TY - JOUR
T1 - Lead chelation therapy and urate excretion in patients with chronic renal diseases and gout
AU - Lin, J. L.
AU - Yu, C. C.
AU - Lin-Tan, D. T.
AU - Ho, H. H.
PY - 2001
Y1 - 2001
N2 - Background. It is known that chronic renal insufficiency (CRI) patients with gout may have subtle lead poisoning. In addition, gout episodes frequently aggravate progressive renal insufficiency because of the use of nephrotoxic drugs and urate deposition. Our study was arranged to evaluate the causal effect of environmental lead exposure on urate excretion in CRI patients. Methods. A cross-section study and a randomized, controlled trial were performed. Initially, 101 patients with CRI and without a history of previous lead exposure received ethylenediamine-tetraacetic acid mobilization tests to assess body lead stores (BLS). Then, a clinical trial was performed; 30 CRI patients with gout and high-normal BLS and the changes of urate excretion in these patients were compared before and after lead chelating therapy. The treated group received four-week chelating therapy, and the control group received a placebo therapy. Results. The BLS of patients with CRI and gout was higher than that of patients with CRI only, and none had subtle lead poisoning. The BLS, not the blood lead level (BLL), significantly correlated to indices of urate excretion in all CRI patients after related factors were adjusted. In addition, after lead chelating therapy, urate clearance markedly improved after a reduction of the BLS of patients with CRI and gout (study group 67.9 ± 80.0% vs. control group 1.2 ± 34.0%, P = 0.0056). Conclusion. Our findings suggest that the chronic low-level environmental lead exposure may interfere with urate excretion of CRI patients. Importantly, the inhibition of urate excretion can be markedly improved by lead chelating therapies. These data shed light on additional treatment of CRI patients with gout; however, more studies are needed to confirm our findings.
AB - Background. It is known that chronic renal insufficiency (CRI) patients with gout may have subtle lead poisoning. In addition, gout episodes frequently aggravate progressive renal insufficiency because of the use of nephrotoxic drugs and urate deposition. Our study was arranged to evaluate the causal effect of environmental lead exposure on urate excretion in CRI patients. Methods. A cross-section study and a randomized, controlled trial were performed. Initially, 101 patients with CRI and without a history of previous lead exposure received ethylenediamine-tetraacetic acid mobilization tests to assess body lead stores (BLS). Then, a clinical trial was performed; 30 CRI patients with gout and high-normal BLS and the changes of urate excretion in these patients were compared before and after lead chelating therapy. The treated group received four-week chelating therapy, and the control group received a placebo therapy. Results. The BLS of patients with CRI and gout was higher than that of patients with CRI only, and none had subtle lead poisoning. The BLS, not the blood lead level (BLL), significantly correlated to indices of urate excretion in all CRI patients after related factors were adjusted. In addition, after lead chelating therapy, urate clearance markedly improved after a reduction of the BLS of patients with CRI and gout (study group 67.9 ± 80.0% vs. control group 1.2 ± 34.0%, P = 0.0056). Conclusion. Our findings suggest that the chronic low-level environmental lead exposure may interfere with urate excretion of CRI patients. Importantly, the inhibition of urate excretion can be markedly improved by lead chelating therapies. These data shed light on additional treatment of CRI patients with gout; however, more studies are needed to confirm our findings.
KW - Chronic renal insufficiency
KW - Environmental lead exposure
KW - Nephrotoxicity
KW - Pollutant
KW - Serum urate
UR - http://www.scopus.com/inward/record.url?scp=0034961669&partnerID=8YFLogxK
U2 - 10.1046/j.1523-1755.2001.00795.x
DO - 10.1046/j.1523-1755.2001.00795.x
M3 - 文章
C2 - 11422760
AN - SCOPUS:0034961669
SN - 0085-2538
VL - 60
SP - 266
EP - 271
JO - Kidney International
JF - Kidney International
IS - 1
ER -