Vitamin D is a common treatment against secondary hyperparathyroidism in renal patients. The rationale for the prescription of vitamin D sterols in chronic kidney disease (CKD) is rapidly increasing due to the coexistence of growing expectancies close to unsatisfactory evidences.
- Renal osteodystrophy is a common complication of chronic renal disease, and the most common complication secondary to impaired renal production of 1,25(OH) D .
- The reduction of serum 1, 25(OH)2D and calcium levels together with total body phosphate expansion are the major causes of secondary hyperparathyroidism.
- This leads to decreased calcium absorption within the gut as well as impaired renal phosphate excretion. The resulting hyperphosphatemia causes a secondary hyperparathyroidism.
Emerging evidence of several pleiotropic effects related to the activation of the vitamin D receptor, several questions were raised that nephrologists should consider dealing with the prescription of nutritional vitamin D or vitamin D receptor activators (VDRA) and with the selection of a VDRA versus a calcimimetic based regimen in Chronic kidney disease-mineral and bone disorder (CKD-MBD) patients.
Burning questions on vitamin D prescription in CKD-MBD
- Are VDRA superior to placebo in terms of cardiovascular events and survival?
- Do vitamin D analogs provide a better achievement of patient centered outcomes compared to calcitriol?
- Is any VDRA superior to the others in achieving KDIGO targets and improving albuminuria, LVH, VC, bone health, hospitalizations, and survival?
- Will paricalcitol ameliorate CKD progression and cardiovascular events through the benefits on albuminuria and LVH?
- Should VDRA be suspended in those patients reaching PTH levels ≤ 150 pg/mL?
Nutritional vitamin D
- Which are the optimal thresholds independently linked to SHPT and survival?
- Which is the best nutritional vitamin D regimen in terms of type and doses to replenish deficiency and treat SHPT?
- Will the replenishment be a cost-effective prevention against SHPT and CKD-MBD?
- Will the replenishment improve CKD progression, diabetes, infections, and survival?
- Will the coadministration of native and active vitamin D be additive against CKD-MBD, infections, diabetes, and mortality?
VDRA or calcimimetic
- Is a VDRA-centered superior to a calcimimetic-centered therapy to control SHPT and survival?
- Which is the best cost-effective strategy in CKD-MBD: VDRA alone, calcimimetic alone, or a balanced association of VDRA and calcimimetic
CKD: chronic kidney disease; SHPT: secondary hyperparathyroidism; LVH: left ventricular hypertrophy; VC: vascular calcification; VDRA: vitamin D receptor activators; kidney disease: improving global outcomes (KDIGO).
- Improvement of renal bone disease should be one of the primary aims of treatment within CKD-MBD, as an increasing body of evidence links impaired bone health and diminished reservoir function (the ability of bone to buffer calcium and phosphorus)with vascular calcification and ultimately, cardiovascular events.
- An expanding body of evidence is rapidly enriching the rationale for vitamin D use in CKD-MBD.
- The traditional action of VDRAs on PTH suppression is now flanked by encouraging data on their pleiotropic effects on microalbuminuria and LVH.
- Nutritional Vitamin D is receiving a growing interest as a preventive and treating strategy against SHPT as well as a protective intervention on immune responses, insulin resistance, and inflammation even in renal patients.
- At present the need to for more studies remains. The clear cut superiority of one approach over the other with respect to all parameters has not emerged over these many studies.
Rationale for the prescription of vitamin D sterols in chronic kidney disease is rapidly increasing due to the coexistence of growing expectancies close to unsatisfactory evidences.