Internal Medicine

0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 4, 2007 21:13

758 Hyperphosphatemia

■Chronic hyperphosphatemia in renal failure is associated with vas-

cular calcification and increased mortality

tests

■Basic blood tests: Serum phosphorus, creatinine

differential diagnosis

■Renal failure: Hyperphosphatemia occurs almost exclusively with

impaired GFR

■Other rare causes:

➣Increased renal reabsorption: hypoparathyroidism, acromegaly,

thyrotoxicosis

➣Massive release from intracellular stores in tumor lysis syndrome,

rhabdomyolysis

■Overdose of vitamin D derivatives, phosphate containing enemas

management

What to Do First

■Assess renal function and normalize if possible.

specific therapy

Indications

■All hyperphosphatemia should be treated, but treatment is limited.

Treatment options:

■Acute hyperphosphatemia: intravenous volume repletion with nor-

mal saline will enhance renal excretion, add 10 U insulin and 1

ampule D50 to enhance cellular uptake. Best removal is obtained

with dialysis but this is limited due to non-extracellular location of

phosphorus.

■Chronic hyperphosphatemia: dietary restriction to 800 mg/day

(although very difficult to maintain this diet), phosphate binders

with each meal, calcium acetate or carbonate with each meal, seve-

lamer HCL with each meal, lanthanum carbonate with each meal.

Choice of binder is dependent on serum calcium level and tolera-

bility of agent. Number of pills needs to be titrated to oral intake of

phosphorus and serum levels. For severe hyperphosphatemia, short-

term administration (ideally <1 month) of aluminum hydroxide with

each meal may be necessary.

Side effects of phosphate binders include constipation, diarrhea,

bloating, nausea, anorexia due to taste of binders. Side effect of