Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The glomerular size-selective properties in a patient with "hyponatremic hypertensive syndrome" were investigated before and after administration of the angiotensin-converting enzyme inhibitor enalapril. Hyponatremic hypertensive syndrome is a rare condition of renovascular hypertension characterized by electrolyte abnormalities (hyponatremia, hypokalemia), polyuria, and high renin activity. In this patient a marked increase in urinary protein excretion was observed. Treatment with enalapril normalized BP, corrected electrolyte abnormalities, and reduced proteinuria. Glomerular filtration rate (GFR), renal plasma flow (RPF), and the clearance of neutral dextrans of graded sizes were measured before and after 6 months of enalapril (20 mg/d) administration. Theoretical analysis of dextran and inulin clearance data with a model of glomerular size selectivity were adopted to separate effects of hemodynamic changes on macromolecule filtration from changes of intrinsic membrane selective properties. After enalapril urinary protein excretion decreased, GFR was unchanged and RPF almost doubled. Fractional clearance values of dextran molecules were markedly elevated in comparison with the corresponding values measured in a group of normal controls and were normalized by enalapril. Theoretical calculation of membrane pore characteristics showed that enalapril treatment reduced the radius of all membrane pores by approximately 1 nm. Altogether these results indicate that enalapril normalized glomerular filtration of neutral macromolecules and circulating proteins in a human condition of angiotensin II-induced proteinuria. Enalapril effectively restored glomerular size-selective function, reducing dimensions of membrane pores, independently of its effect on renal hemodynamics.
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PMID:Angiotensin-converting enzyme inhibition ameliorates the defect in glomerular size selectivity in hyponatremic hypertensive syndrome. 247 29

Hyponatremic hypertensive syndrome is a manifestation of severe hypertension related to renal ischemia. The most common underlying cause of hyponatremic hypertensive syndrome in adults is severe atherosclerotic reno-vascular disorder while in children the most common cause of hyponatremic hypertensive syndrome is unilateral congenital renal artery stenosis due to some form of arterial dysplasia. An excessively stimulated renin-angiotensin-aldosterone system is mainly responsible for heavy polyuria, renal electrolyte loss and proteinuria. The neurological manifestations of hyponatremia and/or hypertensive encephalopathy are the main presenting symptoms, and they are not always in linear correlation with the degree of hyponatremia and/or hypertension. The cornerstone of management is the treatment of underlying hypertensive disease, but the correction of hyponatremic dehydration and safe decrease of blood pressure are essential in the emergency phase of hyponatremic hypertensive syndrome. The optimal antihypertensive therapy depends on the underlying condition. Revascularization, either surgical or by percutaneous transluminal angioplasty, is recommended for children with renal artery stenosis. Pharmacological treatment based on ACEI and/or ARB is the most efficient antihypertensive therapy for those with ischemic reno-parenchymal disorder. Nephrectomy is required if an affected kidney contributes less than 10% of the global renal function, if percutaneous transluminal angioplasty fails and the operative risk is too high, or in the case of extensive tumorous lesions.
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PMID:Hyponatremic hypertensive syndrome. 1892 57