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

Lead Nephropathy: Differential Diagnoses & Workup

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

Differential Diagnoses

Light Chain-Associated Renal Disorders
Nephritis, Interstitial
Nephritis, Radiation
Nephropathy, Uric Acid
Nephrosclerosis
Toxicity, Arsenic

Workup

Laboratory Studies

  • The diagnosis of lead nephropathy requires a high index of suspicion. Most important is obtaining a detailed history that includes occupational or environmental lead exposure, followed by the measurement of total body burden of lead. In 1973, Emmerson suggested the following diagnostic criteria for chronic lead nephropathy: (1) features of long-standing, slowly progressive chronic kidney disease; (2) moderate-to-considerable contraction of both kidneys; (3) definitive evidence of excessive past lead exposure; and (4) exclusion of alternative causes for chronic kidney disease.
  • CBC count
    • A CBC count may serve to identify lead suppression of hematopoiesis and anemia of chronic kidney disease.
    • Peripheral blood smear analysis may show a hypochromic microcytic anemia and basophilic stippling in red blood cells.
  • Chemistries
    • Acute lead nephrotoxicity is associated with hypophosphatemia and non–gap metabolic acidosis secondary to Fanconi syndrome and occasionally even hypocalcemia.
    • Chronic lead nephrotoxicity causes loss of kidney function and consequent elevated blood urea nitrogen and creatinine levels. Hyperuricemia is common.
  • Heme enzymes
    • Erythrocyte aminolevulinic acid dehydratase (ALAD) activity is strongly inhibited by lead because lead oxidizes ALAD's sulfhydryl group and removes zinc from its active site. Consequently, ALAD activity levels are decreased in persons with lead poisoning. Iron deficiency can increase ALAD activity and may mask the lead-induced inhibition of ALAD activity at least in the initial stages; thus, determining iron reserves before examining ALAD activity levels is important.

      • Uremic patients, besides those with lead exposure, may also have lower ALAD activity. The ratio of ALAD to restored ALAD has been suggested as a superior marker of chronic lead exposure.
      • Erythrocyte ALAD levels can be restored by replacing the lead with zinc and by the negative sulfhydryl donor, dithiothreitol. Restored ALAD is increased following exposure to lead, presumably as a compensatory effect. In a 2002 study, Fontanellas et al found that patients with a history of chronic lead exposure and those with renal failure and positive EDTA chelation test results showed a marked reduction in the ratio of ALAD to restored ALAD (0.16 and 0.19, respectively). In contrast, normal controls and patients with chronic kidney disease and normal lead excretion (ratio 0.5 and 0.47) had higher ratios.
      • Inhibition of ALAD results in an increase in blood and urinary concentrations of aminolevulinic acid. The urinary excretion of aminolevulinic acid has also been widely used as a measure of the biologic effect of lead in workers who are occupationally exposed.
    • Similarly, heme enzymes, such as zinc-protoporphyrin and free erythrocyte protoporphyrin, are known to be altered by lead and have been used in the past for lead detection. Results from these tests reflect lead exposure in the previous 3 months (approximate life of a red blood cell) and cannot be used to assess the body burden of lead. Furthermore, erythrocyte protoporphyrin levels are elevated in persons with iron deficiency anemia.
  • Urinary markers
    • Chronic lead nephropathy occurs as a progressive interstitial nephropathy, which is difficult to diagnose at an early stage. Urinary analysis shows mild-to-moderate proteinuria. Blood urea nitrogen levels, serum creatinine values, and the GFR are abnormal only in late stages of nephropathy, when the changes are already irreversible.
    • A number of potential markers of early kidney changes have been studied in individuals exposed to lead. Of the early markers of nephrotoxicity, urinary N -acetyl-beta-D-glucosaminidase excretion has been shown to increase in early lead nephropathy. However, more recent studies have questioned its usefulness as a marker of chronic lead nephropathy, reporting that the elevation in urinary N -acetyl-beta-D-glucosaminidase activity may be an overly sensitive indicator and the rise could be secondary to concomitant cadmium exposure and even may be secondary to a sharp increase in lead burden, rather than cumulative exposure of lead.
    • The renal excretion of 6-keto-prostaglandin factor 1-alpha is reduced in patients exposed to lead, and excretion of thromboxane is enhanced.
  • Blood lead level
    • In the United States, the average blood lead level in unexposed individuals is 3 mcg/dL. Medical surveillance is needed for children when their blood level exceeds 10 mcg/dL.
    • Acute lead poisoning is recognized when classic symptoms of acute intoxication are present and the blood lead level is elevated (>40 mcg/dL). When the blood lead level exceeds 150 mcg/dL, encephalopathy is common and may be accompanied by fatal seizures. However, blood lead levels correlate best with recent exposure, and a normal value does not exclude remote exposure with an increased body burden of lead. Thus, blood lead levels are not useful for investigating chronic lead nephropathy.
    • The best measure for assessing the total accumulation of lead in the body is CaNa2 EDTA lead mobilization test.
  • CaNa2 EDTA lead mobilization test
    • The test is performed by administering 2 g of CaNa2 EDTA intramuscularly in 2 divided doses 12 hours apart or 1 g intravenously and collecting urine for 24 hours. Patients with kidney disease should collect urine over 3-6 days. EDTA is a chelation agent for lead sequestered in body storage sites and mobilizes it for renal excretion in the form of lead-EDTA chelate. Individuals without any unusual prior exposure to lead would excrete less than 650 mcg of lead over the collection period. Cumulative excretion greater than this level is indicative of excessive lead burden.
    • In children, a dose of 30-50 mg/kg of CaNa2 EDTA is administered intramuscularly or intravenously and urine is collected over 8 hours. A positive mobilization test result is a ratio of the dose of EDTA administered (in mg) to the quantity of lead excreted (in mcg) of greater than 0.6.

