Hemodialysis may be required in severe renal dysfunction especially in tumor lysis syndrome. Phosphate-restricted diet chronic treatment: phos-restricted diet plus phosphate binder Calcium acetate PHOSLO mg tablets, start with two tablets TID with meals Can be useful in patients with hypocalcemia. Nonabsorbable resin avoids problems with Mg, Ca may be preferable for patients on dialysis.
May adsorb some drugs podcast back to contents Please note: The segment on hyperphosphatemia starts at Mechanisms and etiopathogenic classification of hypophosphatemia. FGF fibroblast growth factor Adapted from Bacchetta and Salusky. From the physiopathological perspective, three causes of hypophosphatemia may be established: a. Diminished intestinal absorption of phosphorus: this situation is exceptional, due to the widespread abundance of phosphate in food.
Increased renal phosphorus losses: this is the most common cause of hypophosphatemia. The condition may or may not be mediated by FGF23 Table 3 , and may be of genetic, neoplastic or acquired origin.
Causes of hypophosphatemia due to increased renal phosphate excretion. Other causes are treatment with diuretics such as acetazolamide, thiazides, loop diuretics and mannitol, as well as hyper- and normocalcemic hyperparathyroidism and secondary hyperparathyroidism associated with normal renal function with hypocalcemia. The signs and symptoms of hypophosphatemia appear when the latter is accompanied by the depletion of intracellular phosphate, but not when hypophosphatemia is due only to phosphate displacement toward the cell.
Thus, severe acute hypophosphatemia is seen mainly in hospitalized patients presenting severe medical and surgical conditions, with acute deficiency and pre-existing phosphate depletion. Acute hypophosphatemia without prior chronic phosphate depletion is usually not symptomatic.
The effects upon mineral metabolism: — At the renal level: inhibition of the tubular reabsorption of calcium and magnesium, causing hypercalciuria. At bone level: increased bone resorption, with an increase in serum calcium levels that contributes to hypercalciuria. Rickets and osteomalacia may develop over the long term.
The effects upon other systems due to deficient adenosine triphosphate and 2—3 diphosphoglycerate in erythrocytes:. The decrease in red blood cell 2—3 diphosphoglycerate levels increases hemoglobin affinity for oxygen and reduces oxygen release at the tissue level. The decrease in adenosine triphosphate in turn results in changes in cell functions that require this molecule in order to obtain energy.
These alterations result in symptoms at different levels: — The central nervous system CNS : from mild irritability and paresthesia to more serious manifestations in the form of metabolic encephalopathy, delirium, generalized seizures and coma. This condition has also been associated with ventricular arrhythmias and an increased need for vasoactive drugs in heart surgery.
Skeletal and smooth muscle: proximal myopathy, dysphagia and ileus. Episodes of rhabdomyolysis have also been reported in refeeding syndrome and in alcoholics. Hematological manifestations: hemolysis and impaired leukocyte function reduction of phagocytosis and granulocyte chemotaxis.
Platelet alterations with defective clot retraction and thrombocytopenia may also develop. The etiology of hypophosphatemia is often established from a correct case history. In all other cases, and in the absence of pseudo-hypophosphatemia due to paraproteins, 23 urine phosphate excretion should be measured in h urine; alternatively, the tubular reabsorption of phosphorus can be calculated in an isolated urine sample.
The physiological response at the renal level to a decrease in serum phosphate consists of an increase in phosphate reabsorption, which virtually suppresses phosphaturia. It may also occur in patients with hyperventilation and acute respiratory alkalosis.
At the intestinal level, different mechanisms may result in decreased phosphate absorption, increased transit and secretions in chronic diarrhea, the formation of insoluble salts in treatment with calcium, magnesium, or aluminum supplements, and the inhibition of intestinal transport in concomitant niacin therapy.
In the absence of hyperparathyroidism and altered calcium levels, the presence of genetic forms of hypophosphatemic rickets or of oncogenic osteomalacia OO , a paraneoplastic syndrome, should be considered. Diagnostic management of hypophosphatemia. Analysis of the genes responsible for the synthesis of proteins related to FGF23 degradation serves to establish the diagnosis of the three subtypes known to date.
In adults, the finding of previous normal blood phosphate levels demonstrates the presence of OO, though sometimes patients with ADHR may also exhibit normal levels. Locating the culprit tumor is often a diagnostic challenge in which different radiological and nuclear techniques have been used. However, FGF23 levels are not consistently elevated.
This has been attributed to the presence of quiescent periods in which both phosphorus and FGF23 levels are normal in this group of patients. Lastly, a number of tubular defects have been associated with increased renal phosphate loss.
