Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
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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

Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during long-term vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary arteriolar resistance (PAR) than in systemic vascular resistance (SVR) (% delta PAR/% delta SVR greater than 1.0), whereas patients in Group II showed predominant systemic vasodilation (% delta PAR/% delta SVR less than 1.0). Despite similar changes in systemic resistance, patients in Group I showed greater increases in cardiac index, stroke volume index and left ventricular stroke work index (p less than 0.01 to 0.001) but less dramatic decreases in mean systemic arterial pressure (p less than 0.02) than did patients in Group II. Despite similar changes in left ventricular filling pressure, patients in Group I showed greater decreases in mean pulmonary artery and mean right atrial pressures (p less than 0.02 to 0.01) than did patients in Group II. Pretreatment variables in Groups I and II were similar, except that plasma renin activity was higher (8.7 +/- 2.1 versus 3.0 +/- 0.6 ng/ml per h) and serum sodium concentration was lower (133.1 +/- 0.9 versus 137.1 +/- 0.6 mEq/liter) in Group II than in Group I (both p less than 0.05). Both groups improved clinically after 1 to 3 months, but symptomatic hypotension occurred more frequently in Group II than in Group I (36 versus 8%) (p less than 0.005). These findings indicate that changes in the pulmonary circulation modulate alterations in both right and left ventricular performance during the treatment of patients with left heart failure. Hyponatremic patients are likely to experience symptomatic hypotension with captopril because they are limited in their ability to increase cardiac output as a result of an inadequate pulmonary vasodilator response to the drug.
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PMID:Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure. 299 97

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

Hyponatremia, serum sodium < 135 mEq/L, is the most common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the causes of hyponatremia has hampered the delivery of appropriate therapy. This is especially applicable to differentiating syndrome of inappropriate antidiuresis (SIAD) from cerebral salt wasting (CSW) or more appropriately, renal salt wasting (RSW), because of divergent therapeutic goals, to water-restrict in SIAD and administer salt and water in RSW. Differentiating SIAD from RSW is extremely difficult because of identical clinical parameters that define both syndromes and the mindset that CSW occurs rarely. It is thus insufficient to make the diagnosis of SIAD simply because it meets the defined characteristics. We review the pathophysiology of SIAD and RSW, the evolution of an algorithm that is based on determinations of fractional excretion of urate and distinctive responses to saline infusions to differentiate SIAD from RSW. This algorithm also simplifies the diagnosis of hyponatremic patients due to Addison's disease, reset osmostat and prerenal states. It is a common perception that we cannot accurately assess the volume status of a patient by clinical criteria. Our algorithm eliminates the need to determine the volume status with the realization that too many factors affect plasma renin, aldosterone, atrial/brain natriuretic peptide or urine sodium concentration to be useful. Reports and increasing recognition of RSW occurring in patients without evidence of cerebral disease should thus elicit the need to consider RSW in a broader group of patients and to question any diagnosis of SIAD. Based on the accumulation of supporting data, we make the clinically important proposal to change CSW to RSW, to eliminate reset osmostat as type C SIAD and stress the need for a new definition of SIAD.
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PMID:Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia. 2831 39

INTRODUCTION The aim of this study is to determine the prevalence of hyponatremia, its association with long-term medication use and underlying chronic conditions, the rate of hospitalisation and death within 3 months from its discovery and its management in community-dwelling older people. METHODS One year of data for ~5635 patients aged >65 years was extracted from the databases of 19 general practitioners (GPs); 2569 (45.6%) were checked for hyponatremia. RESULTS Hyponatremia occurred in 205 (8.0%) of 2569 checked individuals: 78.5% (161/205) had hypertension, 31.2% (64/205) diabetes, 23.9% (49/205) chronic renal failure; 38.0% (78/205) received diuretics, 36.6% (75/205) renin-angiotensin system antagonists (ACE-I/ARB) and 9.8% (20/205) serotonin reuptake inhibitors. Drug consumption was higher in hyponatremic patients, although only diuretics, ACE-I/ARB, anti-arrhythmics and opioids were significantly associated with hyponatremia. The likelihood of hyponatremia trebled when four drugs were taken, and it was seven-fold higher with the use of six drugs. Hyponatremia was associated with a higher prevalence of chronic illnesses and higher rate of hospitalisation (13.7% vs 7.7%, P = 0.005) and death (3.9% vs 1.8%, P < 0.035). The use of at least one long-term medication was associated with hospitalisation or death in hyponatremic patients (10% vs 6.3%, P = 0.010). Less than 20% of hyponatremic patients had their sodium level checked again after 1 month. DISCUSSION Hyponatremia is not uncommon among community-living older patients, especially in patients taking medications potentially causing hyponatremia. Hyponatremic patients are likely to encounter more serious events, including hospitalisation and death. Targeted training of GPs is desirable to improve their practice.
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PMID:Hyponatremia associated with long-term medication use in the elderly: an analysis in general practice. 3006 72