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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 18  |  Issue : 1  |  Page : 83-86
Chronic lead poisoning: A "forgotten" cause of renal disease

Department of Nephrology and Dialysis, Ibn-Rochd University Hospital Center, Casablanca, Morocco

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Chronic lead nephropathy occurs as a result of years of lead exposure. Nowadays, with the induction of high standards for industrial hygiene, symptomatic lead intoxication has become extremely rare. We report a case of chronic lead nephropathy in a 59­year-old man who worked in a battery-recycling unit and was diagnosed with plumbism during a regular health screening few years ago. The diagnosis was suggested by the following findings: serum creatinine 160 µg/L, creatinine clearance 46 ml/min, daily urine protein excretion 0.1 g, uric acid 9.7 mg/dl, blood lead 9.2 µg/dl, and a urinary excretion of 850 µg lead/72h after a mobilisation test by a Na 2 -Ca-EDTA chelating agent. Renal ultrasound showed bilateral borderline small kidneys. The kidney biopsy revealed moderate focal atrophy, loss of proximal tubules, and prominent interstitial fibrosis. The patient was prescribed angiotensin­converting-enzyme inhibitors to slow the progression of renal insufficiency and control the blood pressure. Hyperuricemia was also treated and controlled. During the regular follow-up, renal function remained stable with no proteinuria. A high index of suspicion for lead intoxication in chronic kidney disease patients should be practiced, especially in patients with hyperuricemia. Chelation of lead urinary excretion is helpful in the diagnosis of this disease.

Keywords: Lead, Chronic kidney disease, Hypertension, Nephropathy

How to cite this article:
Benjelloun M, Tarrass F, Hachim K, Medkouri G, Benghanem MG, Ramdani B. Chronic lead poisoning: A "forgotten" cause of renal disease. Saudi J Kidney Dis Transpl 2007;18:83-6

How to cite this URL:
Benjelloun M, Tarrass F, Hachim K, Medkouri G, Benghanem MG, Ramdani B. Chronic lead poisoning: A "forgotten" cause of renal disease. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2022 Jun 27];18:83-6. Available from: https://www.sjkdt.org/text.asp?2007/18/1/83/31851

   Introduction Top
Throughout human history, lead has been both a necessity and an evil. It has allowed for great civilizations to rise, and perhaps contributed to their demise. [1] Its toxicity can be either acute and dramatic or chronic and subtle, requiring clinicians to have a high degree of suspicion in diagnosing it.[1],[2] However, the incidence of lead poisoning has decreased dramatically over the last twenty years due to universal screening and education. [2],[3] Nowadays, symptomatic lead intoxication has become extremely rare. [4]

The first report of nephrotoxicity attributable to lead was published in 1863 by Lancereaux. [6] He noted substantial atrophy of the renal cortex and tubular fibrosis in the kidney in an artist who habitually held paintbrushes in his mouth. In the late 1920s, an epidemic of chronic nephritis in Queensland, Australia due to childhood lead poisoning brought to light the full spectrum of lead-induced nephropathy. Subsequently, reports of lead nephropathy appeared among "moonshiners" (ie, distillers of illegal corn whiskey) in the southeast United States and among industrial lead workers. [4],[6]

We report here a case of nephrotoxicity attributable to chronic poisoning in a lead smelting worker. We discuss the clinical and public health issues surrounding chronic adult lead toxicity, including current sources of exposure, diagnosis, and treatment strategies for chronic toxicity.

   Case report Top

A 59-year-old worker in a battery-recycling unit visited our out-patient department two years ago because of weakness, fatigue, and impaired renal function for several months. His past history was remarkable for the diagnosis of plumbism during a regular health screening 12 years prior to the patient presentation two years ago. Findings consisted of recurrent abdominal pain and grayish discoloration of the gingival tooth border consistent with 'lead line', with elevated blood lead level. The patient had also suffered from irregularly treated hypertension for about four years. There was no history of alcohol intake or smoking. On physical exami­nation, the patient's blood pressure was 160/80 mmHg, and the other vital signs were normal. Laboratory investigations revealed a serum creatinine of 160 µg/L, creatinine clearance of 46 ml/min, daily urine protein excretion of 0.1 g, uric acid of 9.7 mg/dl, and blood lead level of 9.2 µg/dl. No anemia was found and liver function tests were normal. Renal ultrasound showed bilateral borderline small kidneys, compatible with chronic gout nephropathy. Since the blood lead level was thought to reflect only recent lead exposure, an infusion of two grams of Na 2 -Ca-EDTA chelating agent by an intramuscular route was administered to assess the whole body lead burden. Urine collection over a 72 h period revealed lead excretion of 850 µg. No adverse effects were noted during the infusion. A kidney biopsy showed moderate focal atrophy with loss of proximal tubules with prominent interstitial fibrosis [Figure - 1]. Immunofluorescent examination did not reveal any deposits. After the diagnosis of chronic interstitial kidney disease secondary to lead intoxication, EDTA chelation therapy was not initiated, because the EDTA mobilization test revealed urinary lead excretion (<1000 µg).[4],[5] The patient was prescribed angiotensin­converting-enzyme inhibitors to slow the progression of renal insufficiency and to control the patient's blood pressure. He was also prescribed a low-salt and low-protein diet. The hyperuricemia was treated and controlled by allopurinol 200 mg q.d. The patient has been regularly followed up as an out-patient every three months. The latest serum creatinine was found to be 180 µg/L, without proteinuria.

