eMedicine Specialties > Nephrology > Drug- and Nephrotoxin-Associated Kidney Disorders

Lead Nephropathy: Treatment & Medication

Author: Pranay Kathuria, MD, MBBS, FACP, FASN, Chief, Section of Nephrology, Associate Professor, Department of Internal Medicine, University of Oklahoma College of Medicine at Tulsa
Coauthor(s): Paresh Jadav, MD, Fellow, Department of Medicine, Division of Nephrology and Hypertension, University of Washington School of Medicine
Contributor Information and Disclosures

Updated: Feb 5, 2008

Treatment

Medical Care

The most important step in treatment is to prevent further exposure to lead. Accurate assessment of environmental and occupational exposure is essential. Modifying children's behavior to decrease hand-to-mouth activity is beneficial.

The US Occupational Safety and Health Administration has recommendations for occupational lead exposure. Under these guidelines, the permissible exposure limit is 50 mcg/m3 for an 8-hour, time-weighted average. Workers with blood lead levels greater than or equal to 60 mcg/dL must be removed from the work place. Additionally, employees should be removed from the work place if the average of their last 3 blood lead levels is 50 mcg/dL or greater. Individuals with blood lead levels greater than or equal to 40 mcg/dL must undergo medical evaluation.

Community-wide preventive actions are recommended when children are found to have blood lead levels greater than or equal to 10 mcg/dL. With blood lead levels from 15-19 mcg/dL, nutritional and educational interventions are recommended. With blood lead levels greater than or equal to 20 mcg/dL, medical evaluations and environmental interventions are recommended.

  • Acute lead poisoning and nephropathy
    • With acute lead poisoning, obtain a plain radiograph of the abdomen. If suggestive radiopacities are observed, gastric lavage, cathartics, or whole bowel irrigation may be used to limit absorption.
    • The indications for chelation therapy are well defined with acute lead poisoning.
    • Institute chelation therapy in children with lead levels greater than or equal to 45 mcg/dL. Treat children with levels greater than or equal to 70 mcg/dL as medical emergencies.
      • Succimer and penicillamine are oral chelation agents. Penicillamine may be used when blood lead levels are 25-40 mcg/dL, especially with a negative CaNa2 EDTA mobilization test result. Succimer may be an alternative; its main indication is in persons with blood lead levels greater than or equal to 45 mcg/dL.
      • Intravenous therapy is preferable with blood lead levels greater than or equal to 70 mcg/dL. Use the combination of British antilewisite (BAL) and CaNa2 EDTA with blood lead levels greater than or equal to 70 mcg/dL and in the presence of lead encephalopathy.
      • The CaNa2 EDTA lead mobilization test is useful for identifying patients in whom therapy will be successful.
    • In adults, consider chelation therapy for patients with blood lead levels greater than or equal to 70 mcg/dL. Also consider chelation therapy in symptomatic adults with blood lead levels exceeding 50 mcg/dL.
      • Available chelation agents for adults are BAL and CaNa2 EDTA.
      • Penicillamine and succimer do not have US Food and Drug Administration approval for treatment, although they are effective treatments.
    • Chelation therapy reverses Fanconi syndrome, transient hypertension, and tubular structural changes observed on histopathology findings.
  • Chronic lead nephropathy
    • Patients with chronic lead nephropathy, in the absence of marked interstitial fibrosis and with only minimal impairment in kidney function, may respond to chelation therapy.
    • Extremely limited data are available regarding the benefits of chelation therapy with documented lead nephropathy. In 1979, Wedeen et al treated patients with occupational lead nephropathy and found a 20% improvement in the GFR in 4 of 8 patients administered EDTA 3 times a week for 6-50 months. The reported improvements in kidney function could be from reversal of acute on chronic lead nephropathy.
    • Lin and coworkers from Taiwan performed 3 well-designed studies addressing populations of patients with high-normal lead levels and chronic kidney disease.
      • The first of these studies included 32 subjects with chronic kidney disease (serum creatinine level of 1.5-4 mg/dL) and mildly elevated lead burden (lead excretion value of 150-600 mcg with the 3-d CaNa2 EDTA lead mobilization test). Subjects were randomized to receive EDTA chelation therapy or placebo weekly for 2 months and were followed for an additional 12 months. The reciprocal of serum creatinine (1/Cr) versus time data suggested that using chelation may slow the progression of renal disease.
      • The same group published results of chelation therapy in 36 subjects (24 study group subjects and 12 controls) with serum creatinine values of 1.5-4 mg/dL and high-normal bone lead burden. This time, chelation therapy with CaNa2 EDTA was administered weekly for 3 months. The treated group had an improvement in CrCl of as much as 10.2%, while kidney function declined by as much as 11% in the control group at 1 year.
      • The third study by Lin et al was published in 2003 and included 202 subjects who were followed for 2 years. Sixty-four with a high-normal body lead burden (urinary lead excretion >80 mcg and <600 mcg after 1 g of CaNa2 EDTA infusion) and serum creatinine levels of less than 4.2 mg/dL were randomized to chelation or placebo. In the initial 3 months, the chelation group received 1 g of CaNa2 EDTA every week and the controls received placebo. In the ensuing 24 months, repeated chelation therapy was administered weekly to patients with high-normal lead unless upon repeated testing the body lead burden fell below 60 mcg. The GFR increased by 11.9% (3.4 mL/min) versus a 3.6% (-1 mL/min) decline in the control group (P <.001) at the end of the initial 3 months. Thereafter, no further improvement in the GFR was observed in these patients.
      • At the end of 27 months, the mean change in GFR was +2.1 mL/min in the chelation group and -6 mL/min in the control group (P <.001) over the 27-month study.
    • These studies suggest that in patients with increased lead burden, chelation with small doses of CaNa2 EDTA at longer intervals might be safe for treating chronic kidney disease. However, repeated and chronic exposure to CaNa2 EDTA may create its own nephrotoxicity; therefore, use caution when deciding to institute chelation therapy. Exclude other causes of kidney disease, and define an endpoint of therapy, such as normalization of the CaNa2 EDTA test results and/or improvement in kidney function.

