Funcion Del Tubulo Renal

Tubular Function and Tubulointerstitial Disease
Prasit Futrakul, MD, Saowani Yenrudi, MD, Narisa Futrakul, MD, Rajanee Sensirivatana, MD, Pornchai Kingwatanakul, MD, Jakchai Jungthirapanich, MD, Thumronkprawat Cherdkiadtikul, MD, Aimon Laohapaibul, MD, Dhevy Watana, MD, Vararat Singkhwa, MD, Sithivudh Futrakul, MD, and Pongsak Pongsin, MS
● Tubular transport determined by the fractionalexcretion (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 withMesP-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 F0.001). In the 27 nephrotic patients with mild FSGS (TIF, 28% 9%), four of five variables of FE solutes (FENa, 1.2 0.7; P F 0.001; FECa, 0.9 0.8; P F 0.001; FEPO4, 17 12; P, not significant; FEUA, 16.5 8; P F 0.001; FEMg, 4.1 1; P F 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 patientswith 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. 1999 by the National Kidney Foundation, Inc. INDEX WORDS: Tubular function; renal plasma flow; nephrosis; tubulointerstitial fibrosis; fractional excretion.

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HERE IS A GENERAL consensus among nephrologists thattubulointerstitial disease or fibrosis is a valid predictor of the clinical outcome of renal disease.1-5 Two patterns of clinicopathologic subsets have been generally delineated in nephrosis; namely, (1) a benign clinicopathologic entity associated with no tubulointerstitial disease, such as minimal change lesion or mild mesangial proliferative nephrosis (MesP-NS), and (2) a progressiveclinicopathologic disease associated with tubulointerstitial

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From the Departments of Pediatrics, Pathology, and Medicine, The King Chulalongkorn Memorial Hospital, Bangkok, Thailand. Received July 27, 1998; accepted in revised form October 16, 1998. Supported in part by the Royal Rachadapiseksompoj Research Grant, Chulalongkorn University, Bangkok, Thailand. Address reprint requests to Prasit Futrakul,MD, Faculty of Medicine, The King Chulalongkorn Memorial Hospital, Rama IV Rd, Bangkok 10330, Thailand. E-mail: yong@md2. chula.ac.th
1999 by the National Kidney Foundation, Inc.

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lesion, such as that observed in focal segmental glomerulosclerosis (FSGS), a moderate to diffuse mesangial proliferation, and membranoproliferative glomerulonephritis. Theclinical course in the former is usually associated with a selflimited disease without renal disease progression, whereas in the latter, a progressive renal disease destined for chronic renal insufficiency and end-stage renal disease is likely to ensue.6,7 Hence, the early recognition of its characteristic nature would help select a proper therapeutic regimen and predict a prognostic outcome. For the...