   Discussion Top

The clinical signs and symptoms of lead poisoning are non-specific [Table - 1], which makes the diagnosis difficult, especially when it is not industrially related. [4]

Chronic lead exposure can affect a variety of organs, including the kidney. [2],[3] Lead exposure causes renal injury through several pathways. It appears to act as a direct tubular toxin, as demonstrated in this patient by the presence of characteristic proximal tubular intranuclear inclusions that contained lead and protein. Chronic tubulointerstitial nephritis with fibrosis reflects previous and possibly ongoing lead-induced tubular injury.[4] Recently published data also demonstrated the importance of reactive oxygen radicals in mediating lead-induced tubulointerstitial damage. Scavengers of these radicals may alleviate some of the damage and thus could provide alternative therapies for this disorder. [7],[8]

Gout and hypertension are the major clinical manifestations of lead nephropathy. [2],[3] The prominent feature of early hyper­uricemia in lead nephropathy may explain the confusion between lead nephropathy and gouty nephropathy. Lead urinary excretion after ethylenediamine tetraacetic acid (EDTA)-lead mobilization testing may help differentiate the diagnosis. [4]

In patients with chronic lead nephropathy, chelation therapy has been used to improve renal function and slow the progression of renal insufficiency. [9],[10] Treatment of lead intoxication with intravenous ethylene­diamine-tetraacetic acid (EDTA) depends on the urinary excretion of chelated lead. In patients with mild chronic kidney disease and an EDTA mobilization test revealing excessive urinary lead excretion (>1000 µg), chelation therapy should be considered. [4],[5]

In summary, exposure and high blood lead levels appear to be common features among individuals who develop lead nephropathy. One should have a high index of suspicion for lead intoxication in chronic kidney disease especially in patients with hyperuricemia. The presence of lead urinary excretion after chelation is helpful in the diagnosis of this disease[11].

   References Top

1.Ritz E, Mann J, Stoeppler M. Lead and the kidney. Adv Neph Necker Hosp.1988;17:241-74.  Back to cited text no. 1    
2.Muntner P, He J, Vupputuri S, Coresh J, Batuman V. Blood lead and chronic kidney disease in the general United States population: results from NHANES III. Kidney Int 2003;63:1044-50.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Batuman V. Lead nephropathy, gout, and hypertension. Am J Med Sci 1993; 305:241-7  Back to cited text no. 3  [PUBMED]  
4.Brewster UC, Perazella MA. A review of chronic lead intoxication: an unrecognized cause of chronic kidney disease. Am J Med Sci 2004;327:341-7.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Weeden RP, Malik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med 1979;139:53-7.  Back to cited text no. 5    
6.Cledes J, Allain P. Chronic lead nephropathy. Epidemiology and diagnosis. Presse Med 1992;21:759-62  Back to cited text no. 6    
7.Gonick HC, Ding Y, Bondy S, Ni Z, Vagiri ND. Lead-induced hypertension: interplay of nitric oxide and reactive oxygen species. Hypertension 1997; 30:1487-92.  Back to cited text no. 7    
8.Vaziri ND, Liang K, Ding Y. Increased nitric oxide inactivation by reactive oxygen species in lead­induced hypertension. Kidney Int 1999;56:1492-8.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Sanchez-Fructuoso AI, Blanco J, Cano M, et al. Experimental lead nephro­pathy: treatment with calcium disodium ethylenedia-minetetraacetate. Am J Kidney Dis 2002;40:59-67.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Lin JL, Ho HH, Yu CC. Chelation therapy for patients with elevated body lead burden and progressive renal insufficiency: a randomized, controlled trial. Ann Intern Med 1999;130:7-13.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Akhtar AJ, Funnye AS, Akanno J. Gunshot-induced plumbism in an adult male. J Natl Med Assoc 2003;95:986-90.  Back to cited text no. 11  [PUBMED]  

Correspondence Address:
Faissal Tarrass
Ibn-Rochd University Hospital Center, Salama 3, Gr 6, “B”, N° 21 20450 Casablanca
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Source of Support: None, Conflict of Interest: None

PMID: 17237897

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  [Table - 1]

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