lead renal dysfunction .pdf

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NR 2001:10

Exposure Assessment
in Epidemiology-.and Practice

x2001 -

Mats Hagberg, Bengt Knave,


Lillienberg and Hakan Westberg (Eds)























Dept of Occupational Medicine

ICOH lndustrial Hygiene

National lnstitute for Working Lite

Renal dysfunction and the lead absorption at the exposed workers in
Algerian battery factory
Boukerma.zCI) ., Touabti.A(2)., Maïza.AC2>., Bouakaz.M<1>.

1. Service de Médecine du travail, Centre Hospitalier Universitaire Sétif 19000 Algérie
email: zboukerma@hotmail.com / zboukerma@yahoo.fr
2. Laboratoire central, Centre hospitalier universitaire Sétif 19000 Algérie.

Although descriptions of chronic nephropathies secondary to lead exposure are ancient (Ollivier in
1863 and Lancereaux in 1882) they are lately adrnitted by everybody. Indeed, in different countries,
various epidemiological, clinical and anatomical survey were accomplished, some ofthem are putting
in doubt the reality of the renal toxic effect, whereas others are confirming it.
It is true that these nephropathies, that are a belated complications of the lead exposure, are difficult
to appreciate. Indeed until these last years, the diagnosis of these renal diseases is essentially based
upon the presence or the absence of a more and less important urinary protein that will condition the
pursuit of the renal explorations.
But, currently, the present biochemical means allow the exploration of the glomerular and the tubular
function. Indeed, it exists a hundred ofurinary enzymes which permit the renal disease diagnosis (117) and provide a biochemical biopsy that give more information about the site and the importance of
the renal lesion.

This survey concemed 100 male workers. Their mean age was 43 years (interval 30-60 years) and
their mean exposure was 15 years (interval 8-24). These workers have always been exposed to
concentrations of lead in the atrnosphere between 1.66 and 3.83 g/m 3 of air according to work post.
The aim ofthis survey is to study the renal lesion at workers, who have been chronically exposed
to the inorganic lead. This survey consists to measure out the proteinuria, the microproteinuria and the
urinary enzymes whose activity permit to evaluate the degree and the place ofthese renal damage.
The enzymes dosage, after centrifugation, are made on the moming's urines.
These workers have the following characteristics:
• never have specific treatrnent of the lead poisoning
• have a normal arterial pressure
• have no urinary infections.
• don't present a mellitus diabetes
Otherwise the dosage of the blood "creatinine", and the dosage of the blood and urinary urea are
Because offeasibility, the dosage is made on the 12 hours urines that are collected at 7 hours a.m.

Conceming the proteinuria, the results show that only 3% of the exposed workers present a proteinuria
with an average rate of 510 mg/24 hours. The microproteinuria is also present at 42% of workers with
an average rate of 42.39 mg/24h (Table 1).
The rates of microproteinuria are variable and there is no correlation neither with the age of the
workers nor with the period of the lead exposure Table 2).
Ifwe compare the urinary activity of the enzymes, we note that the NAG and the GGT have a
similar high activity. The intestinal alkaline phosphatase has an average activity; and the urinary
activity of the LDH is very weak. Indeed, the urinary dosage of enzymes shows the presence of the
NAG at 100% ofworkers with a fluctuation rates between 1.07 U/l and 57 U/l (Table 3). The GGT is






also present at 98% of cases with a rate going between IU/l and 37 U/l. The activity of the intestinal
alkaline phosphatase is lower, and we find it at 23% of cases with a rates varying between 1U/l to 12
U/l. At Last the LDH, is present at only one person.
Table 1 - mean and peak (SEM) urinary enzymes (mg/!) and correlation according to age

on the



31 -35
41 -45

72.55 (87 .38)
17 (25 .79)
42.31 (73 .68)
42.88 (67.86)
38.61 (45.82)
30 (31.11)


42,39 (64.85)



0.01 (0.1)



1.05 (2.83)
0.41 (1.00)
0.36 (0 .83)
0.11 (0.32)
0.23 (0.43)
2.11 (2.71)

1.45 (0.29)
2.16 (0.14)
2.68 (0.19)
3.58 (0.41)
19.25 (6.13)

2.72 (1.27)
4.64 (7.60)
3.63 (3 .78)
3.63 (7.41)
2.92 (1.1 1)
3.33 (2.94)

0.52 (1.54)

3.95 (5 .31)

3.97 (5.31)





Table 2- mean and peak (SEM) urinary enzymes (mg/!) and correlation according to
exposure duration

11 -15




0.70 (2.30)
0.27 (0.76)
0.41 ( 1.08)
0.68 (1.52)


