Abstract
Chronic kidney disease is a health problem whose prevalence is increasing worldwide. The kidney plays an important role in the metabolism of minerals and bone health and therefore, even at the early stages of CKD, disturbances in bone metabolism are observed. In the course of CKD, various bone turnover or mineralization disturbances can develop including adynamic hyperparathyroid, mixed renal bone disease, osteomalacia. The increased risk of fragility fractures is present at any age in these patients. Nutritional treatment of patients with advanced stages of CKD is aiming at prevention or correction of signs, symptoms of renal failure, avoidance of protein-energy wasting (PEW), delaying or prevention of the occurrence of mineral/bone disturbances, and delaying the start of dialysis. The results of studies suggest that progressive protein restriction is beneficial with the progression of renal insufficiency; however, other aspects of dietary management of CKD patients, including changes in sodium, phosphorus, and energy intake, as well as the source of protein and lipids (animal or plant origin) should also be considered carefully. Energy intake must cover patients’ energy requirement, in order to enable correct metabolic adaptation in the course of protein-restricted regimens and prevent negative nitrogen balance and protein-energy wasting.
Highlights
bone mineral density (BMD) and T scores (p < 0.0001); Higher protein diets were associated with higher BMD in the femoral neck, trochanter, intertrochanteric, and total femoral areas (p = 0.032, 0.0036, 0.008, and 0.0039, respectively); Such increased BMD benefits of a higher protein diet were not observed in Conclusions: Higher protein diets resulted in higher femoral BMD only in subjects without Chronic kidney disease (CKD)
Restricted protein diet with keto acid (KA) significantly preserved eGFR and decreased proteinuria, serum phosphate, parathyroid hormone (PTH) level, systolic BP, diastolic BP, and serum cholesterol; VLPD with KAs could be superior to low-protein diets (LPD) with KAs in slowing the decline in eGFR; Only VLPD with KAs considerably improved serum PTH, systolic and diastolic BP; Only LPD with KAs considerably increased serum albumin and serum calcium
Serum FGF23 levels may be a useful marker to monitor the effects of a low-protein diet in early and advanced stage CKD
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The worsening of renal function is associated with the retention of phosphate resulting in hypocalcemia, hyperphosphatemia, and low 1,25(OH)2D3, all promoting parathyroid hormone (PTH) secretion which in consequence leads to increased phosphate excretion and the development of secondary hyperparathyroidism in advanced stages of CKD [1,18]. Increased levels of PTH are associated with abnormal osteoblastic function and osteocyte stimulation with the receptor activator of NF-κB (RANK) ligand (RANK-L) leading to CKD mineralization defects, high bone turnover ROD, and bone resorption [46]. Recent studies have suggested that other factors may modulate osteoblast function and may be involved in the development of the mineralization disorder of CKD leading to high turnover renal osteodystrophy, surplus bone resorption, skeletal frailty, and increased fracture risk [43,55]. The utilization of this approach allows for the maintenance of proper protein intake including foods with low PPR, avoidance of a high phosphate load, and the appropriate inclusion of low phosphate vegetables, fruits, and cereals into the diet [79]
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