Please wait a minute...
Frontiers of Medicine

ISSN 2095-0217

ISSN 2095-0225(Online)

CN 11-5983/R

Postal Subscription Code 80-967

2018 Impact Factor: 1.847

Front. Med.    2008, Vol. 2 Issue (3) : 286-289    https://doi.org/10.1007/s11684-008-0054-6
Serum erythropoietin and transferrin in children with idiopathic nephrotic syndrome
LU Hongzhu1, LIU Dan1, ZHANG Wanming1, YUAN Yuesha1, KUANG Hongyan1, WANG Lin2, FAN Qihong2
1.Department of Pediatrics, Clinical Medical College, Yangtze University; 2.Department of Pediatrics, the First Hospital of Jingzhou;
 Download: PDF(60 KB)   HTML
 Export: BibTeX | EndNote | Reference Manager | ProCite | RefWorks
Abstract Idiopathic nephrotic syndrome (INS) is characterized by marked urinary excretion of albumin and other intermediate-sized plasma proteins, such as transferrin and vitamin D-binding protein. Some cases even develop anemia. The aim of this study was to investigate the changes in serum iron, transferrin, and erythropoietin, and the relationships between serum and urine transferrin and erythropoietin. Thirty-seven children with INS and 35 age- and sex-matched healthy children were investigated. The indexes related to iron metabolism, including serum iron, ferritin, transferrin, total iron-binding capacity (TIBC), transferrin saturation, and hematological parameters [hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH)], and urinary transferrin and erythropoietin were measured in 37 children with INS before treatment and at the remission stage. Thirty-five age- and sex-matched healthy children served as controls. Serum iron levels (18.8 ± 3.8) ?mol/L in INS patients before treatment were significantly lower than those of the healthy controls (22.2 ± 3.8) ?mol/L and those measured at the remission stage (21.0 ± 3.5) ?mol/L (all P < 001). Serum transferrin levels in INS patients before therapy (1.9 ± 0.3) g/L also decreased compared with the healthy controls (3.1 ± 0.5) g/L and the measures at the remission stage (2.9 ± 0.6) g/L (all P < 0.01). In contrast, serum TIBC and transferrin saturation were significantly higher in INS patients before treatment than in the healthy controls [TIBC (56.4 ± 9.2) ?mol/L vs (50.7 ± 6.8) ?mol/L, P < 0.01; transferrin saturation (55.7±9.2)% vs (46.4 ± 8.2)%, P < 0.01] and they were also higher than the measures at remission stage [(51.9 ± 7.7) ?mol/L and (47.4 ± 13.3) ?mol/L] (all P < 0.01). Serum transferrin was positively correlated with serum albumin (r = 0.609, P < 0.01) and negatively correlated with urinary transferrin (r = -0.550, P < 0.01) in INS patients before treatment. We conclude that serum iron, transferrin and erythropoietin levels are markedly decreased in INS patients, which may be partially related to the urinary loss of these indexes.
Issue Date: 05 September 2008
 Cite this article:   
WANG Lin,LU Hongzhu,KUANG Hongyan, et al. Serum erythropoietin and transferrin in children with idiopathic nephrotic syndrome[J]. Front. Med., 2008, 2(3): 286-289.
 URL:  
https://academic.hep.com.cn/fmd/EN/10.1007/s11684-008-0054-6
https://academic.hep.com.cn/fmd/EN/Y2008/V2/I3/286
1 Grymonprez A, Proesmans W, Van Dyck M, Jans I, Goos G, Bouillon R . VitaminD metabolites in childhood nephrotic syndrome. Pediatr Nephrol, 1995, 9(3): 278–281.
doi:10.1007/BF02254183
2 Deegens J K, Wetzels J F . Fractional excretion of high–and low–molecular weight proteins and outcome in primary focalsegmental glomerulosclerosis. Clin Nephrol, 2007, 68(4): 201–208
3 Varghese S A, Powell T B, Budisavljevic M N, Oates J C, Raymond J R, Almeida J S, Arthur J M . Urine biomarkerspredict the cause of glomerular disease. J Am Soc Nephrol, 2007, 18(3): 913–922.
