Acute renal failure mercury exposure

In addition to intensive supportive care, prompt chelation with oral or intravenous unithiol, intramuscular dimercaprol, or oral succimer may be of value in diminishing nephrotoxicity after acute exposure to inorganic mercury salts. Vigorous hydration may help to maintain urine output, but if acute renal failure ensues, days to weeks of hemodialysis or hemodiafiltration in conjunction with chelation may be necessary. Because the efficacy of chelation declines with time since exposure, treatment should not be delayed until the onset of oliguria or other major systemic effects. 

Environmental/ industrial exposure to heavy metals, light hydrocarbons, pesticides and sdicon-containing compounds all have heen associated with the development and/or progression of renal failure. Exposure to heavy metals, more particularly lead, cadmium and mercury has heen linked with the development of acute or chronic renal failure. The current hterature also contains a growing hody of information linking solvent exposure wifh renal injury. To what extent exposure to environmental/ occupational... 

The association between metal exposure and renal failure can be approached from two points of view. On the one hand environmental/industrial exposure to heavy metals, more particularly, lead, cadmium and mercury and other inorganic substances such as silicon has been linked to a reduced renal function and/or the development of acute or chronic renal failure [1]. This issue has been dealt with in other chapters of this book. On the other hand patients with chronic renal failure, especially those treated by dialysis are at an increased risk for trace element disturbances (Figure 1). Indeed in these subjects the reduced renal function, the presence of proteinuria, metabolic alterations associated with renal insufficiency, the dialysis treatment, medication etc. all may contribute to either accumulation or deficiency of trace metals. With regard to aluminum intensive research on the element s toxic effects has been performed in the past. Recently, new metal-containing medications have been introduced of which the potential toxic effects should be considered and put in a justified context. 

The kidney plays a key roll in the absorption of mercury in the body. Kidney tissue contains a thiol-rich protein called metaUothionein. Exposure of the kidney to mercury and other toxic metals causes production of this protein which binds the metals tightly, and retains it in the kidney in a relatively harmless form. As long as the kidney is not overwhelmed by the influx of the toxic metal, the excretion of mercury will eventually balance intake so that worsening of adverse symptoms will be limited. However, acute levels can lead to renal failure. 

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