Hereditary hypophosphatemic rickets with hypercalciuria is a genetic disorder characterized by a loss of function of one of the sodium-phosphate cotransporter subtypes at renal level. Elevated calcium levels and the presence of hypercalciuria contribute to the diagnosis, together with genetic analysis.
In X-linked recessive hypophosphatemia, or Dent's disease, the biochemical alterations are similar to those seen in hereditary hypophosphatemic rickets with hypercalciuria, though female carriers only present hypercalciuria. As in hereditary hypophosphatemic rickets with hypercalciuria, elevated calcitriol concentrations have been reported. The treatment of hypophosphatemia depends on the underlying cause and on other factors such as chronicity, severity, clinical manifestations, the presence of hypercalcemia or hypocalcemia, and renal function.
In acute hypophosphatemia with phosphate depletion, phosphate supplementation may be carried out via the oral or intravenous route. Oral replacement is safer, but absorption is unpredictable and can cause gastrointestinal adverse effects such as diarrhea. Intravenous supplementing corrects hypophosphatemia faster, but poses the risk of causing hypocalcemia, arrhythmias, ectopic calcifications and acute renal failure.
In these cases, doses ranging from 0. Strict monitoring of calcium and phosphorus levels is necessary in order to reduce the risk of ectopic calcifications and other complications. Chronic hypophosphatemia results from gastrointestinal or renal phosphate losses.
Correction of the cause of hypophosphatemia sometimes requires the suppression of phosphate binders, diuretics, or the correction of hypomagnesemia. In mild cases, increased dietary phosphorus intake half a liter of skimmed cow's milk provides about mg of phosphorus may be sufficient. Conventional treatment of disorders involving FGF23 includes high dose phosphate supplementing 2—4 g daily in fractionated doses, and calcitriol 0. Recently, a monoclonal antibody targeted to FGF23 called burosumab has been developed and found to be effective in application to different forms of genetic or acquired hypophosphatemia.
It may sometimes be caused by increased tubular reabsorption, redistribution from the intracellular to the extracellular compartment, or increased supply. Spurious hyperphosphatemia or pseudo-hyperphosphatemia is attributable to interference with the analytical methods: hyperglobulinemia, hyperlipidemia, hemolysis and hyperbilirubinemia, treatment with high doses of liposomal amphotericin B, sample contamination with recombinant tissue plasminogen activator, or heparin.
Hyperphosphatemia is usually mild and asymptomatic; however, chronic hyperphosphatemia is an important factor in the development of secondary hyperparathyroidism in CKD. In severe acute hyperphosphatemia, the clinical manifestations arise from hypocalcemia caused by the formation of insoluble calcium phosphate salts: musculoskeletal weakness, tetany and increased neuromuscular excitability.
At the central nervous system level seizures and cognitive impairment may develop. The clinical manifestations of chronic hyperphosphatemia are related to the location of ectopic soft tissue calcification, and comprise pruritus, tendon rupture, band keratopathy and vascular calcification. These can be found in small arterioles and capillaries calciphylaxis , causing necrotic skin lesions and subungual bleeding in medium-caliber arteries.
Calcification may result in acute coronary syndrome ACS and cardiac arrhythmias, prolongation of the QT interval, or valve disease. Other studies have not observed this association, however.
In establishing the etiological diagnosis, it is advisable to measure serum hydroxyvitamin D, calcitriol, PTH, calcium corrected for albumin, magnesium, creatinine, urea, alkaline phosphatase, serum pH, and urine creatinine, calcium and phosphorus. Diagnostic management of hyperphosphatemia. The treatment of hyperphosphatemia depends on its cause, the rapidity of onset, and the presence or absence of renal failure Fig. Therapeutic management of hyperphosphatemia.
Acute hyperphosphatemia. It is essential to identify and suspend any exogenous source of phosphate; aluminum hydroxide antacids reduce its intestinal absorption and favor the binding of phosphate secreted by the intestine. Hemodialysis is the most effective treatment for hyperphosphatemia, and should be considered in severe cases characterized by acute onset. Chronic hyperphosphatemia.
In patients with CKD on predialysis, the treatment of progressive or persistent hyperphosphatemia is indicated. Phosphorus binders cause a slight decrease in phosphorus levels in blood and in h urine. The available chelating agents comprise carbonate and calcium acetate calcium binders , and sevelamer and lanthanum non-calcium binders. The authors declare that they have no conflicts of interest. Endocrinol Diabetes Nutr.
