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Fluid & Electrolyte Disorders
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glycosuria and hypouricemia together with hypophosphatemia indicate Fanconi s syndrome In chronic depletion, radiographs and biopsies of bones show changes resembling those of osteomalacia
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Other causes are listed in Table 21 11 Children normally have higher serum phosphate levels than adults
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Clinical Findings
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A Symptoms and Signs
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The clinical manifestations are those of the underlying disorder (eg, CKD) of hypocalcemia Inadequately treated hyperphosphatemia in CKD leads to secondary hyperparathyroidism, renal osteodystrophy, and extraosseous calcification of soft tissues In patients who have had prior myocardial infarction, an increased serum phosphate level, even if within the normal range, is linked to an increased risk of cardiovascular events and death
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Treatment
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Treatment is best directed toward prophylaxis by including phosphate in repletion and maintenance fluids A rapid decline in calcium levels can occur with parenteral administration of phosphate; therefore, when possible, oral replacement of phosphate is preferable Moderate hypophosphatemia (10 25 mg/ dL) is usually asymptomatic and does not require treatment The hypophosphatemia in patients with diabetic ketoacidosis will usually correct with normal dietary intake Chronic hypophosphatemia can be treated with oral phosphate repletion Phosphate salts are available in skim milk (approximately 1 g [33 mmol]/L) Tablets or capsules of mixtures of sodium and potassium phosphate may be given to provide 05 1 g (18 32 mmol) per day For severe, symptomatic hypophosphatemia (serum phosphorus 1 mg/dL), an infusion should provide 279 310 mg (9 10 mmol)/12 h until the serum phosphorus exceeds 1 mg/dL and the patient can be switched to oral therapy The infusion rate should be decreased if hypotension occurs Because the response to phosphate supplementation is not predictable, monitoring of plasma phosphate, calcium, and potassium every 6 hours is necessary A magnesium deficit often coexists and should be treated simultaneously Contraindications to therapy with phosphate salts include hypoparathyroidism, advanced stages of CKD, tissue damage and necrosis, and hypercalcemia When hyperglycemia due to any cause is treated, phosphate accompanies glucose into cells, and hypophosphatemia may ensue
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Amanzadeh J et al Hypophosphatemia: an evidence-based approach to its clinical consequences and management Nat Clin Pract Nephrol 2006 Mar;2(3):136 48 [PMID: 16932412] Berman E et al Altered bone and mineral metabolism in patients receiving imatinib mesylate N Engl J Med 2006 May 11;354(19):2006 13 [PMID: 16687713] Gaasbeek A et al Hypophosphatemia: an update on its etiology and treatment Am J Med 2005 Oct;118(10):1094 101 [PMID: 16194637] Sheldon GF Treatment of hypophosphatemia J Am Coll Surg 2004 Jul;199(1):171 [PMID: 15217649]
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B Laboratory Findings
In addition to elevated phosphate, blood chemistry abnormalities are those of the underlying disease
Treatment
In acute kidney injury and in advanced stages of CKD, dialysis will reduce serum phosphate Absorption of phosphate can be reduced by administration of calcium carbonate, 05 15 g three times daily with meals (500 mg tablets) Another phosphate binder is sevelamer hydrochloride, which can be titrated to target phosphorus levels using 800 1600 mg three times daily with meals (400 and 800 mg tablets and 403 mg capsules) Because this agent does not contain calcium or aluminum, it may be especially useful for patients with hypercalcemia Despite its usefulness, it has been suspected of producing mild hyperchloremic metabolic acidosis in patients with CKD Lanthanum carbonate has been used successfully as a phosphate binder in patients with CKD
Table 21 11 Causes of hyperphosphatemia
Massive load of phosphate into the extracellular fluid Exogenous sources Hypervitaminosis D Laxatives or enemas containing phosphate Intravenous phosphate supplement Endogenous sources Rhabdomyolysis (especially if chronic kidney disease coexists) Cell destruction by chemotherapy of malignancy, particularly lymphoproliferative diseases Metabolic acidosis (lactic acidosis, ketoacidosis) Respiratory acidosis (phosphate incorporation into cells is disturbed) Decreased excretion into urine Chronic kidney disease (advanced stages) Acute kidney injury Hypoparathyroidism Pseudohypoparathyroidism Excessive growth hormone (acromegaly) Pseudohyperphosphatemia Multiple myeloma Hypertriglyceridemia Cell lysis
HYPERPHOSPHATEMIA
ESSENTIALS OF DIAGNOSIS
Advanced stage of CKD is the most common cause Hyperphosphatemia in the presence of hypercalcemia imposes a high risk of metastatic calcification
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