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[Hypertension, CKD and bone metabolism]
Hironori Nakagami1, Ryuichi Morishita
1Division of Vascular Medicine and Epigenetics, Osaka University, United Graduate School of Child Development.
Insights
Hypertension and Chronic Kidney Disease (CKD) contribute to osteoporosis through complex mechanisms involving calcium, phosphorus, and hormonal pathways. Understanding these links can inform targeted treatments for bone health in affected patients.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Hypertension and Chronic Kidney Disease (CKD) are frequently comorbid with osteoporosis.
- Mechanisms linking these conditions to bone loss are multifactorial, involving mineral imbalances and hormonal dysregulation.
Purpose of the Study:
- To elucidate the specific pathways through which hypertension and CKD contribute to osteoporosis.
- To investigate the role of the renin-angiotensin system in hypertension-associated bone loss.
Main Methods:
- Review of existing literature on hypertension, CKD, and osteoporosis.
- Analysis of the effects of Angiotensin II on osteoblast and osteoclast activity.
- Examination of the impact of phosphorus and FGF23 in CKD-related bone disease.
Main Results:
- Hypertension can lead to increased urinary calcium and secondary hyperparathyroidism, promoting bone resorption.
- The renin-angiotensin system, specifically Angiotensin II, upregulates RANKL, activating osteoclasts.
- CKD-induced hyperphosphatemia and altered vitamin D metabolism contribute to osteoporosis progression.
Conclusions:
- Both hypertension and CKD are significant risk factors and contributing factors to the development of osteoporosis.
- Targeting the renin-angiotensin system and managing mineral imbalances may be crucial for preventing bone loss in these patient populations.
Abstract:
The patients with "Hypertension" and "Chronic Kidney Disease (CKD) " are accompanied with an osteoporosis. In hypertension patients, excess urinary calcium secretion induces secondary parathyroidsim to increase serum calcium (Ca) level, which may lead to Ca release from bone. In this aspect, there are several reports that anti-hypertensive drugs, especially thiazides, increase bone mineral density and decrease the incidence of bone fracture. In addition, we demonstrated that renin-angiotensin system can be involved in the process of osteoporosis. Angiotensin II significantly induced the expression of RANKL (receptor activator of NF-κB ligand) in osteoblasts, leading to the activation of osteoclasts, while these effects were completely blocked by an Ang II type 1 receptor blockade. As for CKD, excess phosphorus (P) due to renal dysfunction induces secondary parathyroidism to decrease serum P level, which similarly leads to osteoporosis. Moreover, excess P can increase FGF23 expression and decrease activated vitamin D, which also resulted in progression of osteoporosis. Both "Hypertension" and "Chronic Kidney Disease (CKD) " are inducible factor to osteoporosis.
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