Consultations

  • Toxicologist
  • Nephrologist

Diet

The diet should be adequate in energy (caloric) intake and replete in calcium, zinc, and iron. Data from the Normative Aging Study suggest that low dietary intake of vitamin D may increase accumulation of lead in bones, while low dietary intake of vitamin C and iron may increase lead levels in blood in subjects who range in age from middle-aged to elderly. Similar data associate calcium and iron deficiency with lead absorption in children. Although no studies have specifically addressed treatment of lead exposure with calcium and iron supplementation, it is a logical therapy to help limit the absorption of lead.

Medication

The mainstay of treatment is chelation therapy. Chelation agents contain sulfhydryl groups that bind lead, and the resulting complex is excreted either renally or hepatically. Oral chelation agents are succimer and penicillamine, while dimercaprol and CaNa2 EDTA are administered parenterally.

Chelation agents

Reduce blood levels and depot stores in lead poisoning.


Edetate calcium disodium (Calcium EDTA, Calcium disodium versenate)

Water-soluble compound. Can be used either IV/IM. Chelation only for extracellular lead. May induce CNS toxicity if BAL therapy is not initiated first when blood lead levels are >70 mcg/dL in children and 100 mcg/dL in adults and in encephalopathy. To prevent hypocalcemia, only CaNa2 EDTA should be used for chelation in heavy metal toxicity. When used IM, same daily dose is administered in 2-6 divided doses. Irritating and painful to muscles (lidocaine with IM preparation lessens pain). Must be used diluted in D5W or NS to <30 mg/mL.

Adult

Acute lead intoxication
1000-1500 mg/m2/d IV for 5 doses, dilute in 500 mL D5W or 0.9% NaCl and infuse IV over 8-12 h (for IM administration divide daily dose into 2-6 administrations); may repeat in 2 d if indicated; if blood levels >70 mcg/d, use with dimercaprol
Chronic lead nephropathy
Serum creatinine <2 mg/dL: 1000 mg/m2/d for 5 d
Serum creatinine 2-3 mg/dL: 500 mg/m2/d for 5 d; repeat qmo until lead excretion levels are normal
Serum creatinine 3-4 mg/dL: 500 mg/m2 q48h for 3 doses; repeat qmo until lead excretion levels are normal
Serum creatinine >4 mg/dL: 500 mg/m2 qwk; repeat qmo until lead excretion levels are normal

Pediatric

Administer as in adults

Enhances hypoglycemic effects of insulin in patients with diabetes; IV incompatibility with lactated Ringer solution and D10W; do not admix in same syringe as BAL

Documented hypersensitivity; kidney failure

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Ensure adequate hydration and diuresis prior to therapy; check kidney and hepatic function and urinalysis prior to and during therapy; monitor for cardiac rhythm changes; patients with lead encephalopathy may develop increased intracranial pressure during therapy; adverse effects include pain and local thrombophlebitis at injection site, flulike symptoms, histaminelike reaction, hypotension, arrhythmias, GI tract upset, paresthesias, elevated LFTs, acute renal failure, renal tubular acidosis, and transient bone marrow suppression
Do not confuse with the similarly named product edetate disodium (Endrate), which is indicated for hypercalcemia and ventricular arrhythmia secondary to digitalis toxicity; each of these 2 products are commonly referred to as EDTA and as a result, the 2 products are easily mistaken for each other when prescribing, dispensing, and administering; deaths in patients when mistakenly given edetate disodium instead of edetate calcium disodium or when edetate disodium was used for chelation therapy; for more information, see the FDA MedWatch Safety Information


Dimercaprol (British Anti-Lewisite, BAL in Oil)

DOC for treatment of lead toxicity. Chelation of intracellular and extracellular lead and is excreted in urine and bile. May be administered to patients with kidney failure. First made available during World War II and was first chelation agent used in lead encephalopathy. Sulfhydryl groups combine with ions of heavy metals to form soluble, nontoxic complexes that are excreted renally. Combination therapy with BAL and CaNa2 EDTA is recommended in all cases of severe, acute intoxication, particularly when encephalopathy is present. Administered IM q4h, mixed in a peanut oil base.

