Our understanding of phosphate regulation is changing as newer mediators such as fibroblast growth factor 23 (FGF-23) emerge. Parathyroid hormone (PTH) and phosphate balance is an integral part of chronic disease kidney care. In a teaching case recently published in the American Journal of Kidney Diseases, Leaf and Wolf discuss a physiologic-based approach to the diagnosis of a patient with hyperphosphatemia. The following questions will test your knowledge of phosphate metabolism.
1. A patient with chronic kidney disease stage 3 is noted to have hyperphosphatemia. The regulators of serum phosphate concentration include all of the following except:
D. 1,25 vitamin D
2. A 34-year-old man with normal kidney function is noted to have an elevated phosphorus level, and pseudohyperphosphatemia is suspected. The causes of pseudohyperphosphatemia are all of the following except:
B. Lactic acidosis
C. Multiple myeloma
3. Reduced PTH levels are seen in all of the following except:
B. Autosomal dominant hypoparathyroidism
4. A 20-year-old woman was referred for investigation of hypocalcemia. She reports carpo-pedal spasm and seizures during childhood. Her corrected calcium is 7 mg/dL. Her kidney function is normal, and a spot urine calcium/creatinine ratio is elevated at 1.95 (0.06–0.45). PTH is low normal at 10 pg/mL and serum magnesium is 0.8 mEq/L. Her 2-year-old daughter has also been found to have hypocalcemia. What is the most likely diagnosis?
C. Autosomal dominant hypoparathyroidism
D. Familial tumoral calcinosis
5. The highest levels of FGF-23 are seen in which of the following conditions?
C. Vitamin D toxicity
D. Chronic kidney disease
E. Familial tumoral calcinosis
Post prepared by Dr. Chinmay Patel and Dr. Shailaja Chidella from Hofstra North Shore-LIJ School of Medicine and edited by Dr. Kenar Jhaveri, eAJKD Blog Editor.
To see the answers, please click here.