Renal failure, acute hypocalcemia

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

Severe - Leukopenia (less than 1000/mm ) 2.8% hypoglycemia (less than 25 mg/dL) 2.4% thrombocytopenia (less than 20,000/mm ) 1.7% hypotension (less than 60 mm Hg systolic) 0.9% acute renal failure (serum creatinine greater than 6 mg/dL) 0.5% hypocalcemia (0.2%) Stevens-Johnson syndrome and ventricular tachycardia (0.2%) fatalities caused by severe hypotension, hypoglycemia, and cardiac arrhythmias. 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

Insights in the renal handling of 2,4-dichloroph-enoxyacetic acid have contributed to a better knowledge of the extent of occupational exposure to this widely used herbicide [107-111]. Recently, Kancir et al. [112] reported on a case of oliguric acute renal failure complicated by profound and recurrent hypocalcemia, severe hyperphosphatemia, and inappropriately high urinary sodium concentrations following exposure to this compound. In the studies of Manninen et al. [Ill] the peak herbicide concentration which was noted during the first 12 hours post exposure turned out... 

Acute renal failure due to cisplatin therapy is usually partially reversible with time and supportive care, including dialysis. Serummag-nesium concentrations should be monitored frequently and hypomagnesemia corrected (see Chap. 50). Hypocalcemia and hypokalemia may be difficult to reverse until hypomagnesemia is corrected. Progressive chronic kidney disease due to cumulative toxicity may not be reversible and in some cases may require chronic dialysis support. 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

B. Complications. Myoglobin released by damaged muscle cells may precipitate in the kidneys, causing acute tubular necrosis and renal failure. This is more likely when the semm CPK level exceeds several thousand lU/L and if the patient is dehydrated. With severe rhabdomyolysis, hyperkalemia, hyperphosphatemia, hypemricemia, and hypocalcemia may also occur. 

C. Acute ingestion may cause gastrointestinal burns, severe vomiting and abdominal pain, and diarrhea with smoking stools. Systemic effects include headache, delirium, shock, seizures, coma, and arrhythmias (atrial fibrillation, QT prolongation, ventricular tachycardia, and fibrillation). Metabolic derangements, including hypocalcemia and hyperphosphatemia (or hypophosphatemia), may occur. Fulminant hepatic or renal failure may occur after 2-3 days. 

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