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Co-Director, State University of New York Downstate Medical Center College of Medicine

After 3­5 weeks of copper loading resulting in tissue damage, the copper levels in the liver begin to decline and the tissue begins to regenerate (Haywood and Loughran 1985). It is believed that the mechanism involved in tolerance development is the increased synthesis of metallothionein (Evering et al. Studies in monkeys, dogs, and ferrets provide strong evidence that copper-induced emesis results from stimulation of the vagus nerve. Abdominal vagotomy resulted in a dramatic decrease in the occurrence of emesis in dogs (Fukui et al. In rats, dietary exposure to 16 mg Cu/kg/day for 13 weeks resulted in an increase in alanine aminotransferase activity; chronic active liver inflammation was observed at 66 mg Cu/kg/day. In contrast, no evidence of liver damage was observed in mice exposed to 814 mg Cu/kg/day for 13 weeks. Most of the experimental data on the toxicity of copper come from studies in which rats were used; however, the relevance of this species to human toxicity has not been fully evaluated. It is unlikely that humans would tolerate prolonged exposure to a copper dose that is 50 times higher than the dietary requirement (0. Chemicals with this type of activity are most commonly referred to as endocrine disruptors. The terminology endocrine modulators has also been used to convey the fact that effects caused by such chemicals may not necessarily be adverse. Many scientists agree that chemicals with the ability to disrupt or modulate the endocrine system are a potential threat to the health of humans, aquatic animals, and wildlife. However, others believe that endocrine-active chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist in the natural environment. Examples of natural hormone mimics include the isoflavinoid phytoestrogens (Adlercreutz 1995; Livingston 1978; Mayr et al. These chemicals are derived from plants and are similar in structure and action to endogenous estrogen. Stated differently, such compounds may cause toxicities that are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering, for example, metabolic, sexual, immune, and neurobehavioral function. However, in the case of ambient human exposures, the validity of these possibilities has yet to be established conclusively. There is no evidence that copper interferes with the normal function of the neuroendocrine axis. Potential effects on offspring resulting from exposures of parental germ cells are considered, as well as any direct or indirect effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. They may differ from adults in their exposures and in their susceptibility to hazardous chemicals. Children may differ from adults in their susceptibility to hazardous chemicals, but whether there is a difference depends on the chemical (Guzelian et al. There are critical periods of structural and functional development during both prenatal and postnatal life at which particular structures and/or functions will be most sensitive to perturbation. There are often differences in pharmacokinetics and metabolism between children and adults. Whether differences in xenobiotic metabolism make the child more or less susceptible also depends on whether the relevant enzymes are involved in activation of the parent compound to its toxic form and/or in detoxification. In addition, children and adults may differ in their capacity to repair damage from chemical insults. In general, children also have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly relevant to the development of cancer. Certain characteristics of the developing human may increase exposure or susceptibility to certain toxicants, whereas others may decrease susceptibility to the same toxicant. Copper is an essential element required for normal growth and development and for a variety of metabolic functions including iron metabolism, cross-linking of connective tissue, and lipid metabolism.

Diseases

• Fetal hydantoin syndrome
• Shellfish poisoning, diarrheal (DSP)
• Serum sickness
• Microcephaly mesobrachyphalangy tracheoesophageal fistula syndrome
• Legionellosis
• Hypoxanthine guanine phosphoribosyltransferase deficiency
• Acute non lymphoblastic leukemia (generic term)

These disorders and treatments generate metabolic alkalosis, which complicates the chronic respiratory alkalosis. If nausea and vomiting occur, they generate a simultaneous or sequential metabolic alkalosis through loss of acidic gastric fluids. Although the final arterial pH is typically acid, it may sometimes become normal or even alkaline if the alkalosis is more severe than the acidosis. This mixed acid-base disorder may be suspected based on the clinical history and physical exam (see next section). This mixed disorder can be suspected on the basis of the history, clinical setting, and physical exam. If the vomiting improves but the diarrhea continues, overt hyperchloremic metabolic acidosis and acidemia may be revealed. Other forms of mixed acid-base disorders are combinations of different metabolic acidosis disorders or, much less commonly, metabolic alkalosis disorders. For example, it is not uncommon for ketoacidosis to coexist with lactic acidosis; similarly, hyperchloremic acidosis caused by diarrhea or renal tubular acidosis may present in conjunction with lactic acidosis or uremic acidosis. Mixed respiratory acid-base disorders can also develop, and they are usually suspected on the basis of the history and clinical setting rather than any specific laboratory results. The patient with chronic obstructive lung disease, who presents with recent pulmonary deterioration caused by a mucus plug or pneumonia, may have chronic respiratory acidosis and a superimposed acute respiratory acidosis. A pregnant woman with underlying hyperventilation who ingests an overdose of sedating drugs and develops respiratory depression will have chronic respiratory alkalosis and a superimposed acute respiratory acidosis. This is the clue to the double disorder of metabolic acidosis and metabolic alkalosis. If the patient represented by Case 1 develops severe extracellular fluid volume depletion, then lactic acidosis may ensue (Case 3). Mixed Mixed metabolic metabolic acidosis and acidosis and respiratory respiratory acidosis alkalosis Simple metabolic acidosis Mixed Mixed respiratory respiratory acidosis and acidosis and metabolic metabolic acidosis alkalosis Simple respiratory acidosis Alkalemia (pH 7. Szerlip 13 Metabolic acidosis describes a process in which nonvolatile acids accumulate in the body. For practical purposes, this can result from either the addition of protons or the loss of base. The consequence of this process is a decline in the major extracellular buffer, bicarbonate, and, if unopposed, a decrease in extracellular pH. However, depending on the existence and the magnitude of other acid-base disturbances, the extracellular pH may be low, normal, or even high. Because the body tightly defends against changes in pH, decreased pH sensitizes peripheral chemoreceptors, and that triggers an increase in minute ventilation. This compensatory respiratory alkalosis helps offset what would otherwise be a marked fall in pH. Because increased ventilation is a compensatory mechanism stimulated by acidemia, increased ventilation never returns the pH to normal. The vast majority of acid production results from the metabolism of dietary carbohydrates and fats. As long as ventilatory function remains normal, this volatile acid does not contribute to changes in acidbase balance. Nonvolatile, or fixed, acids are produced by the metabolism of sulfate- and phosphate-containing amino acids. In addition, incomplete oxidation of fats and carbohydrates results in the production of small quantities of lactate and other organic anions, which, when excreted in the urine, represent loss of base. Individuals consuming a typical meat-based diet produce approximately 1 mmol/kg/day of hydrogen ions. Fecal excretion of a small amount of base also contributes to total daily acid production. The kidney is responsible not only for the excretion of the daily production of fixed acid, but also for the reclamation of the filtered bicarbonate.

