Early dietary phosphorus restriction and calcium supplementation in the prevention of renal osteodystrophy

Maschio, Giuseppe; Tessitore, Nicola; D’Angelo, Angela; Bonucci, E.; Lupo, Antonio; Valvo, E.; Loschiavo, C.; Fabris, Antonia; Morachiello, P; Previato, G.; Fiaschi, E

doi:10.1093/ajcn/33.7.1546

Cited by 42 publications

(9 citation statements)

References 5 publications

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“…How ever, it is also possible that an increase of the blood levels of l,25-(OH)2D3 may be important. In fact, the restriction of the phosphorus intake has been found to exert such an effect with a consequent increase of the intestinal absorp tion of calcium and of the calcemic response to PTH [9], Secondary hyperparathyroidism of renal failure was prevented in dogs with experimental renal failure by re stricting their phosphorus intake [17], The same results were obtained with a low-phosphorus diet in renal patients with a GFR of 45-75 ml/min [9] and in patients with a GFR of 15-35 ml/min [12].…”

Section: Discussionmentioning

confidence: 68%

“…The present investigation shows that the standard low-protein diet (SLPD), which prevents secondary hyperparathyroid ism in patients with early renal failure [9,12], is not effective in severe uremics. Secondary hyperparathyroidism may be reversed in such cases with a very low-protein and lowphosphorus diet supplemented with essential amino acids and keto-analogues and with calcium carbonate (EAA and KA diet).…”

Section: Introductionmentioning

confidence: 81%

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Reversal of Hyperparathyroidism in Severe Uremics Following Very Low-Protein and Low-Phosphorus Diet

Barsotti¹,

Morelli²,

Guiducci³

et al. 1982

Nephron

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Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 81%

Reversal of Hyperparathyroidism in Severe Uremics Following Very Low-Protein and Low-Phosphorus Diet

Barsotti¹,

Morelli²,

Guiducci³

et al. 1982

Nephron

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“…This observation has been subsequently confirmed both in patients with a moderate impairment of renal function and in those with severe renal failure [Hirata, 1979;Kluthe, 1979;Maschio et al, 1979;Gior dano, 1981;Barsotti et al, 1981;Bergstrom et al, 1982;Sitprija and Suvanpha, 1983].…”

Section: Slowing O F the Rate O F Decline O F Rena! Functionmentioning

confidence: 83%

Dietary Treatment of Chronic Renal Failure: Why Is It Not Used More Frequently?

Giovannetti

1985

Nephron

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“…A remarkable stabilization in renal function in a case series of patients maintained on very low phosphate diet (7 mg/kg) was reported in 1983 by Barsotti et al [28]. In the 1980s, low-phosphate diets were considered a promising treatment strategy to attenuate calcitriol deficiency and secondary hyperparathyroidism [29] and progression to ESRD [30], but interest in the possibility of modifying the evolution of renal diseases by this intervention faded away thereafter. A recent study by Di Iorio et al [31] is fully in line with the possibility that low phosphate intake may exert favorable effects on proteinuria in progressive nephropathies.…”

Section: Phosphate Fgf23 and Ckd Progressionmentioning

confidence: 99%

FGF23: A Mature Renal and Cardiovascular Risk Factor?

2013

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High FGF23 predicts renal function loss in chronic kidney disease (CKD) patients and graft failure in transplant patients. FGF23, parathyroid hormone and serum phosphate are all interrelated but among these CKD-MBD biomarkers only FGF23 is independently related with CKD progression. High FGF23 associates with endothelial dysfunction in CKD patients and in elderly individuals in the general population. Furthermore, independently of serum phosphate, high FGF23 associates with mortality and left ventricular hypertrophy in dialysis patients and with atherosclerosis in elderly individuals in the general population. FGF23 also predicts a high risk for death and cardiovascular events in predialysis CKD patients and in subjects with coronary artery disease. A recent trial in CKD patients showed that low phosphate intake associated with a phosphate binder produces a 35% decrease in plasma FGF23. Yet in this and in another trial testing several phosphate binders, FGF23 levels remained well beyond the upper limit of the normal range. Of note, in this latter study, calcification of the coronary arteries and abdominal aorta actually increased, rather than decreased, during treatment with these drugs in the face of evidence of negative phosphate balance and amelioration of hyperparathyroidism. Mechanistic studies are still needed before testing the hypothesis that FGF23 is implicated in a causal manner in cardiovascular and renal diseases. Given the modest effects of phosphate binders on serum FGF23 in CKD patients, pharmacologic interventions antagonizing the effects of this growth factor rather than phosphate-lowering interventions should be put in place to properly test this hypothesis in the clinical scenario in CKD.

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Early dietary phosphorus restriction and calcium supplementation in the prevention of renal osteodystrophy

Cited by 42 publications

References 5 publications

Reversal of Hyperparathyroidism in Severe Uremics Following Very Low-Protein and Low-Phosphorus Diet

Reversal of Hyperparathyroidism in Severe Uremics Following Very Low-Protein and Low-Phosphorus Diet

Dietary Treatment of Chronic Renal Failure: Why Is It Not Used More Frequently?

FGF23: A Mature Renal and Cardiovascular Risk Factor?

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