Phosphorus hyperphosphatemia

All of these actions are directed at increasing serum calcium levels and decreasing serum phosphorus levels, although the activity of calcitriol also increases phosphorus absorption in the GI tract and mobilization from the bone, which can worsen hyperphosphatemia. Calcitriol also decreases PTH levels through a negative feedback loop. These measures are sufficient to correct serum calcium levels in the earlier stages of CKD. 

The first-line treatment for the management of hyperphosphatemia is dietary phosphorus restriction to 800 to 1000 mg per day in patients with stage 3 CKD or higher who have phosphorus levels at the upper limit of the normal range or elevated iPTH levels.39 Foods high in phosphorus are also high in protein, which can make it difficult to restrict phosphorus intake while maintaining adequate protein intake to avoid... 

The most common cause of hyperphosphatemia is decreased phosphorus excretion, secondary to decreased glomerular filtration rate. 

Equilibrium constants for formation of iron(III) complexes of several oxoanions, of phosphorus, arsenic, sulfur, and selenium, have been reported. The kinetics and mechanism of complex formation in the iron(III)-phosphate system in the presence of a large excess of iron(III) involve the formation of a tetranuclear complex, proposed to be [Fc4(P04)(0H)2(H20)i6]. The high stability of iron(III)-phosphate complexes has prompted suggestions that iron-containing mixed hydroxide or hydroxy-carbonate formulations be tested for treatment of hyperphosphatemia. " ... 

In rabbits burned once with an unknown amount of white phosphorus, semm hypocalcemia and hyperphosphatemia were observed (Bowen et al. 1971). No longer term dermal (bum) exposure studies were located. 

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). 

Bowen TE, Whelan TJ Jr, Nelson TG. 1971. Sudden death after phosphorus bums experimental observations of hypocalcemia, hyperphosphatemia, and electrocardiographic abnormalities following production of a standard white phosphorus bum. Ann Surg 174 779-784. 

The normal range of free inorganic phosphate, in plasma, is expressed as 2.0-4.3 mg phosphorus/1(K) ml. Hyperphosphatemia is defined as the condition where plasma phosphate levels rise above 5.0 mg phosphorus/100 ml. Hyperphosphatemia can result from overuse of laxatives or enemas that contain phosphate. Phosphate enemas are used in the hospital prior to examinations of the intestines for disease, such as colon cancer. However, hyperphosphatemia has occurred in the home situation with accidental drinking of enema formulas. Enema drinking... 

Hypocalcemia commonly occurs during the first I or 2 days of life in premature, low-birth-weight infants. The exact mccKaiusm is not clear. Hypocalcemia can also present in newborns fed cow milk, because cow milk contains calcium and phosphorus in a ratio of about 1.34/1.0, by weight. Mother s milk contains relatively less phosphate the calcium/phosphorus ratio is 2.25/1,0. The excess phosphate in cow milk promotes hyperphosphatemia in the newborn. It is thought that plasma phosphate, in elevated concentrations, fonns a complex with plasma calcium. Formation of this complex reduces the levels of free calcium, resulting in symptoms of hypocalcemia. The newborn is not as able to make hormonal adjustments to maintain plasma calcium levels as is the older infant (Mizrachi et al., 1968). 

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. 

Hyperphosphatemia occurs without specific clinical signs in horses with strangulating intestinal lesions (Arden Stick 1988) and severe colitis (Svendsen et al 1979). The clinical findings reported in small animals include diarrhea, hypocalcemia, hypernatremia and an increased propensity to metastatic soft-tissue calcification. The treatment recommended in small animals includes i.v. fluids to correct any acidosis and promote renal phosphorus excretion and dextrose-containing fluids to promote translocation of phosphorus into cells (Macintire 1997). 

Hyperphosphatemia occurs when the serum phosphorus level is greater than 4.5 mg/dl. This is caused by ... 

Increased phosphorus levels during the last trimester of pregnancy Signs and symptoms of hyperphosphatemia are ... 

Management of hyperphosphatemia, calcium balance, and secondary hyperparathyroidism includes dietary phosphorus restriction, use of phosphate binding agents, and vitamin D therapy. 

Serum phosphorus concentration is so closely regulated by the kidneys that it is unusual for hyperphosphatemia (serum phosphorus concentration >4.5 mg/dL) to develop in patients with normal renal function. The most frequent causes of hyperphosphatemia are decreases in urinary phosphorus excretion, and increases in phosphate entrance into the extracellular fluid via either exogenous administration or endogenous intracellular phosphate release. 

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). 

Hypoparathyroidism results in increased renal tubular reabsorption of phosphorus and may result in hyperphosphatemia. Hyperphosphatemia associated with hypoparathyroidism is usually less severe than that associated with severe renal failure or excessive exogenous or endogenous introduction of phosphorus into the ECR Hypoparathyroidism is the most important cause of increased tubular phosphorus reabsorption. Acromegaly and thyrotoxicosis may also cause hyperphosphatemia by reducing urinary phosphorus excretion. 

---