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Why Low Protein Diet For Kidney Disease
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Chronic Kidney Disease (ckd)
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Dadvice Tv:low Protein Diet For Kidney Disease Patients: Tips And Advice From A Renal Dietitian
Division of Molecular Food Science and Technology, Medical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan
Received: 6 April 2018 / Revised: 19 April 2018 / Accepted: 25 April 2018 / Published: 27 April 2018
A low-protein diet (LPD) is expected to delay decline in kidney function in the early stages of chronic kidney disease (CKD), including diabetic kidney disease (DKD), and is recommended for healthy people. Regarding the molecular mechanisms of LPD versus DKD, previous animal studies have shown that LPD provides protection with most improvements in glomerular hyperfiltration/hypertension due to reduction in intraglomerular pressure. On the other hand, we showed that LPD, specifically LPD (VLPD), ameliorated tubule-mediated destruction, inflammation, and fibrosis by restoring autophagy through downregulation of mammalian toll-like receptor complex 1 (mTORC1) in animal models of type 2 diabetes and obesity. . Thus, based on animal studies, VLPD may show beneficial effects against advanced DKD. Previous clinical reports have also shown that VLPD, and not moderate LPD, slows the progression of renal dysfunction in patients with chronic glomerular nephritis. However, there are insufficient clinical data on the beneficial effects of VLPD against DKD. In addition, patients with CKD, including DKD, are a high-risk group for malnutrition, such as protein-energy wasting (PEW), sarcopenia, and frailty. Therefore, LPD, including VLPD, should be prescribed to patients when the benefits of LPD outweigh the risks, taking into account compliance, age, and nutritional status. As a future prediction, the development of VLPD replacement therapy without malnutrition can be expected to protect against high levels of DKD, through regulation of mTORC1 activity and stimulation of adequate autophagy. However, further studies are needed to elucidate the detailed mechanisms by which VLPD confers protection.
The prevalence of diabetes mellitus has been increasing worldwide in recent years. Long-term diabetes causes vascular changes and dysfunction. Complications of diabetes are the leading causes of morbidity and mortality in diabetic patients. Among the vascular complications of diabetes, diabetic kidney disease (DKD) is recognized as both a major cause of end-stage renal disease (ESRD) and an independent risk factor for cardiovascular disease (CVD) [ 1 , 2 ]. Multifactorial management including diet therapy, optimal glycemic control, blood pressure (BP) control using the renin-angiotensin system (RAS), lipid control using a statin or fibrate is recommended to control progression of DKD [3, 4, 5, 6]. Recently, new antidiabetic agents, including incretin-related drugs such as dipeptidyl peptidase-4 (DPP-4) inhibitor, glucagon-like peptide-1 (GLP-1) receptor agonist, and sodium-glucose cotransporter 2 ( SGLT2), showed a nasoprotective effect in DKD [7, 8, 9, 10, 11]. However, some patients with particularly advanced DKD rapidly progress to ESRD despite adequate multidisciplinary therapy.
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Dietary therapy is fundamentally important in both diabetes and DKD to maintain glucose control and control the progression of renal damage . Regarding diet therapy, especially in high levels of kidney disease, a low-protein diet (LPD) has been shown to protect kidney function in chronic kidney disease (CKD), including DKD [13, 14, 15, 16]. . However, the protective effect of LPD in DKD is controversial because previous clinical trials failed to show reliable results. This was due to the difficulty of adhering to a daily LPD and the insufficiency of clinical data on the optimal amount of protein intake [17, 18, 19, 20, 21]. Several early clinical reports have shown that high LPD (VLPD) may provide a more beneficial antineoprotective effect than conventional LPD, in patients without DKD [22,23]. However, there are no large clinical studies showing that VLPD has a beneficial effect on preserving renal function in patients with DKD, compared to conventional LPD. Moreover, the actual performance of LPD, especially VLPD, in a clinical setting has many nutritional risks, despite the benefits of relapse protection when treatment is appropriate, including enough energy, which has not been done.
On the other hand, the molecular mechanisms underlying the protective effects of LPD, particularly VLPD, against DKD have been demonstrated in many previous animal studies, including ours. However, its detailed mechanisms have not yet been fully elucidated. Elucidation of the mechanisms will lead to the development of new therapeutic options for DKD as an alternative treatment for VLPD.
In this review, we discuss (1) the molecular mechanisms of LPD, particularly VLPD, and its effects on kidney damage in advanced diabetes, based on data from animal studies; (2) current understanding of the protective effect of LPD against the development of DKD in a clinical setting; (3) Nutritional issues in CKD patients and their relationship with LPD. (4) the expected future prospects for new therapies as alternatives to VLPD.
Hyperfiltration is clinically important because of its ability to cause renal damage, which is associated with albuminuria, glomerular hypertension, and glomerulosclerosis . Glomerular hyperfiltration and hypertension seen in the diabetic state are closely involved in the initiation and progression of DKD [ 25 , 26 , 27 ]. The number of functional nephrons decreases in advanced renal injury, which leads to further glomerular hyperfiltration and hypertension in the remaining nephrons, accelerating the progression of renal dysfunction and functional deterioration. Therefore, reducing the workload of a nephron and improving glomerular hyperfiltration and hypertension may lead to renal protection. Although RAS inhibitors have been shown in many basic and clinical studies  to have renoprotective effects against CKD, including DKD, the mechanism by which these agents also exert protective effects through the mechanism of reducing glomerular hypertension is not clear. clear. . Recently, SGLT2 inhibitors have also been shown to have renoprotective effects, including reduction of albuminuria and reduced renal function, perhaps through glomerular hyperfiltration through enhancement of the tubular response system (TGF) [28,29]. When focused on dietary protein intake, high-protein diets dilate afferent arterioles and increase intraglomerular pressure, leading to an increase in glomerular filtration rate (GFR) [30,31]. However, glomerular hyperfiltration ultimately activates mesangial cell signaling, leading to increased transforming growth factor-β (TGF-β) release and advanced renal fibrosis and damage [ 32 ]. On the other hand, previous animal studies have shown that low protein intake can control glomerular afferent arterioles and reduce intraglomerular pressure and improve glomerular hypertrophy, which may lead to prevention of onset and slowing of progression. of DKD [30, 31, 33 , 34] (Figure 1).
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The degree of interstitial tubular damage (rather than glomerular damage) predictably correlates with reduced renal function . Therefore, protection of renal tubular cells against diabetes-induced tubular damage leads to preservation of renal function. However, there are few reports on whether LPD exhibits a protective effect on renal tubular cells, along with glomeruli and glomerular cells, in diabetic kidneys. Furthermore, it is unclear whether invasive LPD therapy ameliorates diabetes-induced advanced kidney damage, including tubule-mediated destruction. Previously, we clearly demonstrated that LPD, especially VLPD intervention, ameliorated advanced DKD, especially tubular lesions, including fibrosis, tubular cell damage, inflammation, and apoptosis in fatty Wistar (fa/fa) rats (WFRs) , which are an animal model of type 2 diabetes and obesity . We also investigated the detailed mechanism by which LPD ameliorated advanced tubular interstitial destruction in diabetes, focusing on autophagy and the mammalian target of rapamycin complex 1 (mTORC1) pathway. Autophagy plays a
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