49.22 (78 .71)
42.27 (66.97)
42.17 (69.05)
34.40 (34.45)
42.39 (64.85)

0.01 (0 .1)

0.52 (1.54)



3.18 (1.96)
6.57 (12.60)
2.97 (1.04)
3.55 (1.17)

2.81 (1.07)
2.78 (0.95)
3.67 (3.49)
6.90 (9.86)

3.95 (5 .31)


(5 .31)




Table 3: percentage ofpositivity
-- e

Alcaline phosphatase

60 % (macroproteinuria 6% - microprotéinuria 54%)
23 %
100 %



We always suspected the renal toxicity of the lead, nevertheless the doubt persists conceming
the primary responsibility of the lead or of the arterial hypertension in the renal disease. To
palliate to that, the survey has been lead on 1OO persans exposed to the inorganic lead, and
who never received any treatment for the lead poisoning and who have a normal arterial
The nephrotoxicity of the inorganic lead can express itself through either a glomerular
and/or a tubular affection.
The presence of microproteinuria is considered as a precocious glomerular lesion. In our
survey the urinary protein dosage showed that 60% of workers present a glomerular lesion
among which, 54% at a precocious degree.
To this stadium the dosage of proteins by the test strip procedure used of a systematic manner
in occupational health doesn't permit to question a possible glomerular affection, of where the
interest of the urinary research of microproteins.
Indeed the microproteinuria, (2-9-10) is defined as being the presence of abnormally high
urinary proteins without clinic proteinuria.
The microproteinuria is present when its rate is included between 20 and 200 mg/min (1215), rate to which the test with the test strip procedure is negative (9) and that corresponds
approximately to rates included between 30 and 300 mg/24h (2- 6-11-12) .
If the enzymes usually provided information on organs, which are affected by the illness,
as the myocardial infarction, it is not the case for the kidney. The reason ofthis failing is due
extensively to the fact that the dosage of only one urinary enzyme can not give a reliable
information on the site, the type and the extent of the renal damage. The simultaneous use of
several enzymes as the N-acethyl-beta-D-glucosaminidase (NAG), the gama-glutamyltransferase (GGT) the intestinal alkaline phosphatase (PAL) and the lactate deshydrogenase
(LDH) permit an early and precise diagnosis.
In our survey, ail the exposed workers to the inorganic lead have a tubular lesion attested
by the presence in the urines of N-acethyl-beta-D-Glucosaminidase (NAG) at 100% and the
presence ofGGT at 98% ofworkers.
Indeed, witnesses of an irreversible and early proximal tubular damage (17-11-1) the NAG,
and the GGT (6) have a high activity at the level of the kidneys in comparison to other tissue
such as the Jung and the liver (4). These two enzymes are respectively found at 100% and
98% of workers exposed to the inorganic lead. There are no correlations between the values
of these two enzymes and the age or the exposure period of the workers. lt is explained by
the fact that the activity of the NAG reflects the severity of damages of the renal tissue (14);
but the possibility to find some normal values can also mean an irreversible partial
disturbance due to the tubular cell exhaustion (18).
The dosage of the intestinal alkaline phosphatase permits us to conclude to a tubular effects
extended to the S3-segment of the proximal tubule in 23% of cases. Indeed different studies
confirmed this enzyme as an indicator of the effect on the S3 segment of the proximal tubule
The LDH, found in 1% of cases, cornes to complete other enzymatic dosages, and its
presence signs the cellular death (7).

This survey shows that, outside of ail arterial hypertension, the inorganic lead is directly
responsible of the renal dysfunction. There is nota correlation neither between the tubular
lesion and the age, nor between the tubular damage and the period of exposure.


>i ts conceming
disease. To
Jic lead, and
ial arteri al

The renal dysfunction are situated at the level of proximal tubule and can be extended to
the S3 segment. Moreover the glomérular attack attested by microproteinuria could
complicated the tubular lesion.
Making a real biochemical biopsy, the dosage of the microproteinuria and the urinary
enzymes are a supplementary and important tool for the precocious nephrotoxicity diagnosis
and for the surveillance of exposed persons to toxic risks.



on. In our
nilar lesion


crnatic manner
ofwhere the


mally high


: mg/min (12orresponds



: · the illness,
failing is due
! reliable
eous use of

on attested
00°/o and the

. -1) the NAG,
other tissue
00% and




141516~ t

al tubule


di ts


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Toxicology Letters, 1989, 46: 193.196
Feldkamp.C.S and Mckenna.J.M. Microalbumin, American association for clinical chemistry, 1989,
Vol.8 N°6, p7.
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