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Hyponatraemia is well recognised in hypothyroidism, especially in the severe forms. The hypothyroidism is usually primary, but there are reports of hyponatraemia in patients with anterior hypopituitarism and corticotropin deficiency, and in these cases sodium concentrations return to normal with corticosteroid, rather than thyroid, replacement. Hyponatraemia in hypothyroidism has long been known to be associated with increased total body sodium, suggesting an important role for water retention. Hypothyroid patients, hyponatraemic or not, have a diminished ability to excrete free water, fail to achieve maximum urine dilution, and show delayed excretion of a water load.' Although the mechanism of water retention remains largely unexplained, arginine-vasopressin (AVP) may be involved.
In hypothyroid patients with plasma sodium concentrations between 130 and 142 mmol/L, 75% had raised plasma AVP concentrations which did not suppress normally after water ingestion.' To assess the response of AVP to an osmotic stimulus, Iwasaki et al infused eight patients with severe primary hypothyroidism with hypertonic saline.2 The rise in plasma AVP with rising plasma osmolality was normal in all patients, suggesting that the high plasma AVP in hypothyroid patients may be due to a non-osmotic stimulus, presumably hypovolaemia,' resulting in urine concentration even when plasma osmolality is low.
The hypovolaemia could be explained by both prerenal and renal mechanisms. Patients with hypothyroidism have a 50-60% increase in peripheral vascular resistance and a 30-50% reduction in cardiac output,4 with proportionate reduction in glomerular filtration rate (GFR) and renal plasma flow. Micropuncture studies in thyroidectomised rats reveal a marked reduction in single-nephron GFR, caused by decreased renal plasma...