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Signs and symptoms of hypophosphatemia

Authors
Alan S L Yu, MB, BChir
Jason R Stubbs, MD
Section Editor
Stanley Goldfarb, MD
Deputy Editor
Albert Q Lam, MD

INTRODUCTION

When combined with phosphate depletion (that is, when not due solely to phosphate movement into the cells), hypophosphatemia can cause a variety of signs and symptoms [1,2]. The manifestations depend, in large part, upon the severity and chronicity of the phosphate depletion, with the plasma phosphate concentration usually being below 1 mg/dL (0.32 mmol/L) in symptomatic patients.

The major conditions associated with symptomatic hypophosphatemia are chronic alcoholism, intravenous hyperalimentation without phosphate supplementation, urinary phosphate-wasting syndromes (such as Fanconi syndrome or tumor-induced osteomalacia), and the chronic ingestion of antacids or other phosphate binders. Significant hypophosphatemia is also observed in patients receiving continuous renal replacement therapies, yet the clinical relevance of this finding remains uncertain. (See "Causes of hypophosphatemia" and "Hypophosphatemia in the alcoholic patient".)

Severe hypophosphatemia can also be seen during treatment of diabetic ketoacidosis and with prolonged hyperventilation; however, symptoms are unusual in these settings since the hypophosphatemia is acute and there is no preexisting chronic phosphate depletion [3]. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Phosphate depletion'.)

Except for the effects on calcium and magnesium metabolism, the clinical manifestations of hypophosphatemia are primarily due to the consequences of intracellular phosphate depletion, which can affect many organ systems. The signs and symptoms of hypophosphatemia will be reviewed here. The diagnostic approach to and treatment of hypophosphatemia are discussed separately. (See "Evaluation and treatment of hypophosphatemia".)

EFFECTS OF HYPOPHOSPHATEMIA ON MINERAL METABOLISM

Prolonged hypophosphatemia produces a number of effects on both the kidney and bone. Distal tubular reabsorption of calcium and magnesium are inhibited, and striking hypercalciuria ensues. This response to phosphate depletion is dramatic, but the mechanism is unknown. A number of patients with idiopathic hypercalciuria have mild hypophosphatemia, and it has been suggested that impaired phosphate balance may be the primary abnormality, with enhanced calcium excretion representing a secondary effect.

          

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Literature review current through: Nov 2016. | This topic last updated: Mon Jul 25 00:00:00 GMT+00:00 2016.
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References
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