Encephalopathy lead nephropathy

The exposure to lead based paints and subsequent lead nephropathy and encephalopathy, in the USA, is concentrated in substandard housing [162]. Individuals at the lower end of our economic ladder often are denied access to preventative health care thus putting them at additional risk for toxin exposure. Another example is the consumption of "moonshine" whiskey that has been associated with the development of lead nephropathy [167]. 

In children with lead encephalopathy, proximal tubule reabsorptive defects characterized by the Fanconi syndrome have been observed [13]. The Fanconi syndrome appears when blood lead levels approach 150 //g/ dL. It is rapidly reversed by chelation therapy designed to treat the far more dangerous lead encephalopathy. The proximal tubule reabsorptive defect can regularly be induced experimentally in rats fed dietary lead [14]. In both children and experimental animals, acute lead nephropathy is consistently associated with acid-fast intranuclear inclusions in proximal tubule... 

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Exposure to lead in adults has been associated with hypertension, nephropathy, decreased hearing acuity, anemia, peripheral neuropathy, and encephalopathy. Onset of symptoms may be slow with chronic exposure. Anemia, common in chronically exposed adults and children, tends to be more severe in children. The life span of red blood cells decreases when lead concentrations in blood increase. In the past, the morphology of various blood cells was used to diagnose lead poisoning. Zero content is allowed in food (Food and Drug Administration). 

Lead (tap water, leaded paint chips, herbal remedies, gas-sniffing, glazed kitchenware, etc.) Acute N and V, GI distress and pain, malaise, tremor, tinnitus, paresthesias, encephalopathy (red or black feces) Chronic multisystem effects—anemia (X heme synthesis), neuronathv (wrist dronL nephropathy (proteinuria, failure), hepatitis, mental retardation (from pica), >1 fertility and 1 stillbirths Decontamination—gastric lavage + dimercaprol (severe) or EDTA or succimer (penicillamine if unable to use dimercaprol or succimer) Children succimer PO... 

With blood levels in excess of 80 mcg/dL, serious overt intoxication may occur, including abdominal pain (lead colic) and nephropathy. Encephalopathy and neuropathy are usually associated with levels over 100 mc dL. 

This chapter describes the acute and chronic nephrotoxic effects of lead in human populations. These effects have long been recognized in chronic adult occupational lead exposures and in nonoccupational adult exposures arising from dietary Pb intakes, producing disorders such as gouty nephropathy. In acute childhood Pb exposure, severe kidney effects in the form of Fanconi syndrome were identified in the early pediatric literature. The syndrome often co-occurred with acute encephalopathy. 

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