Tubular transport determined by the fractional excretion (FE) of filtered s
olutes was studied in 129 nephrotic patients; 72 patients with mesangial pr
oliferation (MesP-NS) and intact tubulointerstitium (group 1), 13 patients
with MesP-NS and superimposed tubulointerstitial fibrosis (TIF; group 2), 2
7 patients with mild focal segmental glomerulosclerosis (FSGS; group 3), an
d 17 patients with severe FSGS (group 4). In the 72 nephrotic patients with
MesP-NS and normal tubulointerstitium (no TIF), tubular transport was inta
ct (FE of sodium [FENa], 0.5 +/- 0.5; FE of calcium [FECa], 0.3 +/- 0.3; FE
of phosphate [FEPO4], 14 +/- 13; FE of uric acid [FEUA], 9.8 +/- 0.5; FE o
f magnesium [FEMg], 1.3 +/- 0.5). In the 13 nephrotic patients with MesP-NS
and superimposed TIF (4.9% +/- 2%), there was no difference in FE solutes
from those in group 1 except for FEMg (3.3 +/- 0.9; P < 0.001). In the 27 n
ephrotic patients with mild FSGS (TIF, 28% +/- 9%), four of five variables
of FE solutes (FENa, 1.2 +/- 0.7; P < 0.001; FECa, 0.9 +/- 0.8; P < 0.001;
FEPO4, 17 +/- 12; P, not significant; FEUA, 16.5 +/- 8; P < 0.001; FEMg, 4.
1 +/-; P < 0.001) were significantly different from those of patients with
MesP-NS without TIF, and two of five variables (FECa, FEMg) were statistica
lly different from those of patients with MesP-NS with TIF. In the severe c
ategory of FSGS (TIF, 69% +/- 19%), all FE solutes were statistically diffe
rent from the other groups (FENa, 4.8 +/- 3; FECa, 2 +/- 1; FEPO4, 47 +/- 2
4; FEUA, 37 +/- 18; FEMg, 12 +/- 6). Thus, the results imply that (1) norma
l tubular transport reflects an underlying intact tubulointerstitial struct
ure, whereas tubular dysfunction indicates an underlying tubulointerstitial
disease, and (2) FEMg is the most sensitive index to detect an early abnor
mality of tubular structure and function. (C) 1999 by the National Kidney F
oundation, Inc.