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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). |