Drugs that cause direct nephrotoxicity, such as aminoglycosides and intravenous radiocontrast, should be avoided. Selected use of renal ultrasound is useful for identifying hydroureter and/ or hydronephrosis indicative of a postrenal cause. Lower urinary tract obstruction can be identified and treated by bladder catheterization showing a large postvoid residual urine volume, whereas nephrostomy tubes or ureteric stents can be used to treat upper urinary tract obstruction. Hematuria and proteinuria should prompt further investigations for causes of glomerulonephritis, whereas white bloods cell casts should prompt a careful assessment for causes of interstitial nephritis, including a review of medication exposures. Readers are referred elsewhere in the Primer for a review of specific aspects of treatment for acute interstitial nephritis, glomerulonephritis, urinary obstruction, and systemic diseases involving the kidney. Attempts are usually made to avoid further exposure to nephrotoxic agents to the greatest extent possible without compromising management of other comorbidities. Doses of medications cleared by the kidney should be adjusted for the level of kidney function. Hyponatremia may result from impaired free water excretion, whereas hypernatremia is common in patients with inadequate free water intake, hypotonic fluid losses, or large-volume intravenous saline infusions for resuscitation. These abnormalities may be corrected by modifying free water intake or the composition of intravenous fluids. Acid generation can be reduced by dietary protein restriction, although this may be undesirable in hypercatabolic patients. Alkaline intravenous fluids such as sodium bicarbonate may be provided to correct metabolic acidosis, although volume overload and pulmonary edema may limit this intervention. Beta-agonists, insulin, and sodium bicarbonate can shift potassium out of the plasma and into cells. Attempts to eliminate potassium through the gastrointestinal tract using ion exchange resins may be used; however, these agents are slow to take effect, have limited efficacy, have been associated with bowl necrosis or perforation, and are unlikely to be adequate in patients with severe hyperkalemia. Strategies to maintain hemodynamic stability include the use of intravenous fluids, vasopressors/inotropic medications, and protocols for hemodynamic monitoring to guide the use of these therapies. A positive fluid balance has been associated with increased mortality in observational studies. Colloid solutions such as albumin and starches are theoretically attractive alternatives for intravenous volume expansion given their oncotic properties, but their appropriate use remains controversial. Aggressive fluid resuscitation remains of paramount importance in these patients; however, after intravascular volume has been repleted, vasopressors such as norepinephrine, dopamine, and vasopressin may be required to maintain hemodynamic stability. One randomized trial showed a reduction in in-hospital mortality for patients with septic shock managed according to a protocol for early provision of intravenous fluids, blood transfusion, vasopressors, and inotropes based on specific goals for blood pressure, central venous pressure, serum lactate, central venous oxygen saturation, and urine output. Nonetheless, diuretics can be used effectively to achieve fluid balance, and may facilitate mechanical ventilation in volume-overloaded patients. Nutritional protein administration is therefore usually increased to meet the greater metabolic demands of hypercatabolic patients. Consultation with a registered dietician is valuable to estimate the appropriate energy and protein requirements for an individual patient. Electrolytes (potassium, phosphate) should be monitored following initiation of enteral feeding. Parenteral nutrition may be required in some patients to supplement the enteral route, or in patients without functional gastrointestinal tracts. Low-dose dopamine is associated with increased renal blood flow, increased urine output, and small improvements in creatinine clearance. Fenoldopam is a dopamine type 1 receptor agonist that also increases renal blood flow, although it decreases systemic vascular resistance. However, given its risk of hypotension along with limitations of the existing published trials, further trials are necessary to support the use of fenoldopam for this indication. Although insulin-like growth factor-1 showed promising results on recovery of kidney function in animals, small trials have failed to demonstrate beneficial results in humans. Available resources, expertise, hemodynamic stability, and patient comorbidities usually influence the decision of renal replacement modality. Ultrafiltration in excess of replacement fluid necessary for fluid removal None 1000 to 1500 mL/hr for neutral fluid balance.

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