? Nephrotic syndrome (NS) in children has been associated with a systemic circulating permeability factor. studied. Data are reported as mean standard deviation. Differences between groups were calculated using the Mann-Whitney U-test, and < 0.05 was considered significant. ? Each study group consisted of 10 patients [NS patients: 4 boys, mean age of 7.3 4.1 years; control patients: 6 boys, mean age of 7.2 4.7 years (= nonsignificant)]. In the group with NS, 8 patients were diagnosed by biopsy as having focal segmental glomerulosclerosis, and 2 as having minimal-change disease. At study entry, patients with NS had hourly urinary protein losses of 398 313 mg/m2 and daily peritoneal protein losses of 3.4 1.9 g/m2, compared with LAMC1 29.9 31 mg/m2 and 1.5 1.1 g/m2 respectively in the control group (< 0.05). The same statistical difference was found 6 months later. We observed no statistical differences in PET results, daily exchange volume, and mean dextrose concentration of dialysate. Similarly, no significant between-group differences were observed for Kt/V, DPI, nPNA, and biochemical parameters. ? Hispanic children with NS on PD show higher peritoneal protein losses than do their control counterparts. Such differences could be secondary to increased peritoneal permeability caused by a systemic permeability factor. (8) identified a focal segmental permeability protein factor associated with a low molecular weight fraction from plasma and showed that the proteins activity correlates with severity of disease and risk of recurrence. McCarthy recently proposed that cardiotrophin-like cytokine factor 1 (CLCF1) could be an active factor in FSGS. Soluble urokinase receptor has been also recognized in the plasma of individuals with recurrent FSGS (11). Steroid-resistant individuals with NS show poor prognosis; most progress to end-stage renal failure (ESRF) and dialysis over time. If steroid-resistant NS were to be associated with the systemic permeability element shown by Sharma then peritoneal protein deficits should be higher in NS individuals on peritoneal dialysis (PD) than in a non-NS dialyzed human population. The implications of improved peritoneal protein deficits include further exacerbation of malnutrition, improved risk of illness, growth retardation, developmental delay, and improved mortality in pediatric PD individuals with NS (12). To day, only one study has showed that peritoneal protein deficits are higher in children with NS on PD, and medical observations suggest that these individuals need careful nourishment and dialytic supervision (13). The objective of the present study was to evaluate peritoneal protein deficits in Hispanic children with steroid-resistant NS on PD therapy, comparing them with dialyzed individuals not having NS. METHODS Our retrospective 4-yr analysis (2003 - 2007) evaluated chronic PD individuals with ESRF secondary to NS. All individuals were going to the Luis Calvo Mackenna Childrens Hospital, University or college of Chile, Santiago, Chile. Data from the KU-60019 2nd and 6th month on PD were analyzed. Age, sex, weight, height, KU-60019 and time on PD were recorded. Biochemical data included serum creatinine (Jaffe reaction), electrolytes, blood urea nitrogen (enzyme assay), calcium, phosphate, parathyroid hormone [PTH (Advantage Nichols Intact PTH Assay: Pursuit Diagnostics Nichols Institute, San Juan Capistrano, CA, USA)], serum albumin, and KU-60019 protein (turbidimetric assay). At the beginning and end of follow-up, 24-hour protein deficits and nitrogen were measured in dialysate and urine. Thimerosal was added to the urine and dialysate samples to avoid urea generation secondary to bacterial activity..