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).

Erythropoietin synthesis

Anaemia is often associated with chronic renal disease. The normochromic normocytic anaemia is due primarily to failure of erythropoietin production. Biosynthesized human erythropoietin may be used to treat the anaemia of CRF.

 Water and sodium intake should be carefully matched to the losses. Dietary sodium restriction and diuretics may be required to prevent sodium overload.

 Hyperkalaemia may be controlled by oral ion-exchange resins (Resonium A).

 Hyperphosphataemia may be controlled by oral aluminium or magnesium salts, which act by sequestering ingested phosphate in the gut.

 The administration of hydroxylated vitamin D metabolites may prevent the development of secondary hyperparathyroidism. There is a risk of hypercalcaemia with this treatment.

 Dietary restriction of protein, to reduce the formation of nitrogenous waste products, may give symptomatic improvement. A negative nitrogen balance should, however, be avoided.

Dialysis

Haemodialysis and peritoneal dialysis will sustain life when other measures can no longer maintain fluid, electrolyte and acid–base balance. The key to dialysis is the provision of a semipermeable membrane through which ions and small molecules, present in plasma at high concentration, can diffuse into the low concentrations of a rinsing fluid. In haemodialysis, an artificial membrane is used. In peritoneal dialysis, the dialysis fluid is placed in the peritoneal cavity, and molecules move out of the blood vessels of the peritoneal wall. Continuous ambulatory peritoneal dialysis (CAPD) is an effective way of removing waste products. The dialysis fluid is replaced every 6 hours.

Note that haemodialysis and peritoneal dialysis may relieve many of the symptoms of chronic renal failure and rectify abnormal fluid and electrolyte and acid–base balance. These treatments do not, however, reverse the other metabolic, endocrine or haematological consequences of chronic renal failure.

Renal transplant

Although transplant of a kidney restores almost all of the renal functions, patients require long-term immunosuppression. For example, ciclosporin is nephrotoxic at high concentrations and monitoring of both creatinine and ciclosporin is necessary to balance the fine line between rejection and renal damage due to the drug.