Phosphate disorders and the clinical management of hypophosphatemia and hyperpho ISSN: Previous article Next article. Issue 3. Pages March More article options. Phosphate disorders and the clinical management of hypophosphatemia and hyperphosphatemia. Download PDF. Corresponding author.
This item has received. Article information. Show more Show less. Table 1. Mechanisms and etiopathogenic classification of hypophosphatemia.. Table 3. Causes of hypophosphatemia due to increased renal phosphate excretion.. In this document, members of the Mineral and Bone Metabolism Working Group of the Spanish Society of Endocrinology and Nutrition review phosphate disorders and provide algorithms for adequate clinical management of hypophosphatemia and hyperphosphatemia.
Palabras clave:. Full Text. Figure 1. Table 2. Causes of hypophosphatemia. Elevated FGF Figure 2. Table 4. Causes of hyperphosphatemia.
Increased supply intravenous, oral, rectal Phosphate salts oral or rectal laxatives Fosphenytoin Liposomal amphotericin B B. Phosphate transcellular changes: metabolic or respiratory acidosis C.
Catabolism or rapid cell lysis Catabolic states Tissue damage: hyperthermia, crush injury, fulminant hepatitis Cell lysis: hemolytic anemia, rhabdomyolysis, cytotoxic treatment, severe leukemia. Figure 3. Figure 4. Goretti Penido, U. Phosphate homeostasis and its role in bone health. Pediatr Nephrol, 27 , pp. Regulation of calcium and phosphate metabolism [Monograph on the Internet]. Bonekey Rep, 3 , pp. Blaine, M. Chonchol, M.
Renal control of calcium, phosphate, and magnesium homeostasis. Clin J Am Soc Nephrol, 10 , pp. Felsenfeld, B. Am J Kidney Dis, 60 , pp. Weisinger, E. Lancet, , pp. Kinoshita, S. X-linked hypophosphatemia and FGFrelated hypophosphatemic diseases: prospect for new treatment.
Endocr Rev, 39 , pp. The expanding family of hypophosphatemic syndromes. J Bone Miner Metab, 30 , pp. Bacchetta, I. Evaluation of hypophosphatemia: lessons from patients with genetic disorders. Am J Kidney Dis, 59 , pp. Manghat, R. Sodi, R. Ann Clin Biochem, 51 , pp.
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Endocr Connect, 3 , pp. Malloy, D. Genetic disorders and defects in vitamin D action. Rheum Dis Clin North Am, 38 , pp. Evaluation and treatment of hypophosphatemia [Monograph on the Internet]. Lorenz-Depiereux, A. Benet-Pages, G.
Eckstein, Y. Defects in renal excretion of phosphate in the absence of chronic kidney disease Chronic Kidney Disease Chronic kidney disease CKD is long-standing, progressive deterioration of renal function. Symptoms develop slowly and in advanced stages include anorexia, nausea, vomiting, stomatitis, dysgeusia Hyperphosphatemia occasionally results from a transcellular shift of phosphate into the extracellular space that is so large that the renal excretory capacity is overwhelmed. This transcellular shift occurs most frequently in.
Diabetic ketoacidosis Diabetic Ketoacidosis DKA Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with Nontraumatic rhabdomyolysis Rhabdomyolysis Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle tissue.
Symptoms and signs include muscle weakness, myalgias, and reddish-brown urine, although this triad is Tumor lysis syndrome Tumor Lysis and Cytokine Release Syndromes Adverse effects are common in patients receiving any cancer therapy. Patients may also have adverse effects resulting from their cancer. Successfully managing these adverse effects is important Hyperphosphatemia can also occur with excessive oral phosphate administration and occasionally with overzealous use of enemas containing phosphate.
Hyperphosphatemia can be spurious in cases of hyperproteinemia eg, in multiple myeloma Multiple Myeloma Multiple myeloma is a cancer of plasma cells that produce monoclonal immunoglobulin and invade and destroy adjacent bone tissue.
Common manifestations include lytic lesions in bones causing Manifestations may include hyperviscosity, bleeding, recurring infections Principal causes include hyperparathyroidism, vitamin Soft-tissue calcification in the skin is one cause of excessive pruritis in patients with end-stage renal disease who are on chronic dialysis.
Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis Most patients with hyperphosphatemia are asymptomatic, although symptoms of hypocalcemia Symptoms and Signs Hypocalcemia is a total serum calcium concentration 8. Soft-tissue calcifications are common among patients with chronic kidney disease; they manifest as easily palpable, hard, subcutaneous nodules often with overlying scratches. Imaging studies frequently show vascular calcifications lining major arteries.
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