Adult

75 mg/m2 IM q4h for 5 d; not to exceed 24 mg/kg/d

Pediatric

Evidence of encephalopathy: Administer as in adults
Symptomatic without encephalopathy: 50 mg/m2/d
Asymptomatic with blood lead >45 mcg/dL: 50 mg/m2/d

Toxicity may increase when coadministered with selenium, uranium, iron, or cadmium; do not admix in same syringe with CaNa2 EDTA; may decrease iodine I 131 thyroidal uptake

Documented hypersensitivity; peanut allergy; concurrent iron supplementation therapy

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May be nephrotoxic and may cause hypertension; maintain urine alkalinity to prevent nephrotoxicity; caution when administering to patients with oliguria or G-6-PD deficiency; may induce hemolysis in patients with G-6-PD deficiency; adverse effects include tachycardia, GI tract upset, convulsions, myalgias, paresthesias, neutropenia and thrombocytopenia, fever, and burning sensation of eyes, lips, throat, and penis


Succimer (Chemet)

Analog of dimercaprol used in lead poisoning. Particularly useful in children with lead blood levels >45 mcg/dL. Generally well-tolerated following PO administration and produces linear dose-dependent reduction in serum lead concentration. Forms water-soluble chelate with heavy metals and is excreted in urine.

Adult

10 mg/kg PO q8h for 5 d followed by 10 mg/kg PO q12h for 14 d; allow 2 wk minimum between courses if repeat courses are indicated

Pediatric

Administer as in adults

Do not administer concomitantly with CaNa2 EDTA or penicillamine

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in kidney or hepatic impairment; to prevent toxicity, patient should be well hydrated; adverse reactions include fever, dizziness, nausea, vomiting, appetite loss, metallic taste, back pain, rash, flulike symptoms, mild-to-moderate neutropenia, and reversible elevation of AST, ALT, and alkaline phosphatase


Penicillamine (Cuprimine, Depen)

Recognized therapy for Wilson disease and cystinuria. Used as an oral lead chelation agent but has never been licensed for this indication by FDA.

Adult

25-35 mg/kg/d PO divided tid/qid, initiate therapy at 25% of dose and increase gradually to full dose in 2-4 wk to minimize adverse effects, continue until blood lead level <60 mcg/dL

Pediatric

Administer as in adults

Increases effects of immunosuppressants, phenylbutazone, and antimalarials; decreases digoxin effects; effects may decrease with coadministration of zinc salts, antacids, and iron

Documented hypersensitivity; renal insufficiency; previous penicillamine-related aplastic anemia; concomitant administration of hematopoietic-depressant drugs (eg, gold, immunosuppressants, antimalarials)

Pregnancy

D - Unsafe in pregnancy

Precautions

Urinalysis, CBC count, and liver and kidney function should be assessed weekly; caution in penicillin allergy; has been associated with fatalities related to aplastic anemia, agranulocytosis, Goodpasture syndrome, myasthenia gravis, and thrombocytopenia; other adverse effects include rash, urticaria, hypogeusia, arthralgias, edema, fever, pancreatitis, hepatitis, optic neuritis, nephrotic syndrome, drug-induced lupus, lymphadenopathy, and adverse GI tract effects

More on Lead Nephropathy

Overview: Lead Nephropathy
Differential Diagnoses & Workup: Lead Nephropathy
Treatment & Medication: Lead Nephropathy
Follow-up: Lead Nephropathy
Multimedia: Lead Nephropathy
References
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Further Reading

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Keywords

saturnine nephropathy, lead toxicity, lead poisoning, industrial lead exposure, lead exposure, lead paint, lead intoxication, nephrotoxicity, lead-induced nephropathy, acute lead poisoning, chronic lead nephropathy, interstitial nephritis, lead hypertension, lead encephalopathy, kidney transplant, renal replacement, chronic renal failure, CRF, end-stage renal disease, ESRD, end stage renal disease, pica, saturnine gout, hyperuricemia, hypertension, illegal corn whiskey, moonshine, huffing, gun shot wound, GSW, kohl, surma, Fanconi syndrome, Fanconi's syndrome

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Contributor Information and Disclosures

Author

Pranay Kathuria, MD, MBBS, FACP, FASN, Chief, Section of Nephrology, Associate Professor, Department of Internal Medicine, University of Oklahoma College of Medicine at Tulsa
Pranay Kathuria, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation
Disclosure: Nothing to disclose.

Coauthor(s)

Paresh Jadav, MD, Fellow, Department of Medicine, Division of Nephrology and Hypertension, University of Washington School of Medicine
Paresh Jadav, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, and American Medical Student Association/Foundation
Disclosure: Nothing to disclose.

Medical Editor

James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine, Director of Nephrology Training Program, Kidney Disease Program, University of Louisville School of Medicine; Director, Metabolic Stone Clinic
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Roche Honoraria Consulting

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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