Hyperphosphatemia
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Serum phosphorus greater than 4.5 mg/dL (see Box 5.6).
Incidence
A.Hyperphosphatemia is most common in renal impairment (acute or chronic).
B.Sustained hyperphosphatemia is rare in the absence of renal disease.
Pathogenesis
A.Homeostasis of phosphate is maintained through gastrointestinal (GI) absorption and renal excretion. Imbalances in either of these mechanisms can result in hyperphosphatemia.
Predisposing Factors
A.Excessive intake is rare, but potential cause.
B.Patients with renal failure.
BOX 5.6
Phosphorus in Humans
•85% of total body phosphorus is located in bones.
○Approximately 14% is intracellular.
○Remaining 1% is extracellular.
•Two-thirds of ingested phosphorus is excreted in the urine with the remainder excreted in stool.
•Normal serum phosphorus is 2.5 to 4.5 mg/dL.
•Many physiological functions.
○Bone and cell membrane composition.
○Nerve conduction.
○Muscle function.
○Energy-rich bonds of adenosine triphosphate.
Subjective Data
A.Common complaints/symptoms.
1.Most common and significant manifestations are signs/symptoms of hypocalcemia due to calcium-phosphate precipitation with decrease in ionized calcium.
2.Can lead to soft-tissue calcification due to precipitation of calcium-phosphate crystals in soft tissues producing symptoms of pruritus, dermatologic changes, and (in severe cases) calciphylaxis.
Physical Examination
A.Respiratory examination.
B.Musculoskeletal examination.
C.Dermatological examination.
Diagnostic Tests
A.Serum phosphorus.
B.Serum total calcium, ionized calcium.
C.Venous CO2.
D.Renal function evaluation (blood urea nitrogen [BUN] and serum creatinine).
Differential Diagnosis
A.Renal failure or decreased renal excretion.
1.In chronic dialysis patients, poor compliance with phosphorus binding medications.
B.Increased intestinal absorption: Rapid shifts from intracellular to extracellular.
1.Acidosis (respiratory or metabolic).
2.Hemolysis.
3.Rhabdomyolysis.
4.Tumor lysis syndrome.
C.Hypoparathyroidism.
D.Vitamin D toxicity.
E.Phosphorus containing laxatives or enemas.
F.Hypocalcemia (reciprocal rise).
G.Thyrotoxicosis, acromegaly (rare).
Evaluation and Management Plan
A.Step 1—Volume expansion despite fluid volume status.
1.Initial bolus resuscitation.
2.Continue isotonic intravenous hydration.
B.Step 2—Emergency treatment for acute and severe hyperphosphatemia due to risk of renal failure.
1.Calcium replacement (see section “Hypocalcemia“). Acute, severe hyperphosphatemia can cause reciprocal hypocalcemia.
2.Emergency treatment: Continuous renal replacement therapy. Consult nephrology.
3.Additional management.
a.Phosphorus binders (as noted in the text that follows) at large doses with three meals, snacks, plus a dose at bedtime.
b.Consultation with a renal dietician for dietary counseling.
i.Tightly restrict unnecessary sources of phosphorus in the diet such as food preservatives and higher phosphorus grains and vegetables.
ii.Choose an individualized target for protein intake that will not place the patient at risk for nutrition deficiencies or allow excessive phosphorus intake from protein sources.
c.Continuation of isotonic intravenous hydration. Consider loop diuretics if needed to increase urine output.
C.Step 3—If nonemergent, assess for cause of hyperphosphatemia.
1.Hyperphosphatemia management is oral phosphate binders and dietary restriction in patients with chronic renal disease.
a.Give phosphate binders with food in order to bind dietary phosphorus in the intestinal tract and prevent absorption.
b.Avoid magnesium- and aluminum-based binders because of risk of accumulation in renal disease.
2.Phosphorus binders should not be given to patients with acute kidney injury (AKI) due to risk for overcorrection (hypophosphatemia) during recovery.
3.Current available formulations.
a.Calcium-based (calcium acetate or calcium carbonate).
b.Sevelamer.
c.Lanthanum.
d.Iron-based (ferric citrate or sucroferric oxyhydroxide).
e.Dose is specific to formulation used.
D.Step 4—Treat underlying cause if possible.
E.Step 5—Treat other electrolyte and acid–base disorders.
Follow-Up
A.Calcium levels, phosphate levels, and renal function should be monitored at intervals consonant with the severity of the underlying disorder.
Consultation/Referral
A.Nephrology may be consulted if the hyperphosphatemia is associated with renal failure.
Endocrinology may be consulted if the patient has hypoparathyroidism.
Special/Geriatric Considerations
A.Elderly patients with chronic kidney disease (CKD) are at risk for hyperphosphatemia.
Bibliography
Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). Treatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62(16), 1663–1682. doi:10.2146/ajhp040300
Moe, S. M., &Daoud, J. R. (2014). Disorders of mineral metabolism: Calcium, phosphorous, and magnesium. In D. D. Gipson, M. A. Perazella, & M. Tonelli (Eds.), National Kidney Foundation’s primer on kidney diseases (6th ed., pp. 100–112). Philadelphia, PA: Elsevier Saunders.
Stubbs, J. R., … Yu, A. S. L. (2017). Overview of the causes and treatment of hyperphosphatemia. In S. Goldfarb … A. Q. Lam(Eds.), UpToDate, Waltham, MA: Retrieved from https://www.uptodate.com/contents/overview-of-the-causes-andtreatment-of-hyperphosphatemia