A 64-year-old man comes to the office with fatigue. He has hypertension and poorly controlled diabetes complicated by nephropathy and peripheral neuropathy. His renal function has declined steadily over the last few years. On examination, his conjunctivae are pale and he has bilateral 1+ peripheral edema. Laboratory results are as follows: On the graph below, area "C" shows the normal relationship between serum concentrations of free calcium and parathyroid hormone. Which of the following areas most likely represents this patient's current metabolic state?

Question

A 64-year-old man comes to the office with fatigue.  He has hypertension and poorly controlled diabetes complicated by nephropathy and peripheral neuropathy.  His renal function has declined steadily over the last few years.  On examination, his conjunctivae are pale and he has bilateral 1+ peripheral edema.  Laboratory results are as follows:  On the graph below, area "C" shows the normal relationship between serum concentrations of free calcium and parathyroid hormone.  Which of the following areas most likely represents this patient's current metabolic state?

Quizplus · Accepted Answer

11ec160b_3a2e_f5c6_9249_0bc8f9157952_MD0001_00 In the physiologic state, parathyroid hormone (PTH) causes an overall increase in serum calcium (Ca²⁺) and a decrease serum phosphate (PO₄) via the following effects: PTH production is very sensitive to small changes in serum free Ca²⁺ and is regulated by a negative feedback mechanism: increased Ca²⁺ will suppress PTH, but decreased Ca²⁺ will increase PTH. In chronic kidney disease (CKD), PO₄ clearance declines due to the fall in GFR. The increased PO₄ binds free serum Ca²⁺, resulting in hypocalcemia. Loss of normal renal parenchyma reduces 1,25-dihydroxyvitamin D synthesis, resulting in a significant decline in intestinal Ca²⁺ absorption and Ca²⁺ release from bone. This further exacerbates the hypocalcemia, which along with hyperphosphatemia and low calcitriol, stimulates PTH production (secondary hyperparathyroidism). (Choice B) In primary hyperparathyroidism, serum Ca²⁺ is elevated but does not suppress PTH due to autonomous gland function. In longstanding CKD, PTH release may become independent of Ca²⁺ levels due to chronic parathyroid cell stimulation; PTH remains elevated despite 1,25-dihydroxyvitamin D and Ca²⁺ supplementation (tertiary hyperparathyroidism). However, this is less common than secondary hyperparathyroidism and is usually seen in patients with end-stage renal disease (ie, on dialysis). (Choice C) Calcitriol and Ca²⁺ supplementation in patients with CKD often returns PTH and Ca²⁺ levels to normal. (Choice D) Low PTH with hypocalcemia and hyperphosphatemia is seen in hypoparathyroidism. (Choice E) High serum Ca²⁺ with low PTH is seen in patients with PTH-independent causes of hypercalcemia, which include hypercalcemia of malignancy, vitamin D toxicity, excessive Ca²⁺ ingestion, thyrotoxicosis, and immobilization (Ca²⁺ resorbed from inactive bones). Educational objective: Chronic kidney disease usually causes hyperphosphatemia (binds serum Ca²⁺) and low 1,25-dihydroxyvitamin D (decreases intestinal Ca²⁺ absorption and Ca²⁺ release from bone). The resulting hypocalcemia stimulates release of parathyroid hormone, causing secondary hyperparathyroidism. __________ References: Hyperparathyroidism in chronic kidney disease patients: an update on current pharmacotherapy. (http://www.ncbi.nlm.nih.gov/pubmed/23521343) Secondary and tertiary hyperparathyroidism. (http://www.ncbi.nlm.nih.gov/pubmed/23267748)

A 64-Year-Old Man Comes to the Office with Fatigue