Abstract
Use of nutritional therapy (NT) in chronic kidney disease (CKD) patients is still debated among nephrologists, but it represents a fundamental point in the conservative treatment of CKD. It has been used for years and it has new goals today, such as (1) the reduction of edema, diuretics, and blood pressure values with a low sodium-content diet; (2) the dose reduction of phosphate levels and phosphate binders; (3) the administration of bicarbonate with vegetables in order to correct metabolic acidosis and delay CKD progression; (4) the reduction of the number and the doses of drugs and chemical substances; and (5) the lowering of urea levels, the cure of intestinal microbioma, and the reduction of cyanates levels (such as indoxyl-sulphate and p-cresol sulphate), which are the most recent known advantages achievable with NT. In conclusion, NT and especially very low protein diet (VLPD) have several beneficial effects in CKD patients and slows the progression of CKD.
Highlights
Nephrologists replaced the Shakespearean doubt “to be or not to be” with “nutritional therapy (NT) in chronic kidney disease (CKD) patients: yes or not?”There is still a great debate among nephrologists regarding the efficacy of NT in CKD patients [1,2,3]
A high percentage of CKD patients are treated with diuretics to reduce edema, anti-hypertensive drugs, ACE-inhibitors to treat proteinuria, phosphate binders to prevent secondary hyperparathyroidism and vascular calcification, sodium bicarbonate to correct metabolic acidosis, and erythropoietin to treat anemia [5]
Several recent papers focus on the tight connection between gut and kidney, showing that intestinal endothelial alterations and its permeability are caused by both intestinal microbioma modification and high urea levels in CKD patients [6,27,28,29]
Summary
Nephrologists replaced the Shakespearean doubt “to be or not to be” with “nutritional therapy (NT) in chronic kidney disease (CKD) patients: yes or not?”. As far as we know, there are no publications in the scientific literature in which NT is considered as a pharmacological therapy, a coadjuvant treatment, or a tool to reduce the number and the doses of medications. A high percentage of CKD patients are treated with diuretics to reduce edema, anti-hypertensive drugs, ACE-inhibitors to treat proteinuria, phosphate binders to prevent secondary hyperparathyroidism and vascular calcification, sodium bicarbonate to correct metabolic acidosis, and erythropoietin to treat anemia [5]. There is a growing evidence that serum urea is a toxin [6,7] and there is no pharmacological therapy to treat and reduce its levels. The multivariate analysis showed a significant correlation between phospUhsaeteolfeNveTlspilnacnrte-adseeri(vOeRd 1a.l1l1o;w9e5d%aClIes1s.0i4n–t1e.s1t9in; apl-vaablsuoerp0.t0io3)n, uorfinpahroyspphhaotsepahnadte tihnecnreaasbeeOttRer 1p.2h2o;s9p5h%ateClIe1v.e1l2s–c1o.3n7tr;opl-vwailtuhea0l.e0s2s)e,raunsdeuosfedoruf gNsT[5w].ith a higher protein content (OR 1.85; 95% CI 1.51–2.23; p-value 0.005) (26)
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