The magnitude of the glomerular nitrate requires very special mechanisms for the conservation of water and two of them, the exchange of sodium for potassium in the distal tubule under the control of renin and aldosterone and the control of free water excretion in the collecting duct by vasopressin (antidiuretic hormone, ADH), are under endocrine control.

Hyponatremia

All babies teeter on the brink of salt and water loss, because the osmolality of the renal medulla has not attained the level it needs for adequate reabsorption of water from the loop of Henle, even though a decreased glomerular perfusion protects the immature renal tubules. In early postnatal life, blood is distributed preferentially to the juxtamedullary area to nephrons with a higher capacity than the superficial ones to reabsorb sodium, but obligatory sodium reabsorption in the proximal tubule is limited so the neonate has a greater dependence on distal tubular function. Preterm infants are especially at risk of hyponatremia.

The renin–angiotensin system is functional in the fetus, and levels of renin activity, angiotensin and aldosterone are very high in the newborn. If these mechanisms are defective in any way, urinary sodium loss can rapidly cause serious salt depletion, even though the absolute loss of sodium may not be very great.

There is considerable clinical variability in the presentation of a salt-losing state ranging from moderate failure to thrive to a life-threatening salt-losing crisis. The serum sodium concentration alone may be misleading in such a situation.