Subject(s)
Abscess/diagnosis , Fever/diagnosis , Kidney Diseases/diagnosis , Klebsiella Infections/diagnosis , Klebsiella pneumoniae/isolation & purification , Puerperal Infection/diagnosis , Abscess/microbiology , Abscess/therapy , Adult , Combined Modality Therapy , Drainage , Female , Fever/microbiology , Fever/therapy , Hematuria/microbiology , Hematuria/therapy , Hematuria/urine , Humans , Kidney Diseases/microbiology , Kidney Diseases/therapy , Klebsiella Infections/complications , Klebsiella Infections/therapy , Klebsiella pneumoniae/enzymology , Postpartum Period , Pregnancy , Puerperal Infection/microbiology , Puerperal Infection/therapy , Pyuria/microbiology , Pyuria/therapy , Pyuria/urine , Treatment Outcome , Urinalysis , Urine/microbiology , beta-Lactamases/analysisABSTRACT
Studies indicate that environmental exposure to lead is associated with reduced renal function. Whether lead affects progressive diabetic nephropathy is unclear. Eighty-seven patients with type II diabetes and diabetic nephropathy (serum creatinine of 1.5-3.9 mg/dl) with normal body lead burden and no lead exposure history were observed over a 12-month period. Thirty subjects with high normal body lead burdens (80-600 microg) were randomly assigned to a chelation and control group. For 3 months, the 15 chelation-group patients underwent lead-chelation therapy with calcium disodium ethylenediaminetetraacetic acid weekly until body lead burden fell <60 microg, and the 15 control group subjects received a weekly placebo. During the following 12 months, renal function was regularly assessed at 3-month intervals. The primary outcome was an elevation of serum creatinine to 1.5 times baseline value during the observation period. A secondary outcome was temporal changes in renal function following chelation therapy. Twenty-six patients achieved the primary outcome. Basal blood lead levels and body lead burden were the most important risk factors in predicting progressive diabetic nephropathy. Following chelation, the rates of decline in glomerular filtration rates in the chelation group and the control group, respectively, were 5.0+/-5.7 ml and 11.8+/-7.0 ml/min/year/1.73 m(2) of body surface area (P=0.0084) during follow-up, although both groups had similar rates of progression of renal function during the 12-month observation period. We concluded that low-level environmental lead exposure accelerates progressive diabetic nephropathy and lead-chelation therapy can decrease its rate of progression.
Subject(s)
Chelating Agents/therapeutic use , Diabetes Mellitus, Type 2/complications , Diabetic Nephropathies/etiology , Diabetic Nephropathies/prevention & control , Edetic Acid/therapeutic use , Environmental Exposure/adverse effects , Lead Poisoning/complications , Adult , Aged , Disease Progression , Female , Humans , Male , Middle Aged , Prospective StudiesABSTRACT
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 ethylenediaminetetraacetic 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.
