A liberal fluid intake should be ensured, to provide for both the obligatory urinary water loss and normal daily fluid requirement. When the latter occurs, other causes should also be considered. If metabolic acidosis is found in a patient with sickle cell disease, renal hydrogen ion excretion should be evaluated to determine whether it plays a role in the process. If it is present, it should be corrected by judicious therapy with sodium bicarbonate. Impaired renal tubular potassium excretion has also been described in sickle cell disease and, in some cases, can result in a tendency toward modest hyperkalemia, which is hyporesponsive to kaliuretic agents such as furosemide.
Hyperkalemia can increase as patients age.
This condition is due to the increase in urate production associated with accelerated erythropoiesis coupled with a decreased renal clearance of urate. Hyperuricemia in SS disease responds poorly to uricosuric agents, but the uric acid level can be lowered with the use of allopurinol. Uric acid nephropathy is rare, but if recurrent uric acid stone formation occurs, urinary alkalinization with oral sodium bicarbonate is recommended. Clinical gout is uncommon in sickle cell disease. The bleeding is usually painless, although clot formation in the renal pelvis or ureter can produce renal colic.