@ Dr. FSUSTC, on the role of renal papillary necrosis in the manifestation of dehydration in sickle cell disease.
This is a very interesting remark!
However I am not so sure of the actual contribution of this mechanism in the context of dehydration in SCD. I mean, yes you are right that renal papillary necrosis is evident in SCD patients. But the major site of action of ADH, with regard to its water regulatory properties, is the collecting duct (through the down-regulation of water channels and the urea countercurrent mechanism), and to a lesser extent the thick ascending limb of Henle's loop (action on the Na-K-2Cl co-transporter). The renal papilla is where the collecting system ends up, but I think the major work of water reabsorption has already been accomplished in the collecting tubules themselves, before they reach the papilla. Of course, the relatively ischemic tubular cell is not functioning properly, but is this the main reason of dehydration in SCD pt's? Am I missing something on this mechanism?


