EARLY DETECTION AND THE COURSE OF GLOMERULAR INJURY IN PATIENTS WITH SICKLE-CELL-ANEMIA

We performed a cross sectional analysis of glomerular function in 34 a dult patients with sickle cell anemia (SSA). Patients were divided acc ording to GFR and albumin excretion rate (AER): SSA controls (normal G FR and AER, N = 10), albuminuria (increased AER, but normal GFR, N = 7 ) and chronic renal failure (CRF, low GFR, N = 17). GFR did not correl ate with age (that is, duration of disease), but was inversely related to AER and IgG excretion rates (I = -0.61 and -0.69, respectively, P < 0.001) and directly related to the hematocrit (r = 0.56, P < 0.001). Renal plasma flow was disproportionately higher than GFR, so that fil tration fraction was low in all groups, Albuminuria was accompanied, e ven in patients with normal GFR, by a reduction in ultrafiltration coe fficient (16 +/- 3 in albuminuria vs. 25 +/- 3 in controls, P < 0.05). A more severe loss of ultrafiltration coefficient and glomerular perm selectivity occurred in CRF. We conclude that renal failure in SSA occ urs because of glomerular injury with loss of ultrafiltration coeffici ent and glomerular permselectivity. The earliest clinically detectable abnormality is an increase in albumin and IgG excretion. When albumin uria is present, the ultrafiltration coefficient is already diminished even if GFR is preserved. Detection of albuminuria can identify estab lished glomerular injury in SSA.