PMID- 16609688
OWN - NLM
STAT- MEDLINE
DCOM- 20060810
LR  - 20181201
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 69
IP  - 7
DP  - 2006 Apr
TI  - Proinflammatory effects of iron sucrose in chronic kidney disease.
PG  - 1259-63
AB  - Inflammation is a central component of progressive chronic kidney disease (CKD). 
      Iron promotes oxidative stress and inflammatory response in animals and promotes 
      progressive CKD. Parenteral iron provokes oxidative stress in patients with CKD; 
      however, its potential to provoke an inflammatory response is unknown. In 20 
      veterans with CKD, 100 mg iron sucrose was administered intravenously over 5 min 
      and urinary excretion rate and plasma concentration of monocyte chemoattractant 
      protein-1 (MCP-1) were measured at timed intervals over 24 h. Patients were then 
      randomized to placebo or N-acetyl cysteine (NAC) 600 mg b.i.d. and the experiment 
      was repeated at 1 week. Iron sucrose markedly increased plasma concentration and 
      urinary excretion rate of MCP-1 at baseline and at 1 week visits (P < 0.0001 for 
      time effect). Urinary excretion peaked at 30 min and plasma concentration at 15 
      min. Plasma MCP-1 concentration fell from 164 +/- 17.7 to 135 +/- 17.7 pg/ml with 
      NAC, whereas it remained unchanged from 133 +/- 12.5 to 132 +/- 17.7 pg/ml with 
      placebo (P=0.001 for visit x antioxidant drug interaction). There was a reduction 
      in MCP-1 urinary excretion rate from visit 1 to 2. At the baseline visit, the 
      urinary excretion rate averaged 305 +/- 66 pg/min and at the second visit 245 +/- 
      67 pg/min (mean difference 60 +/- 28 pg/min, P = 0.030). There was no improvement 
      in urinary MCP-1 excretion with NAC. In conclusion, iron sucrose causes rapid and 
      transient generation and/or release of MCP-1 plasma concentration and increases 
      urinary excretion rate, and systemic MCP-1 level but the urinary excretion rate 
      is not abrogated with the antioxidant NAC. These results may have implications 
      for the progression of CKD with parenteral iron.
FAU - Agarwal, R
AU  - Agarwal R
AD  - Indiana University School of Medicine and Richard L Roudebush VA Medical Center, 
      Indianapolis, Indiana 46202, USA. ragarwal@iupui.edu
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Ferric Compounds)
RN  - FZ7NYF5N8L (Ferric Oxide, Saccharated)
RN  - QLZ991V4A2 (Glucaric Acid)
SB  - IM
MH  - Aged
MH  - Chemokine CCL2/blood/urine
MH  - Chronic Disease
MH  - Ferric Compounds/*toxicity
MH  - Ferric Oxide, Saccharated
MH  - Glucaric Acid
MH  - Humans
MH  - Inflammation/*chemically induced
MH  - Kidney Diseases/blood/*physiopathology/urine
MH  - Kidney Failure, Chronic/blood/*physiopathology/urine
MH  - Reproducibility of Results
EDAT- 2006/04/13 09:00
MHDA- 2006/08/11 09:00
CRDT- 2006/04/13 09:00
PHST- 2006/04/13 09:00 [pubmed]
PHST- 2006/08/11 09:00 [medline]
PHST- 2006/04/13 09:00 [entrez]
AID - S0085-2538(15)51631-1 [pii]
AID - 10.1038/sj.ki.5000164 [doi]
PST - ppublish
SO  - Kidney Int. 2006 Apr;69(7):1259-63. doi: 10.1038/sj.ki.5000164.