Sodium and water metabolism

Most CRF patients retain the ability to reabsorb sodium ions, but the renal tubules may lose their ability to reabsorb water and so concentrate urine. Polyuria, although present, may not be excessive because the GFR is so low. Because of their impaired ability to regulate water balance, patients in renal failure may become fluid overloaded or fluid depleted very easily.

Potassium metabolism

Hyperkalaemia is a feature of advanced CRF and poses a threat to life (Fig 19.1). The ability to excrete potassium decreases as the GFR falls, but hyperkalaemia may not be a major problem in CRF until the GFR falls to very low levels. Then, a sudden deterioration of renal function may precipitate a rapid rise in serum potassium concentration. An unexpectedly high serum potassium concentration in an outpatient should always be investigated with urgency.

Acid–base balance

As CRF develops, the ability of the kidneys to regenerate bicarbonate and excrete hydrogen ions in the urine becomes impaired. The retention of hydrogen ions causes a metabolic acidosis.

Calcium and phosphate metabolism

The ability of the renal cells to make 1,25-dihydroxycholecalciferol falls as the renal tubular damage progresses. Calcium absorption is reduced and there is a tendency towards hypocalcaemia. Phosphate retention, along with low calcium, induces a rise in parathyroid hormone (PTH), and the latter may have adverse effects on bone if this is allowed to continue (renal osteodystrophy; Fig 19.2).