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Abstract: FR-PO702

Pseudohyperphosphatemia in Multiple Myeloma

Session Information

Category: Trainee Case Report

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Chavez Morales, Efren Alejandro, New York Presbyterian - Columbia University Irving Medical Center, New York, New York, United States
  • Al-Awqati, Qais, Columbia University, New York, New York, United States
Introduction

Hyperphosphatemia commonly occurs in renal failure or hypoparathyroidism. If severe it can cause severe hypocalcemia leading to cardiac or neurologic symptoms. Pseudohyperphosphatemia is rarely seen and it is due to interference by other serum elements in the phosphorous assay.

Case Description

We present here a 58 year old woman with refractory IgG kappa multiple myeloma.
SCr was 0.6 mg/dL, eGFR >60 ml/min, Pi 34 mg/dL, iCa 1.06 mmole/L, PTH 32 pg/mL, uric acid 6.2 mg/dL, LDH 212 U/L, IgG 7888 mg/dL, total protein 13.2 g/dL, serum globulin 10.3 g/dL
In the setting of normal renal function, normal PTH, no laboratory evidence of tumor lysis syndrome and discrepancy between serum phosphorus and calcium levels we suspected this was a case of pseudohyperphosphatemia.

Discussion

It has been stated that paraproteins interfere with spectroscopic measurement of phosphomolybdate which is the actually measured adduct in the routine laboratory phosphorous (P) assay. The inherent flaw in the design of this test is its dependence on light penetration into the sample, thus any condition that increases the turbidity of the sample would falsely elevate the reading.<span style="font-size:10.8333px"> </span>Also, the abnormal serum proteins may themselves bind phosphate which may spuriously increase the total serum phosphate, but not the biologically active form of phosphate. The level of serum phosphate returns to normal when it is measured after deproteinization with sulfosalicylic acid or trichloroacetic acid<span style="font-size:10.8333px">.</span>
Instead of precipitating the proteins we performed a mixing study using normal serum with a Pi of 1.3 mg/d and performed serial dilutions. The patient’s serum diluted fourfold only increased the Pi level of the mixture to 2.1 mg/dL indicating that the upper bound of our patient’s true Pi level is around 4.5 mg/dL.
We can also calculate the free Pi concentration from association constant of calcium and phosphorus, which is 2.3x10 -7 mole2/L2. When the ionized calcium is 1 mmole/L the free serum Pi level has to be 0.23 mmol/L. Using an activity coefficient of Pi of 0.23, the patient’s actual plasma Pi is about 1 mmole/L or ~ 3mg/dL.
It is interesting that a falsely elevated Pi level does not occur in every patient with paraproteinemia thus it is likely that the type of paraprotein produced by the clone may have specific chemical attributes that leads to the spurious measurement.