Case Report

Severe Hyperphosphatemia in a Patient with Mild Acute Kidney Injury

Table 2

Evaluation of hyperphosphatemia.

CategoriesSpecific sourcesPatient data

PseudohyperphosphatemiaHeparinBlood drawn by routine phlebotomy not via heparinized central line; patient not on heparin
ParaproteinemiaParaproteinemia not checked in a young patient without any suspicious signs/symptoms
HyperlipidemiaTotal cholesterol 138 mg/dL, low density lipoprotein 71 mg/dl, high density lipoprotein 53 mg/dL, triglycerides 70 mg/dL
Liposomal amphotericinPatient was receiving liposomal amphotericin

IngestionFood sourcePatient receives hospital food, hyperphosphatemia from food ingestion is unlikely
Phosphate-containing medications (e.g., accidental ingestion of phosphate-containing enemas)

Gastrointestinal absorptionHypervitaminosis DVitamin D, 25-OH level 33 pg/mL

Cellular shiftCell death (e.g., rhabdomyolysis, hemolysis, tumor lysis, and bowel infarction)Clinical exam was benign lactate dehydrogenase 106 U/L and creatinine phosphokinase 21 U/L
Metabolic acidosis (e.g., lactic acidosis and diabetic ketoacidosis)
Chronic respiratory alkalosis
Venous blood gas was consistent with mild normal anion gap metabolic acidosis (which resolved after recovery of kidney function) and chronic respiratory alkalosis. Respiratory alkalosis was likely associated with pregnancy. See discussion in text regarding contribution of patient’s acid-base disturbances to hyperphosphatemia.

ExcretionReduced kidney excretion (e.g., GFR <30 ml/min/1.73 m2Patient’s estimated GFR >> 30 ml/min/1.73 m2
Hypoparathyroidism, parathyroid hormone resistanceParathyroid hormone 26 pg/ml; serum calcium was in normal range after correction for hypoalbuminemia. Hypoparathyroidism was unlikely
Drug-induced (e.g., bisphosphonates)
Others: acromegaly, familial tumoral calcinosis, reduced fibroblast growth factor-23 (FGF-23) level or function
Patient was not receiving any bisphosphonates. Conditions such as acromegaly and familial tumoral calcinosis were unlikely contributory due to the acute presentation of hyperphosphatemia. FGF-23 level was also not checked due to low suspicion and diagnosis of pseudohyperphosphatemia was already established.