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In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.
In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."
Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.
Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.
Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.
In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.
In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."
Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.
Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.
Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.
In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.
In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."
Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.
Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.
Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.