Confirming reports of the unusual BP findings in patients with sickle cell disease have been published from Jamaica1 and now from the Netherlands. Although the explanation of these findings is unknown, this population represents an invaluable model for investigations into the pathophysiology of hypertension. The explanations that were offered in the June Archives (1981;141:891-894) were not meant to be definitive but to suggest hypotheses to be tested. As such, the comments of de Jong et al regarding the potential role of prostaglandins are welcomed additions.
In regard to salt-losing nephropathy, the reply by Radel et al2 to the letter of DeFronzo and colleagues (de Jong reference 1) arguing for the presence of inappropriate ADH secretion in sickle cell anemia refutes this argument with additional data not included in the original report. Subsequently, DeFronzo et al3 showed that the kidney in sickle cell disease is vasopressin resistant.