title: Tubular function and tubulointerstitial disease.
abstract: Tubular transport determined by the fractional excretion (FE) of filtered solutes was studied in 129 nephrotic patients; 72 patients with mesangial proliferation (MesP-NS) and intact tubulointerstitium (group 1), 13 patients with MesP-NS and superimposed tubulointerstitial fibrosis (TIF; group 2), 27 patients with mild focal segmental glomerulosclerosis (FSGS; group 3), and 17 patients with severe FSGS (group 4). In the 72 nephrotic patients with MesP-NS and normal tubulointerstitium (no TIF), tubular transport was intact (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 +/- 5; FE of 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 nephrotic 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 +/-1; P < 0.001) were significantly different from those of patients with MesP-NS without TIF, and two of five variables (FECa, FEMg) were statistically different from those of patients with MesP-NS with TIF. In the severe category of FSGS (TIF, 69% +/-19%), all FE solutes were statistically different from the other groups (FENa, 4.8 +/- 3; FECa, 2 +/- 1; FEPO4, 47 +/- 24; FEUA, 37 +/- 18; FEMg, 12 +/- 6). Thus, the results imply that (1) normal tubular transport reflects an underlying intact tubulointerstitial structure, whereas tubular dysfunction indicates an underlying tubulointerstitial disease, and (2) FEMg is the most sensitive index to detect an early abnormality of tubular structure and function.
authors.affiliation: Departments of Pediatrics, Pathology, and Medicine, The King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
authors.forename: P
authors.initials: P
authors.lastname: Futrakul
authors.forename: S
authors.initials: S
authors.lastname: Yenrudi
authors.forename: N
authors.initials: N
authors.lastname: Futrakul
authors.forename: R
authors.initials: R
authors.lastname: Sensirivatana
authors.forename: P
authors.initials: P
authors.lastname: Kingwatanakul
authors.forename: J
authors.initials: J
authors.lastname: Jungthirapanich
authors.forename: T
authors.initials: T
authors.lastname: Cherdkiadtikul
authors.forename: A
authors.initials: A
authors.lastname: Laohapaibul
authors.forename: D
authors.initials: D
authors.lastname: Watana
authors.forename: V
authors.initials: V
authors.lastname: Singkhwa
authors.forename: S
authors.initials: S
authors.lastname: Futrakul
authors.forename: P
authors.initials: P
authors.lastname: Pongsin
mesh_terms: D000293:Adolescent; D001692:Biological Transport; D002118:Calcium / Q000652:urine; D002648:Child; D005260:Female; D005920:Glomerular Mesangium / Q000503:physiopathology; D005921:Glomerulonephritis / Q000503:physiopathology / Q000652:urine; D005923:Glomerulosclerosis, Focal Segmental / Q000503:physiopathology / Q000652:urine; D006801:Humans; D007684:Kidney Tubules / Q000098:blood supply / Q000503:physiopathology*; D008274:Magnesium / Q000652:urine; D008297:Male; D009395:Nephritis, Interstitial / Q000503:physiopathology* / Q000652:urine; D009401:Nephrosis / Q000503:physiopathology / Q000652:urine; D010710:Phosphates / Q000652:urine; D011379:Prognosis; D012964:Sodium / Q000652:urine; D014527:Uric Acid / Q000652:urine
chemical_list: D010710:Phosphates; D014527:Uric Acid; D012964:Sodium; D008274:Magnesium; D002118:Calcium