[Idiopathic edema, tubular metabolism of water and sodium].
Paraules clau
Resum
OBJECTIVE
To look for intrinsic changes in renal tubular water and sodium metabolism in idiopathic edema (IE), independent of the underlying hormonal and vascular defects.
METHODS
Prospective controlled study in patients with edema referred to a nephrology clinic.
METHODS
Ten female patients with IE were compared with a control group of 4 healthy women.
RESULTS
Patients and controls were submitted to a base-line test of water loading and lithium clearances, after 12 hours supine position, to study renal tubular handling of Na and H2O in different nephron sites and 5 h water excretion capacity. Patients were then randomized in 2 groups, both receiving standard treatment during 2 months (low-salt diet--70 to 90 mEq of Na per day, stopping diuretics and laxatives, elastic stockings). Group B received in addition carbidopa/levodopa 25/100--3 tabs/day and captopril 6.25 mg q 8 h. At the end of this 2 months period the base-line tests were repeated. We registered a good clinical response, with an average a.m. weight reduction of 2.8 kg and a decrement of the a.m. to p.m. weight gradient from 2.42 +/- 0.3 kg pre-treatment to 0.6 +/- 0.1 kg afterwards. From the several measurements obtained, only global FENa and Proximal Fraccional Reabsorption of Na were significantly different between patients and controls (0.87 +/- 0.09% vs 2.1 +/- 0.2%, p less than 0.001 and 77.4 +/- 2.9% vs 64.0 +/- 3.5%, p = 0.02 respectively), with no difference in distal Na and H2O reabsorption or water excretion capacity. Two months treatment only partially corrected global FENa, and there were no differences in the clinical and physiological effects between the 2 therapeutic groups.
CONCLUSIONS
1--In the absence of orthostatism, H2O and Na metabolism is similar between IE patients and healthy controls, only with an increased selective proximal Na reabsorption in patients. 2--Standard non-pharmacologic therapy was a clinical success, but didn't correct the physiological defect of excessive proximal sodium reabsorption. Treatment results were not improved by pharmacologic intervention.
