Iron homeostasis in relapsing steroid-sensitive nephrotic syndrome of childhood

Citation
Mj. Kemper et al., Iron homeostasis in relapsing steroid-sensitive nephrotic syndrome of childhood, CLIN NEPHR, 52(1), 1999, pp. 25-29
Citations number
26
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
CLINICAL NEPHROLOGY
ISSN journal
03010430 → ACNP
Volume
52
Issue
1
Year of publication
1999
Pages
25 - 29
Database
ISI
SICI code
0301-0430(199907)52:1<25:IHIRSN>2.0.ZU;2-W
Abstract
Aim: Urinary transferrin loss is a typical feature in relapse of the idiopa thic nephrotic syndrome, however, the impact on serum iron homeostasis and hematological parameters has not been studied systematically so far. Patien ts and methods: Therefore, we investigated serum iron (Fe), erythropoietin (EPO), ferritin (FN), transferrin (TF), total iron-binding capacity (TEBK), transferrin saturation and the soluble transferrin receptor (sTFR) combine d with hematological parameters (hemoglobin, MCV, MCH) in 42 children with relapsing, steroid-sensitive nephrotic syndrome (NS) in remission (RM, n = 26) and relapse (RL, n = 16), including 13 patients who were studied in bot h states. Thirty-three age-matched healthy children served as controls. Res ults: Fe, TEBK and TF were significantly reduced in RL compared to RM in cr oss-sectional as well as in paired studies while ferritin, hematological pa rameters and EPO levels remained unchanged. A significant increase, however , of the soluble transferrin-receptor could be demonstrated in cross-sectio nal analysis comparing RL to RM and healthy controls (3568 +/- 713 mg/ml vs 2625 +/- 576 vs 2646 +/- 697; p < 0.001 respectively) as well as in paired analysis of 13 patients in RL and RM (p < 0.001). Conclusion: We conclude that transient transferrin and iron deficiency occurs in RL of INS but this seems to be counterbalanced by upregulation of the sTFR, a mechanism that might be important in preventing the development of iron deficiency anemia during the active nephrotic state.