach is needed in order to achieve a good control of the symptoms and a significant improvement of quality of life.
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PMID:A case of severe hypoalbuminemia associated with chronic congestive heart failure: the role of the tricuspid regurgitation. 2474 83