Nephropathy in Chronic Lead Poisoning

Abstract

This paper presents a study of renal function in I02 patients with lead poisoning admitted to the Occupational Diseases Clinic in Bucharest during the past IO years; nearly half the patients had no history of lead colic. Every possible cause of renal damage, other than lead, was excluded by a careful differential diagnosis.Renal function was investigated by repeated determinations of blood urea, creatinine and uric acid, urea clearance, and endogenous creatinine clearance tests.Significant decreases of the clearance values (less than 50 ml./min. urea clearance and less than 8o ml./min. creatinine clearance), persistent high blood urea (more than 50 mg./Ioo ml.), and high blood creatinine (more than I-2 mg./ioo ml.) were found in a significant number of cases. These signs of impaired renal function were more frequent in the group of patients with chronic lead poisoning who had had several episodes of colic and an occupational exposure of more than IO years. A high blood pressure was also found more frequently in this group of patients.Undercompensated and decompensated renal failure was found in I7 patients, most of whom had been exposed to lead for more than IO years and had a history of several attacks of colic. Arterial hypertension accompanied the chronic renal failure in 13 patients, the renal impairment generally preceding the rise in blood pressure by several years.The duration of occupational lead exposure, the high absorption in the past, and the long period of observation of these patients, most of whom were repeatedly hospitalized, may explain the relatively high incidence (17 cases) of nephropathy with chronic renal failure in the present group. Impairment of urea clearance seems to be the earliest sign, at a time when the creatinine clearance is still normal. As the duration of exposure lengthens and the patient is subjected to active episodes of poisoning the creatinine clearance also deteriorates. Persistent urea retention and high creatininaemia may follow in time, accompanied rather frequently by arterial hypertension. A study of some of the cases followed for several years demonstrated this progressive evolution of lead nephropathy.A functional and transitory impairment of renal function is very probably caused by an impairment of intrarenal circulation, resulting from marked vasoconstriction of the renal vessels, forming part of the generalized vasoconstriction of lead poisoning. Prolonged exposure and frequently recurring episodes of acute poisoning may lead to progressive impairment of renal function and to the development of organic lesions.Special attention should be paid to renal function tests in all cases with prolonged exposure to lead in order to prevent the development of severe lead nephropathy.The question whether lead poisoning can cause certain pathological states earlier than has been a chronic nephropathy is of interest at the present possible hitherto. time not only in occupational medicine but also inIn the past, many authors have held that chronic paediatrics, general medicin...

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980.

“…Renal effects in man have been described in clinical reports (21,24,35), by studies of renal function (14,23,33,38,47), and by epidemiologic studies. For example, Lane (19,20) Because, as Lane (19) pointed out, animals exposed to lead have shown both tubular and vascular changes in the kidneys, it is of interest that in our study there were excess deaths in both the chronic nephritis and the renal vascular disease categories.…”

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

“…However, like PbB, urinary lead excretion reflects, mainly, recent exposure and, thus, shares many of the same limitations for assessing lead body burden or long-term exposure (Sakai 2000;Skerfving 1988). The measurement is further complicated by variability in urine volume, which can affect concentrations independent of excretion rate (Diamond 1988) and the potential effects of decrements in kidney function on excretion, in association with high, nephrotoxic lead exposures or kidney disease (Lilis et al 1968;Wedeen et al 1975). Urinary lead concentration increases exponentially with PbB and can exhibit relatively high intra-individual variability, even at similar PbBs (Gulson et al 1998a;Skerfving et al 1985).…”

“…Measurements of urinary lead levels have been used to assess lead exposure (e.g., Fels et al 1998;Gerhardsson et al 1992;Lilis et al 1968;Lin et al 2001;Mortada et al 2001;Roels et al 1994). However, like PbB, urinary lead excretion reflects, mainly, recent exposure and, thus, shares many of the same limitations for assessing lead body burden or long-term exposure (Sakai 2000;Skerfving 1988).…”

“…The measurement of lead excreted in urine following an injection (intravenous or intramuscular) of the chelating agent, calcium disodium EDTA (EDTA provocation) has been used to detect elevated body burden of lead in adults (Biagini et al 1977;Lilis et al 1968;Wedeen 1992;Wedeen et al 1975) and children (Chisolm et al 1976;Markowitz and Rosen 1981), and is considered to be a reliable measure of the potentially toxic fraction of the lead body burden (WHO 1995). The assay is not a substitute for blood lead measurements in the clinical setting.…”

Increased Risk of Proteinuria among a Cohort of Lead-Exposed Pregnant Women

“…Excesses in mortality due to nephritis (3,4) and chronic hypertension (not associated with cardiovascular causes) (5) and renal diseases (6-1Q) have been observed among young adults surviving an epidemic of childhood lead encephalopathy in Australia and in workers in lead industries, respectively. Reductions in glomerular filtration rate (GFR) (11,12), creatinine clearance (13), and glucose transport (14) have been reported in adults with prolonged occupational exposure to lead. Together, these observations suggest that long-term, high-dose lead exposure is associated with increased mortality and morbidity due to renal dysfunction.…”