الفهرس 
HEAVY METAL NEPHROPATHYOnly 14 pages are availabe for public view
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Abstract
Toxic nephropathies are an important and relatively
common category of kidney damage. Although they generally
are reversible when detected early, they may be permanent,
leading to chronic kidney disease (CKD). Toxic nephropathies
are defined primarily as kidney injury caused by any number of
medications, diagnostic agents, alternative products, herbal
adulterants, or other toxin exposures, which includes
environmental agents and chemicals. Because the kidney
performs a number of essential bodily functions, including
clearance of endogenous waste products, control of volume
status, maintenance of electrolyte and acid-base balance, and
modulation of endocrine activity, loss of kidney function leads to
a number of clinical problems. Furthermore, metabolism and
excretion of exogenously administered medications and
environmental exposures is a critically important function. In its
role as the primary eliminator of exogenous drugs and toxins, the
kidney is vulnerable to develop various forms of injury.
Heavy metals such as cadmium, mercury, lead, chromium
and platinum are a major environmental and occupational
hazard. Unfortunately, these non-essential elements are toxic at
very low doses and non-biodegradable with a very long
biological half life. Thus, exposure to heavy metals is potentially
harmful. The kidney is the first target organ of heavy metal
toxicity because of its ability to reabsorb and accumulate
divalent metals. The extent of renal damage by heavy metals
depends on the nature, the dose, route and duration of exposure.
Both acute and chronic intoxication have been demonstrated to
cause nephropathies, with various levels of severity ranging from
tubular dysfunctions like acquired Fanconi syndrome to severe
renal failure leading occasionally to death. Very varied pathways
are involved in uptake of heavy metals by the epithelium,
depending on the form (free or bound) of the metal and the
segment of the nephron where reabsorption occurs (proximal
tubule, loop of Henle, distal tubule and terminal segments).
Cadmium nephropathy has been described in industrial
workers exposed mainly by inhalation and in the general
population exposed via contaminated foods. There is now a
consensus among scientists to say that in chronic cadmium
poisoning the kidney, which is the main storage organ of
cadmium, is the first organ to display signs of toxicity.
Cadmium, a metal ordinarily obtained as a by- product of
zinc refining, is used industrially in plating of steel, pigments,
plastics, alloys, and nickel-cadmium batteries, and in nuclear and
electronic engineering. Because the biologic half-life of
cadmium is long (more than 30 years), prolonged low-level
exposure leads to excessive accumulation in certain tissues,
especially the kidney.
Primary exposure sources of cadmium for the general
population include food and tobacco smoking. Oral ingestion of
polluted food is the major route of exposure for the nonsmoking
general population.
A successful prevention of renal diseases induced by
occupational exposure to cadmium and/or lead largely relies on
the capability to detect nephrotoxic effects at a stage when they
are still reversible or at least not yet compromising renal
function.
The aim of this study is to evaluate the prevalence of
nephropathy among cadmium exposed workers.
120 cases were enrolled in this study, 80 Egyptian welding
workers as well as 40 healthy volunteers as a control group
which was age, sex and smoking habits matched.
Cases with past history of renal/urological diseases,
hypertension or diabetes mellitus, family history of
renal/urological diseases or history of exposure to other
potentially or suspected nephrotoxins other than cadmium and
lead were excluded from this study.
Medical and occupational histories were recorded from all
cases with stress on duration of exposure to cadmium and
symptoms suggestive of cadmium toxicity like bony aches,
yellowish discoloration of teeth and anosmia.
All cases underwent general examination, pelviabdominal
ultrasound and laboratory studies included serum creatinine,
urea, sodium, potassium, calcium, phosphrous, hemoglobin
level, complete urine analysis, urinary protein creatinine ratio,
urinary B 2 microglobulin, blood cadmium level and blood lead
level.
The present study showed significantly higher blood
cadmium level in group (1) compared to group (2) (8.1± 2.9
versus 3.4 ±1.6 μg/l, P = 0.004).
The present study showed significantly higher blood lead
level in group (1) compared to group (2) (310 ± 52 versus 160 ±
14.9 μg/l, P < 0.000).
It was found that anosmia and yellowish discoloration of
teeth, as symptoms suggestive of cadmium toxicity, are more
prevalent in group (1) compared to group (2) (P< 0.00, 0.00).
In the present study there was highly significant higher
systolic and diastolic blood pressure in group (1) versus group
(2). There was positive correlation between systolic and diastolic
blood pressure and blood cadmium level in group (1) (r = 3.03, P
= 0.04 and r = 4.31, P =0.03 respectively). And a positive
correlation between diastolic blood pressure and cadmium was
found in group (2). (r= 4.12, p= 0.03)
There was significant positive correlation between blood
Cadmium and urinary beta 2 microglobulin/creatinine ratio in
group (1) and (2) (r = 4.34, P = 0.02) and (r = 4.44, P =0.03)
respectively.
There was no significant correlation between blood lead
level and B2MG/Cr ratio in both groups.
There was significant positive correlation between blood
cadmium and serum urea (P value <0.00) in group (1). And there
was significant negative correlation between blood cadmium
level and GFR. (P = 0.03) in group (1).
Blood cadmium has a significant positive correlation with
smoking index in group (2) (r = 5.69, P< 0.00).