Imaging Studies

  • Kidney ultrasound: Kidneys are contracted with chronic lead nephropathy.
  • X-ray fluorescence
    • X-ray fluorescence (XRF) is a safe, noninvasive, and reliable technique to measure lead in the skeleton. XRF works by emitting x-rays at bone to activate electrons in different electron shells. Lead atoms respond to x-ray excitation by fluorescing, with greater fluorescence associated with higher concentrations of lead. The photons are collected in a detector and counted, yielding an estimate of bone lead.
    • Two types of XRF are used. L-line XRF stimulates electrons in the L electron shell, whereas K-line XRF acts only on electrons in the K shell. The L-line XRF uses weakly penetrating radiation, and measurements reflect lead in the subperiosteal bone, which is a mobilizable compartment of lead. Accurate calibration is somewhat difficult with this technique. The latter technique permits detection of lead molecules from the full thickness of bone and allows accurate assessment of the lead-to-calcium ratio. The exposure to radiation in this technique is much less compared with that of a conventional x-ray film.
    • The XRF technique to determine skeletal lead stores has been proposed as an epidemiological tool to help screen large populations because the CaNa2 EDTA mobilization test is too cumbersome, invasive, and expensive to be used in the general population.

Procedures

  • Bone lead measurements
    • More than 90% of the total burden of lead is in bone, with 70% in dense bone. Therefore, a direct measurement of dense bone lead content can be an accurate diagnostic test.
    • In 1988, Wedeen et al suggested that iliac crest bone lead-to-calcium ratios exceeding 100 X 10-6 and transiliac lead-to-calcium ratios exceeding 140 X 10-6 are consistent with the diagnosis of lead nephropathy. However, data from Antwerp, Belgium, have demonstrated that the chelation test provides as accurate an estimate of body lead burden when compared with transiliac biopsy results. Thus, bone biopsies are not indicated for the diagnosis of lead poisoning.
  • Kidney biopsy: Kidney biopsy is not needed for diagnosis. Results may show nonspecific changes of a chronic tubulointerstitial nephritis.

Histologic Findings

The potential effects of lead extend from reversible proximal tubular changes to interstitial nephritis and chronic kidney disease.

Acute lead nephropathy

The characteristic histological finding is the presence of acid-fast nuclear inclusion bodies in the proximal tubular cells, which are lead-protein complexes. Three types of characteristic changes in the nuclei are described: (1) lead-induced nuclear inclusion bodies, (2) clumped granular chromatin, and (3) pseudo inclusions or nuclear invagination of cytoplasmic contents.

Other ultrastructural changes include swollen mitochondria in the tubular lining cells, with distorted cristae. Endoplasmic reticula are swollen and increased in number. Lysosomes are often numerous, some of which may have a laminated appearance and may contain dense bodies of varying sizes. Brush border structures are distorted, with a reduced number of microvilli or with swollen microvilli. Most of these histopathologic changes are reversible with treatment.

Chronic lead nephropathy

Changes in chronic lead nephropathy are nonspecific. Macroscopically, kidneys appear contracted and have a granular surface. The cut surface shows general loss of cortical tissue, corticomedullary demarcation, and vascular markings. The pyramids are small but intact.

Upon histopathologic analysis, the tissue shows varying degrees of relatively acellular interstitial nephritis. Areas of dilated tubules alternate with atrophic tubules, rendering a granular appearance to the kidney surface. A large proportion of glomeruli are lost without leaving a trace, which is a characteristic feature. The remaining glomeruli are irregularly distributed, some with periglomerular fibrosis.

Glomerular cells have nonspecific abnormalities, such as occasional swelling and distortion of organelles in the cytoplasm, but have normal basement membranes. The glomeruli also show adhesive glomerulitis, with damage varying from single adhesions to complete obliteration of the capsular space. The inclusion bodies described in acute lead nephropathy are usually absent. The vessels show arteriolar nephrosclerotic changes. Immunofluorescence reveals a variety of immunoglobulin deposits in glomerular capillaries and tubular basement membranes, suggesting a role for immune mechanisms.

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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