A Case of Renal Osteodystrophy with Unexpected Serum Intact Parathyroid Hormone Concentrations

Abstract

A 64-year-old female with long-standing end-stage renal disease (ESRD),1 status post 2 failed renal transplants, was evaluated for management of renal osteodystrophy with particular concern for adynamic bone disease (ABD). ABD was suspected because of low normal serum intact parathyroid hormone (PTH) concentrations (range 2.5–54 ng/L, reference range 10–65 ng/L), intermittently increased serum calcium concentrations (range 88–107 mg/L, reference range 84–105 mg/L), and severe osteoporosis. However, her mildly increased serum alkaline phosphatase activities (range 149–196 U/L, reference range 30–120 U/L) were inconsistent with the low bone turnover observed in ABD. This discrepant clinical profile prompted investigation into the PTH assay used at our institution. Simultaneous samples were analyzed for intact PTH on our Roche Elecsys 2010 immunoassay analyzer and at a reference laboratory (Quest Diagnostics) on the Siemens Immulite 2000 immunoassay analyzer. Discrepant values of 48 and 786 ng/L were obtained, respectively. Parathyroid hormone functions to maintain serum calcium concentrations within a tight physiologic range. Patients with chronic renal failure develop secondary hyperparathyroidism owing to decreased renal production of 1,25-dihydroxyvitamin D and hyperphosphatemia, both of which result in hypocalcemia. These derangements in mineral metabolism stimulate PTH production to raise serum calcium and promote phosphorus excretion. Increased serum PTH leads to excessive bone resorption through stimulation of osteoblasts and osteoclasts. The combination of secondary hyperparathyroidism and mineralization defects (osteomalacia) represents the most common form of renal osteodystrophy (ROD). In contrast, a subtype of ROD known as adynamic bone disease can be observed in the setting of prolonged peritoneal or hemodialysis, oversuppression of PTH with calcitriol or calcium-based phosphate binders, or the use of bisphosphonates for osteoporosis treatment (1). ABD is characterized by marked suppression of bone remodeling that leads to fracture. Common biochemical hallmarks of ABD include hypercalcemia, low or inappropriately normal PTH concentrations, and reduced markers of bone turnover …