Effect of chelation therapy on progressive diabetic nephropathy in patients with type 2 diabetes and high-normal body lead burdens.
ABSTRACT A previous study in type 2 diabetic patients with high-normal body lead burdens showed that EDTA chelation therapy for 3 months slows progressive diabetic nephropathy during a 12-month follow-up. The effect of a longer course of therapy on kidney function decrease over a longer follow-up is not known.
A 12-month run-in phase, then a randomized single-blind study with a 27-month intervention.
University medical center; 50 patients (serum creatinine, 1.5-3.9 mg/dL) with high-normal body lead burden (≥80-<600 μg) were randomly assigned to the treatment and control groups.
The treatment group received weekly chelation therapy for 3 months to reduce their body lead burden to <60 μg and then as needed for 24 months to maintain this level. The control group received placebo for 3 months and then weekly for 5 weeks at 6-month intervals for 24 months.
The primary end point was change in estimated glomerular filtration rate (eGFR) over time. A secondary end point was a 2-fold increase in baseline serum creatinine level or the requirement for renal replacement therapy.
Body lead burdens were assessed by EDTA mobilization tests and eGFR was calculated using the equation for Chinese patients with type 2 diabetes.
Mean baseline eGFRs in the treatment and control groups were similar. After 3 months of chelation therapy, the change in eGFR in the treatment group (+1.0±4.8 mL/min/1.73 m(2)) differed significantly from that in the control group (-1.5±4.8 mL/min/1.73 m(2); P = 0.04). In the subsequent 24-month intervention, the yearly rate of decrease in eGFR (5.6±5.0 mL/min/1.73 m(2) per year) in the treatment group was slower than that (9.2±3.6 mL/min/1.73 m(2) per year; P = 0.04) in the control group. 17 (68%) control-group patients and 9 (36%) treatment-group patients achieved the secondary end point.
Small sample size, not double blind.
A 27-month course of EDTA chelation therapy retards the progression of diabetic nephropathy in type 2 diabetic patients with high-normal body lead burdens.
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ABSTRACT: The heavy metal lead (Pb) is a major environmental and occupational hazard. Epidemiological studies have demonstrated a strong association between lead exposure and the presence of chronic kidney injury. Some studies have suggested that chelation therapy with calcium disodium ethylenediaminetetraacetic acid (calcium disodium EDTA) might help decrease the progression of chronic kidney disease among patients with measurable body lead burdens. However, calcium disodium EDTA chelation in lead exposure is controversial due to the potential for adverse effects such as acute tubular necrosis. Therefore, we investigated the available randomized controlled trials assessing the renoprotective effects of calcium disodium EDTA chelation therapy. Our meta-analysis shows that calcium disodium EDTA chelation therapy can effectively delay the progression of chronic kidney disease in patients with measurable body lead burdens reflected by increasing the levels of estimated glomerular filtration rate (eGFR) and creatinine clearance rate (Ccr). There appears to be no conclusive evidence that calcium disodium EDTA can decrease proteinuria.Nephrology 01/2014; 19(1):56-9. · 1.69 Impact Factor
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ABSTRACT: In the present review we provide an update of the appropriate use of chelating agents in the treatment of intoxications with compounds of mercury, lead and copper. The relatively new chelators meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercapto-propanesulphonate (DMPS) can effectively mobilize deposits of mercury as well as of lead into the urine. These drugs can be administered orally and have relatively low toxicity compared to the classical antidote dimercaptopropanol (BAL). D-penicillamine has been widely used in copper overload, although 2,3-dimercaptosuccinic acid or tetrathiomolybdate may be more suitable alternatives today. In copper-toxicity, a free radical scavenger might be recommended as adjuvant to the chelator therapy.Journal of Trace Elements in Medicine and Biology 01/2014; · 1.96 Impact Factor
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ABSTRACT: S ince its earliest description in 1863 in France by Lancereaux, chronic lead nephropathy has been recognized in diverse settings, including episodic high exposure in the workplace and continuous low-level environmental exposure. 1 Later, clusters of chronic lead nephropathy cases between 1915 and 1935 were linked to childhood lead poisoning from ingestion of lead-based paint in Queensland, Australia, 2,3 and dur-ing the 1950s, to lead-contaminated moonshine whiskey in the southern United States. 1 Despite continued reports of chronic lead nephropathy from both occupational and nonoccupational settings, 1,4,5 the role of lead in kidney disease has been controver-sial and some authors have even questioned the very existence of chronic lead nephropathy. 6,7 Amidst this growing skepticism, this issue of AJKD presents a study by Chowdhury et al 8 reporting an increased risk of end-stage renal disease (ESRD) in individuals exposed to lead, mostly in the occupational setting. The authors analyzed blood lead values from 58,307 men in 11 states that participated in the Adult Blood Lead Surveillance (ABLES) program sponsored by the National Institute for Occupational Safety and Health. Compared to US general population (adjusted for age, race, sex and calendar), the analysis showed an increased standardized incidence ratio of ESRD at 5 years or later in individuals with at least one blood lead value above 51 mg/dL, with a medianAmerican journal of kidney diseases : the official journal of the National Kidney Foundation. 07/2014; 64(1):1-3.