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Prasit Futrakul, Chulalongkorn Medical School Hospital, Rama IV Road, Bangkok 10330 (Thailand) Dear Sir, Table 1. Renal function studies Tubular insult with various degrees of histopathologic expression has consistently been encountered in nephrotic syndrome associated with focal segmental glomerulosclerosis. However, relating evidence supporting tubular functional abnormality was sporadically documented of which its significance is generally underestimated by the clinician [1–3]. In this respect, we have, therefore, observed tubular functional defect attested during 10–12 h fasting in 18 children with clinically steroid-resistant nephrosis and histopathologically proven FSGS. As depicted in table 1, there was a trend of increased urinary excretions of all the solutes above those of the normal control values during active proteinuria. Nevertheless, the differences were statistically significant only in the fractional excretion of phosphate and uric acid. In addition, simultaneous assessments of effective renal plasma flow using 131I-labeled para-aminohippurate and glomerular filtration rate using 99mTc-labeled DTPA during active proteinuria revealed a preponderantly low effective renal plasma flow compared to glomerular filtration rate yielding a high filtration fraction. Therapeutic combination of prednisolone (1–2 mg/ kg/day), dipyridamole (10–15 mg/kg/day), calcium channel blocker (Nifedipine, 1–3 mg/kg/day) and ACE inhibitor (0.5–2 mg/kg/day) had been medicated to all 18 nephrotics with the duration of treatment varying from 6 to 24 months. Interestingly, reassessments of renal functions following the therapeutic trial revealed a regression of enhanced tubular excretion of solute in conjunction with the improvement of renal hemodynamics. Normal FSGS Remission active