[Differential diagnosis and treatment of hyponatremia].

Hyponatremia is one of the most common metabolic disorders in clinical medicine. The value of Na+ in serum equalling 135 mmol/ l and lower is regarded as hyponatremia. Its clinical manifestations are the following: headaches, nausea, vomiting, seizures, numbness, coma and death. Hyponatremia caused by nonosmotic hypersecretion of vasopressin can be divided into: a) hypovolemic, b) normovolemic and c) hypervolemic. Hyponatremia which is not caused by the hypersecretion of vasopressin is the so  called pseudohyponatremia, water intoxication, cerebral salt loss syndrome. Hypovolemic hyponatremia is caused by the loss of Na+ and fluid loss from the organism. It occurs, for example, after using thiazide diuretics, after recurrent diarrhoea, vomiting, after significant blood loss and other causes. Treatment of this disorder must focus on the producing cause and on the parenteral administration of 0.9% NaCl. Normovolemic hyponatremia can be with or without symptoms. Acute normovolemic hyponatremia is treated by the intravenous administration of 3% NaCl and with the simultaneous use of loop diuretics (20- 40 mg Furosemide/ 24 hrs) and restriction of fluid intake. In the case of chronic normovolemic hyponatremia, refractory to the previous treatment, caused by the inappropriate secretion of arginine  vasopressin, it is recommended to use perorally its V2- receptor blocker, Tolvaptan. Hypervolemic hyponatremia occurs in the case of cardiovascular failure, with hepatic cirrhosis, nephrotic syndrome, renal failure, porphyric disease and other conditions. Symptoms occurring with it are swellings, ascites, distension of jugular veins and the presence of unaccented rales in the lungs, which can be detected during physical examination. For treatment it is recommended to restrict fluid intake and to administer NaCl as well as diuretic therapy. Recently it has been recommended to use Tolvaptan which increases excretion of free water (aquaresis), decreases osmolality in the urine, and leads to the increase in serum Na+. Apart from that, we present our three clinical  laboratory observations in the paper: 1. Contrary to the data in the literature, after the Košice Marathon (42.125 km) the serum concentration of Na+ in the runners increased (from 144.4 ± 2.1 mmol/ l to 147 ± 2.8 mmol/ l, p < 0.01) in spite of a significant reduction in the body weight (from 73.2 ± 5.7 kg to 71.9 ± 5.2 kg, p < 0.05), intensive perspiration and dehydration (blood haemoglobin before the run: 150.4 ± 5.5 g/ l, after the run: 152.1 ± 4.8 g/ l, p < 0.05). Apart from that, we detected a significant decrease in the fractional excretion of sodium (FENa) from 1.16 ± 0.30% to 0.34 ± 0.10%, p < 0.01. 2. One patient with chronic intermittent porphyria displayed the syndrome of inappropriate antidiuretic hormone secretion, which had been positively influenced by the restriction of fluid intake in the long term and by peroral administration of 1- 3 g NaCl/ 24 hrs. 3. In 15 haemodialysed patients with chronic renal failure, who displayed recurrent hypervolemic hyponatremia, we achieved, by means of adequate ultrafiltration and a dialysis solution containing Na+ 145 mmol/ l, the serum concentration of Na+ 142 mmol/ l at the end of haemodialysis.