Plasma arginine vasopressin in hyponatraemic patients receiving diuretics

Abstract

Summary:Random estimations of plasma arginine vasopressin concentration were undertaken in 6 non-oedematous patients receiving diuretic therapy for hypertension, who were admitted to hospital with severe hyponatraemia. Hyponatraemia resolved within 2 weeks of discontinuing the diuretic. Measurable amounts of plasma arginine vasopressin were detected in all 6 patients.Sequential biochemical measurements in one patient, performed when plasma sodium concentration and osmolality were returning to the normal range, disclosed that urine osmolality remained higher than plasma osmolality during the first 5 days, when urine volume and sodium excretion were low. Thus the rise in plasma sodium was not initially related to water diuresis. The ability to excrete a water load was severely limited on the fifth day, but improved progressively by the tenth and seventeenth days.Diuretic-induced hyponatraemia is associated with incomplete suppression of anti-diuretic hormone secretion arising from non-osmotic stimulation, in conjunction with transient impairment of renal diluting ability which could be due to net sodium deficit.

Diuretic-Induced Hyponatremia

“…First, they inhibit electrolyte transport at the cortical diluting sites, thereby raising the minimum urinary osmolality [7,9,10]; but while this effect reduces electrolyte free water clearance [5], it does not reduce urine flow and therefore does not directly predispose to an expansion of total body water. Second, thiazides stimulate antidiuretic hormone (ADH) release [11][12][13]. Third, they decrease the glomerular filtration rate acutely [9,10,14,15] and increase fractional proximal water reabsorption [15], thereby reducing delivery to diluting sites.…”

“…Similarly, Abramow and Cogan [4] found that in some of their patients the fractional urea excretion was high during hyponatremia and fell with correction of the serum sodium. Furthermore, many patients with thiazide-induced hyponatremia appear euvolemic [4,12,[23][24][25][26]. Finally, in some of them water balance was positive during the development of hyponatremia and negative during its correction [4,17,24,25,27].…”

“…However, because thiazides interfere with renal water excretion, they impair this normal osmoregulatory response. Thus, as in most patients with hyponatremia, urine osmolality is inappropriately high relative to the osmolality of plasma and often exceeds it [1,4,12,17,22,23,25,28]. In fact, rejected cations may sometimes be excreted at a total concentration which exceeds that of plasma [17].…”

“…Hypovolemia may stimulate the release of ADH which is elevated in many of these patients [4,12,13,25], though not in all [17,21]. As previously noted, volume depletion may also impair renal water excretion by decreasing the glomerular filtration rate and increasing proximal reabsorption, thereby reducing distal delivery [15,18,33]; this can cause water retention even in the absence of ADH [34].…”

Loop diuretic-induced hyponatremia: a case report

“…Vasopressin receptor antagonists block arginine vasopressin from binding to V2 receptors in the distal nephron and promote the excretion of electrolyte-free water. 16 In recent randomized trials, tolvaptan, an orally active V2 receptor antagonist, has been effective in raising serum sodium in patients with hyponatremia.…”