LAUSR

Introduction: Chronic Kidney Disease related Mineral Bone Disease (CKD-MBD) can occur in all patients with CKD and leads to a variety of clinical manifestations, including bone pain and fractures characterized by abnormalities in the metabolism of calcium, phosphorus, parathyroid hormone (PTH), or vitamin D, abnormalities in bone turnover, mineralization, volume, growth, or strength. We report one case, a 41year-old man with CKD G5D on CAPD (Continous Ambulatory Peritoneal Dialysis) during the last 4 years, fracture of the vertebra with changes in body shape. We suspect this patient is suffering from complications of CKD-MBD, based on complaints, physical examination and other supporting examinations. Methods: A 41 year old man complained of chronic back pain and chest, and also back deformities. The patient also complained of a gradual decrease in his height in the last 5 years. The patient was diagnosed with CKD stage 5 since 7 years ago and underwent CAPD since 3 years ago. There were history of fracture of the humeral bone. Currently, patients ralso consump calcium and cholecalciferol and calcitriol supplements. On physical examination, there was pigeon chest, chyphoscoliosis of the thoracic vertebrae without a history of previous trauma. Laboratory tests showed a significant increase in PTH levels (4081 pg/ml, 62 times of normal values), increased serum inorganic phosphorus (4.9 mg / dl, normal: 2.7-4.5 mg/dl), and normal serum calcium (9.5 mg dl).On thoracolumbar X-ray examination, there were many compression fracture of his vertebra and decreased bone mineralization. From physical examination and support, our patient was diagnosed with CKD-G5D complications with CKD-MBD. In addition to the low phosphate diet, the patient also started giving phosphate binders, lanthanum carbonate, non-calcium phosphate binders. In addition, calcium and cholecalciferol supplementation therapy and calcitriol. Results: The patient is currently undergoing CAPD therapy and complaint of multiple fractures of the vertebral.The pathomechanism that underlies the fracture in CKD-MBD patients is hyperphosphatemia which stimulates the release of PTH resulting in Secondary Hyperparathyroidoism (SHPT) which is induced by hypocalcemia, decreased calcitriol formation by the kidneys and decreased function, decreased FGF-23 production and increased PTH gene expression. In this patient, there was an increase in phosphate levels and an increase in PTH levels up to 62 times the normal value, but the serum calcium levels were normal because the patient had routinely taken calcium supplements, cholecalciferol and calcitriol. The patient had received supplements of calcium, cholecalciferol and calcitriol, but PTH increases. Refractory SHPT can be caused by inadequate therapy, persistent hyperphosphatemia, calcitriol deficiency and hypocalcemia resulting in hyperplasia of the parathyroid glands. Based on KDIGO 2017 recommendations for severe hyperparathyroidism that is very high (> 800 pg/ml) and does not respond to therapy, the next option is surgery for parathyroidectomy. However, because the patient did not agree to this procedure, pharmacotherapy was our main choice, accompanied by adequate hemodialysis in this patient. Conclusions: In this case report we have reported a 41 year old male with CKD-MBD and PGK-G5 on CAPD. Inadequate and delayed therapy in this patient caused complications of CKDMBD. No conflict of interest POS-643