Clinical Outcomes with Active versus Nutritional Vitamin D Compounds in Chronic Kidney Disease

Kalantar-Zadeh, Kamyar; Kövesdy, Csaba P.

doi:10.2215/cjn.02140309

Cited by 89 publications

(92 citation statements)

References 85 publications

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“…More accurate reporting of P content of foods by manufacturers, especially when mandated by the Food and Drug Administration, may result in improved public health nutrition and healthier control of dietary P intake with less risk for developing protein malnutrition in people with illnesses that render them more P intolerant (43,44). Because a high protein intake and a concurrent low P intake and normal serum P seems to be associated with the lowest mortality in patients with ESRD (33), cooking modalities that can reduce P content (e.g., boiling) (48), use of selective vitamin D activators that lead to less intestinal P absorption (23), diligent use of potent P binders with less pill burden (59 -62), and patient-friendly educational tools such as the concept of dietary "phosphate unit" and its relationship with binder dosage (63) also are helpful. Meals that have lower amounts of organic and particularly inorganic P and are rich in high-value protein, along with P binders, can be provided during long hemodialysis treatment sessions to patients with CKD within inside dialysis clinics and monitored in-center by renal dietitians and nephrologists.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated serum P may also suppress serum calcium by causing a saturated serum calcium-P product to precipitate in tissues. These factors can promote increased release of PTH (23). Frequent or sustained elevations of PTH levels can have adverse effects on bone mineral content and architecture, although the significance of such borderline or temporary hyperparathyroidism without kidney dysfunction is unclear (24).…”

Section: Dietary P and Its Metabolismmentioning

confidence: 99%

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Understanding Sources of Dietary Phosphorus in the Treatment of Patients with Chronic Kidney Disease

Kalantar-Zadeh

Gutekunst²,

Mehrotra³

et al. 2010

Clinical Journal of the American Society of Nephrology

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435

321

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In individuals with chronic kidney disease, high dietary phosphorus (P) burden may worsen hyperparathyroidism and renal osteodystrophy, promote vascular calcification and cardiovascular events, and increase mortality. In addition to the absolute amount of dietary P, its type (organic versus inorganic), source (animal versus plant derived), and ratio to dietary protein may be important. Organic P in such plant foods as seeds and legumes is less bioavailable because of limited gastrointestinal absorption of phytate-based P. Inorganic P is more readily absorbed by intestine, and its presence in processed, preserved, or enhanced foods or soft drinks that contain additives may be underreported and not distinguished from the less readily absorbed organic P in nutrient databases. Hence, P burden from food additives is disproportionately high relative to its dietary content as compared with natural sources that are derived from organic (animal and vegetable) food proteins. Observational and metabolic studies indicate nutritional and longevity benefits of higher protein intake in dialysis patients. This presents challenges to providing appropriate nutrition because protein and P intakes are closely correlated. During dietary counseling of patients with chronic kidney disease, the absolute dietary P content as well as the P-to-protein ratio in foods should be addressed. Foods with the least amount of inorganic P, low P-to-protein ratios, and adequate protein content that are consistent with acceptable palatability and enjoyment to the individual patient should be recommended along with appropriate prescription of P binders. Provision of in-center and monitored meals during hemodialysis treatment sessions in the dialysis clinic may facilitate the achievement of these goals.

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Section: Discussionmentioning

confidence: 99%

Section: Dietary P and Its Metabolismmentioning

confidence: 99%

Understanding Sources of Dietary Phosphorus in the Treatment of Patients with Chronic Kidney Disease

Kalantar-Zadeh

Gutekunst²,

Mehrotra³

et al. 2010

Clinical Journal of the American Society of Nephrology

Self Cite

435

321

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“…Vitamin D therapy produced modest or transient increases in serum 25-hydroxyvitamin D (generally 10-15 ng/ml), leaving a considerable proportion of the treated patients (up to ∼50%) showing no clinically meaningful increases in serum 25-hydroxyvitamin D or decreases in plasma iPTH. The overall conclusion from this body of work has been well summarized: ‘Most of these studies have shown either no or minimal to inadequate changes in PTH levels, usually only in some stages of CKD, or changes that still would not satisfy the K/DOQI recommended target ranges for PTH' [12]. …”

Section: Discussionmentioning

confidence: 99%

“…Consensus is lacking on the definition of vitamin D insufficiency with K/DOQI, for example, defining it as <30 ng/ml and the Institute of Medicine (IOM) favoring <20 ng/ml [11]. Supplementation with vitamin D has been found to be inconsistently effective and often inadequate in patients with predialysis CKD, leaving SHPT largely uncorrected [12]. Thus, therapy with vitamin D receptor activators (VDRAs) is required to treat SHPT in many predialysis CKD patients.…”