doi:10.1681/ASN.2006070767
4 Cooper M A, Biddington B, Miller N L, Alfrey A C . Urinary ironspecification in nephrotic syndrome. AmJ Kidney Dis, 1995, 25(2): 314–319.
doi:10.1016/0272‐6386(95)90014‐4
5 Beard J L, Murray-Kolb L E, Rosales F J, Solomons N W, Angelilli M L . Interpretation of serum ferritinconcentrations as indicators of total–body iron stores in surveypopulations: the role of biomarkers for the acute phase response. Am J Clin Nutr, 2006, 84(6): 1498–1505
6 Sun X, Kaysen G A . Albumin and transferrin synthesisare increased in H4 cells by serum from analbuminemic or nephroticrats. Kidney Int, 1994, 45(5): 1381–1387.
doi:10.1038/ki.1994.180
7 Prinsen B H, de Sain-van der Velden M G, Kaysen G A, Straver H W, van Rijn H J, Stellaard F, Berger R, Rabelink T J . Transferrin synthesis is increased innephrotic patients insufficiently to replace urinary losses. J Am Soc Nephrol, 2001, 12(5): 1017–1025
8 Branten A J, Swinkels D W, Klasen I S, Wetzels J F . Serum ferritin levels are increased in patients with glomerular diseasesand proteinuria. Nephrol Dial Transplant, 2004, 19(11): 2754–2760.
doi:10.1093/ndt/gfh454
9 Kemper M J, Bello A B, Altrogge H, Timmermann K, Ludwig K, Müller-Wiefel D E . Iron homeostasis in relapsing steroid–sensitivenephrotic syndrome of childhood. Clin Nephrol, 1999, 52(1): 25–29
10 Castellino P, Cataliotti A . Changes of protein kineticsin nephrotic patients. Curr Opin Clin NutrMetab Care, 2002, 5(1): 51–54.
doi:10.1097/00075197‐200201000‐00010
11 Shibasaki T, Misawa T, Matsumoto H, Abe S, Nakano H, Matsuda H, Gomi H, Ohno I, Ishimoto F, Sakai O . Characteristics of anemiain patients with nephrotic syndrome. NipponJinzo Gakkai Shi, 1994, 36(8): 896–901
12 Cooper M A, Buddington B, Miller N L, Alfrey A C . Urinary ironspecification in nephrotic syndrome. AmJ Dis, 1995, 25(2): 314–319.
doi:10.1016/0272‐6386(95)90014‐4
13 Howard R L, Buddington B, Alfrey A C . Urinary albumin, transferrin, and iron excretion in diabeticpatients. Kidney Int, 1991, 40(5): 923–926.
doi:10.1038/ki.1991.295
14 Feinstein S, Becker-Cohen R, Algur N, Raveh D, Shalev H, Shvil Y, Frishberg Y . Erythropoietin deficiencycauses anemia in nephrotic children with normal kidney function. Am J Kidney Dis, 2001, 37(4):736–742
15 Alfrey A C . Role of iron and oxygen radicals in the progression of chronic renalfailure. Am J Kidney Dis, 1994, 23(2): 183–187
16 Nankivell B J, Boadle R A, Harris D C . Iron accumulation in human chronic renal disease. Am J Kidney Dis, 1992, 20(6): 580–584
17 kaysen G A, Sun X, Jones H Jr, Martin V I, Joles J A, Tsukamoyo H, Couser W G, Bander H . Non-iron-mediated alteration in hepatic transferrin geneexpression in the nephrotic rat. KidneyInt, 1995, 47(4): 1068–1077.
doi:10.1038/ki.1995.153
18 Mähr N, Neyer U, Prischl F, Kramar R, Mayer G, Kronenberg F, Lhotta K . Proteinuria and hemoglobinlevels in patients with primary glomerular disease. Am J Kidney Dis, 2005, 46(3): 424–431.
doi:10.1053/j.ajkd.2005.06.002
19 Terrier B, Fakhouri F, Sultanik P, Delarue R, Hummel A . Urinary erythropoietin excretion:an unknown cause of anemia during nephrotic syndrome. Rev Med Interne, 2006, 27(8): 643–645
20 Vaziri N D, Kaupke C J, Barton C H, Gonzales E . Plasmaconcentration and urinary excretion of erythropoietin in adult nephroticsyndrome. Am J Med, 1992, 92(1): 35–40.
doi:10.1016/0002‐9343(92)90012‐Z
21 Zhou X J, Vaziri N D . Erythropoietin metabolismand pharmacokinetics in experimental nephrosis. Am J Physiol Renal Physiol, 1992, 263(5pt2): F812–F815
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed