End-stage renal disease (ESRD) is the ultimate consequence of damage t
o the renal microvasculature by the sickle red cell. Progression to ES
RD starts with the onset of hyposthenuria, leading to an increase in g
lomerular filtration rate (GFR). Progressive glomerulosclerosis is mar
ked by proteinuria and a decreased GFR. This age-associated cumulative
deterioration can be modulated with appropriate therapy, but not tota
lly prevented.