Renal failure, acute hyperphosphatemia

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. 

Orias M, Mahnensmith RL, Perazella MA. Extreme hyperphosphatemia and acute renal failure after a phosphorus-containing bowel regimen. Am J Nephrol 1999 19 60-3. 

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... 

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). 

Any disorder that results in necrosis of skeletal muscle cells (i.e., rhabdomyolysis) can result in the release of large amounts of intracellular phosphorus into the systemic circulation. This condition is frequently associated with acute renal failure and thus severe hyperphosphatemia may develop due to increased endogenous phosphorus release coupled with decreased renal phosphorus excretion. Bowel infarction, malignant hyperthermia, and severe hemolysis are also conditions that may increase endogenous release of phosphorus. 

Reactions following initial infusions of antibody are common, but these can usually be handled by a cautious rate of infusion, appropriate hydration and diuresis, and, if necessary, praned-ication. Twenty six percent of initial reactions are reported to be mild, 48 % moderate, and 26 % severe. The initial infusion reaction to some mAbs, for example, rituximab (see below), may provoke tumor lysis syndrome, cytokine release syndrome, and systemic inflammatory response syndrome. Tumor lysis syndrome, noted particularly with rituximab, can occur following cancer treatment and sometimes without treatment. It is believed to be the result of breakdown products of cancer cells leading to increased levels of some metabolites and reflected in conditions such as hypercalcemia, hyperkalemia, hyperphosphatemia, acute uric acid nephropathy, and acute renal failure. The syndrome can occur in the early stages of mAb therapy and is potentially life-threatening. Cytokine release syndrome, also called cytokine storm, is commonly seen after... 

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... 

There have been multiple reports of acute kidney injury following the use of oral sodium phosphate solution [13,19-33]. Many of these reports are the subject of a recent review [19] and are best divided into 2 categories. In the first group of cases, the clinical course was dominated by immediate and severe electrolyte disorders including hyperphosphatemia, and renal biopsy was not performed [13, 20-28]. In the second group of patients, the clinical course was less acute and the connection between the use of OSPS and renal failure was confirmed by renal biopsy [19, 29-33]. 

Hyperphosphatemia is usually secondary to the inability of the kidneys to excrete phosphate. In acute or chronic renal failure, a decrease in glomerular filtration rate (GFR) reduces the renal excretion of phosphate, resulting in hyperphosphatemia. Moderate increases of serum phosphate occur in individuals with low PTH (hypoparathyroidism), PTH resistance (pseudohypoparathyroidism), or acromegaly (increased growth hormone) caused by an increased renal phosphate threshold. Growdi hormone is responsible for the increased renal phosphate threshold and higher phosphate concentrations observed in children. EDTA therapy has also been associated with hyperphosphatemia. 

The treatment for acute hyperphosphatemia is administration of phosphate binding salts, calcium, magnesium, and aluminum although aluminum is avoided in renal failure. 

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. 

The diuretic (subacute) phase of acute toxicant-induced renal failure is characterized by hypokalemia, hypernatremia, hyperphosphatemia, decreas urine specific gravity, and a normal blood urea nitrogen (BUN) level. The immature ceiis of the recovering tubule lack the ability to control potassium and sodium balance through the normal sodium pump and exchange mechanisms, producir dilute urine. Because urea is freely filtered, the BUN level may be kept within a normal rar because of the high rate of filtration artd formation of dilute urine. 

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