Section: Introductionmentioning

confidence: 99%

Modified-Release Calcifediol Effectively Controls Secondary Hyperparathyroidism Associated with Vitamin D Insufficiency in Chronic Kidney Disease

et al. 2014

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Background/Aims: Vitamin D insufficiency drives secondary hyperparathyroidism (SHPT) and is associated with increased cardiovascular mortality in patients with chronic kidney disease (CKD). SHPT is poorly addressed by current vitamin D repletion options. The present study evaluated a novel investigational vitamin D repletion therapy: a modified-release (MR) formulation of calcifediol designed to raise serum 25-hydroxyvitamin D in a gradual manner to minimize the induction of CYP24 and, thereby, improve the SHPT control. Methods: This randomized, double-blind, placebo-controlled trial evaluated MR calcifediol in CKD subjects (n = 78) with plasma intact parathyroid hormone (iPTH) >70 pg/ml and serum total 25-hydroxyvitamin D <30 ng/ml. Subjects received daily treatment for six weeks with oral MR calcifediol (30, 60 or 90 µg) or a placebo. Results: More than 90% of subjects treated with MR calcifediol achieved serum 25-hydroxyvitamin D levels ≥30 ng/ml versus 3% of subjects treated with placebo (p < 0.0001). Mean plasma iPTH decreased from baseline (140.3 pg/ml) by 20.9 ± 6.2% (SE), 32.8 ± 5.7 and 39.3 ± 4.3% in the 30, 60 and 90 µg dose groups, respectively, and increased 17.2 ± 7.8% in the pooled placebo group (p < 0.005). No clinically significant safety concerns arose during MR calcifediol treatment. Conclusion: Oral MR calcifediol appears safe and highly effective in treating SHPT associated with vitamin D insufficiency in CKD.

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“…In recent years, there has been a tendency towards lower serum calcium levels in dialysis patients for the following reasons: (1) lowering dialysate fluid (bath) calcium concentrations from higher (3.5 mEq/l) to lower levels (2.5, 2.25 or 2.0 mEq/l); (2) use of calcimimetics; (3) switching from more calcemic active vitamin D (such as calcitriol) to less calcemic agents (such as paricalcitol [15] or maxacalcitol); (4) use of noncalcium-based binders; and (5) recommending lower dietary calcium intakes [7,16,17,18]. The clinical outcomes of dialysis patients whose serum calcium is, on average, relatively low or high over a longer period of time is not clear.…”

Section: Introductionmentioning

confidence: 99%

Association of Cumulatively Low or High Serum Calcium Levels with Mortality in Long-Term Hemodialysis Patients

et al. 2010

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Background: The outcome-predictability of baseline and instantaneously changing serum calcium in hemodialysis patients has been examined. We investigated the mortality-predictability of time-averaged calcium values to reflect the ‘cumulative’ effect of calcium burden over time. Methods: We employed a Cox model using up-to-5-year (7/2001–6/2006) time-averaged values to examine the mortality-predictability of cumulative serum calcium levels in 107,200 hemodialysis patients prior to the use of calcimimetics, but during the time where other calcium-lowering interventions, including lower dialysate calcium, were employed. Results: Both low (<9.0 mg/dl) and high (>10.0 mg/dl) calcium levels were associated with increased mortality (reference: 9.0 to <9.5 mg/dl). Whereas mortality of hypercalcemia was consistent, hypocalcemia mortality was most prominent with higher serum phosphorus (>3.5 mg/dl) and PTH levels (>150 pg/ml). Higher paricalcitol doses shifted the calcium range associated with the greatest survival to the right, i.e. from 9.0 to <9.5 to 9.5 to <10.0 mg/dl. African-Americans exhibited the highest death hazard ratio of hypocalcemia <8.5 mg/dl, being 1.35 (95% CI: 1.22–1.49). Both a rise and drop in serum calcium over 6 months were associated with increased mortality compared to the stable group. Conclusions: Whereas in hemodialysis patients cumulatively high or low calcium levels are associated with higher death risk, subtle but meaningful interactions with phosphorus, PTH, paricalcitol dose and race exist.

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Clinical Outcomes with Active versus Nutritional Vitamin D Compounds in Chronic Kidney Disease

Cited by 89 publications

References 85 publications

Understanding Sources of Dietary Phosphorus in the Treatment of Patients with Chronic Kidney Disease

Understanding Sources of Dietary Phosphorus in the Treatment of Patients with Chronic Kidney Disease

Modified-Release Calcifediol Effectively Controls Secondary Hyperparathyroidism Associated with Vitamin D Insufficiency in Chronic Kidney Disease

Association of Cumulatively Low or High Serum Calcium Levels with Mortality in Long-Term Hemodialysis Patients

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