Complications
Renal osteodystrophy is characterized by abnormal bone turnover and/or mineralization. Extremely low and extremely high parathyroid hormone (PTH) levels predict low and high bone turnover status respectively. There is a U-shaped association between fracture risk and PTH level, where extremely low and extremely high PTH levels are associated with an increased risk of fracture compared with PTH levels within the target range for patients on dialysis with SHPT.[104] However, PTH is a poor marker for bone turnover status when the level is within the target range aimed for controlling SHPT.[105] If there is still suspicion of high bone turnover disease or a mineralization defect, despite achieving acceptable PTH levels (e.g., unexplained hypercalcemia, bone pain, or fractures), bone biopsy may be required to confirm the diagnosis and guide further management.[1]
Osteoporosis can also coexist with renal osteodystrophy in chronic kidney disease (CKD). Bone densitometry can be used to detect reduced bone density and monitor its response to treatment. However, bone densitometry is a poor tool to predict fracture risk in CKD stages 4 to 5. There is also a lack of evidence that any intervention (including medical treatment to control SHPT) can prevent renal osteodystrophy or reduce fracture risk in severe CKD.
Osteoporosis is the loss of bone mass due to the dysregulation of bone formation to bone resorption. During the cycle of the development and course of SHPT (and in many cases exacerbated by the underlying disease) either too much bone is removed and/or too little bone is reconstructed, leading to skeletal fragility and fractures.
Osteoporosis can also coexist with renal osteodystrophy in chronic kidney disease (CKD). Bone densitometry can be used to detect reduced bone density and monitor its response to treatment. However, bone densitometry is a poor tool to predict fracture risk in CKD stages 4 to 5.
This is a vascular and tissue manifestation of chronic hypercalcemia. This primarily occurs in patients with SHPT and chronic kidney disease.[106] Other more specific names used for this condition are calcific uremic arteriolopathy, uremic small-vessel disease, uremic gangrene syndrome, and uremic small-artery disease with medial calcification and intimal hyperplasia. As these terms imply, calciphylaxis is characterized by systemic calcification of the tunica media of small vessels. This leads to the clinical manifestation of tissue ischemia and necrosis. Affected areas initially manifest as painful, purpuritic, nodular plaques and typically progress to necrotic ulcers with eschar. Mortality remains between 60% and 87%, usually as a result of overwhelming infection and sepsis.[107]
Uremic small-artery disease has been found to occur in 4% of patients on dialysis. Females are more commonly affected. A superimposed event such as local tissue trauma from injection of medications can lead to the development of wounds in these sensitized patients. A calcium-phosphate product of 70 or more increases the likelihood of developing calciphylaxis. Other factors that might contribute to calciphylaxis are type 1 diabetes mellitus, protein C or protein S deficiency, calcium carbonate usage, prednisone, and administration of warfarin.[107]
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