A 43-year-old haemodialysis individual was admitted to hospital because of paroxysmal pain in the upper abdominal region radiating to the back. mentionedFineman 199937F10 yearsThoracicIncipient paraplegia456 (10C55)47.3 (1.0C5.7)Azria 200040FYes, after failed renal transplantThoracicBack painMasutani 200139F11 yearsThoracicParaplegia139 191 (150C500)aVandenbussche 200437F3 yearsThoracicBack pain, incipient paraplegia2500259.3 (not mentioned)Tarrass 200642M10 yearsSacralCauda equina compression1456 (10C65)151 (1.0C6.7)Ren 200847M6 yearsThoracicIncipient paraplegia1301 (0C62)134.9 (0C6.4)Mak 200965F10 yearsThoracicBack pain, incipient paraplegia93.2 (1.2C5.7)Current case201043M1 yearThoracicBack pain69 (1.3C6.8) Open in a separate window iPTH, intact parathyroid hormone; CRF, chronic renal failure; F, female; M, male; conversion factor PTH pg/mL into pmol/L (SI units): 9.643. aThese PTH measurements were not performed with an intact PTH assay and therefore inactive PTH fragments were inaccurately measured. Radiographically, brown tumours appear as lytic solitary or multifocal, sharply demarcated expansile lesions [7,18]. Bone scintigraphy shows multiple hot spots, owing to osteoclast activity, suggestive of a metastatic disease. However, the clinical history of renal failure and severe secondary hyperparathyroidism combined with increased alkaline phosphatase raises suspicion for a brown tumour. When diagnostic uncertainty persists, histological investigation of a lesion is recommended [3,8]. Our patient responded insufficiently Navitoclax pontent inhibitor to cinacalcet. A possible explanation is that enlarged parathyroid glands ( 1 cm), with nodular hyperplasia, express less calcium-sensing receptors and may therefore be hyporesponsive to cinacalcet . We have several hypotheses why our patient developed a brown tumour. First, most likely the duration of severe hyperparathyroidism plays a role. Our patient had severe secondary hyperparathyroidism for several years, which was refractory for medical treatment including cinacalcet. Recently, a case report described a patient who developed a brown tumour due to secondary hyperparathyroidism (PTH twice the upper normal limit) only 2 years after a biliopancreatic diversion for severe obesity . Second, cinacalcet reduces PTH levels maximally 2C4 h after administration and therefore induces daily fluctuations. Intermittently high levels of PTH which increase osteoblast survival and ABL stimulate the formation of fibroblasts , are known to have a different impact compared with continually high PTH amounts. Third, osteoblasts express calcium-sensing receptors . Cinacalcet may induce mitogenic actions on osteoblasts via calcium-sensing receptors in a high-calcium environment. The progressive increment of the amount of serum total alkaline phosphatase (marker of bone formation) after beginning cinacalcet suggests improved osteoblast activity. We conclude that, although uncommon, a brownish tumour of the backbone is highly recommended in ESRD individuals with serious secondary hyperparathyroidism and fresh onset neurologic symptoms. The brownish tumour created despite a 1-season treatment of the individual with cinacalcet, which nevertheless did not create a major reduction in serum Navitoclax pontent inhibitor iPTH concentrations (from 110 to 69 pmol/L: 37% decrease). The tumour ultimately caused serious myelum compression that emergent decompressive neurosurgery to protect neurologic function was needed. With hindsight, a parathyroidectomy must have been performed previous in our individual, provided the persistently elevated PTH and alkaline phosphatase. Extra elements that could possess backed the indication for parathyroidectomy consist of Navitoclax pontent inhibitor huge parathyroid glands ( 1 cm) on ultrasound or a bone biopsy revealing osteitis fibrosa cystica . Navitoclax pontent inhibitor Acknowledgments We are indebted to Dr Eric Melse for his graph and insightful observation. em Conflict of curiosity statement /em . non-e declared..