Protein restriction for diabetic renal disease

Robertson, Lynn; Waugh, Norman; Robertson, Aileen

doi:10.1002/14651858.cd002181.pub2

Cited by 155 publications

(109 citation statements)

References 64 publications

(37 reference statements)

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“…An increasing body of evidence suggests that dietary pattern intake rather than a sole focus on individual nutrients may offer a more practical approach to dietary management of chronic diseases (122-124). (126)(127)(128)(129)(130)(131)(132)(133).Theeffectsofalow-protein (daily intake of 0.6 g protein/kg ideal body weight), low-phosphorus (500-1,000 mg/day) diet were compared with those of a control diet containing $1.0 g protein/kg ideal body weight per day and $1,000 mg phosphorus per day in 35 patients with type 1 diabetes and DKD. Study participants on the lowprotein, low-phosphorus diet had a slower rate of decline in iothalamate GFR over the course of the study.…”

Section: Sodium-glucose Cotransporter 2 Inhibitorsmentioning

confidence: 99%

Diabetic Kidney Disease: A Report From an ADA Consensus Conference

Tuttle

Bakris

Bilous

et al. 2014

American Journal of Kidney Diseases

648

616

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The incidence and prevalence of diabetes mellitus have grown significantly throughout the world, due primarily to the increase in type 2 diabetes. This overall increase in the number of people with diabetes has had a major impact on development of diabetic kidney disease (DKD), one of the most frequent complications of both types of diabetes. DKD is the leading cause of end-stage renal disease (ESRD), accounting for approximately 50% of cases in the developed world. Although incidence rates for ESRD attributable to DKD have recently stabilized, these rates continue to rise in high-risk groups such as middle-aged African Americans, Native Americans, and Hispanics. The costs of care for people with DKD are extraordinarily high. In the Medicare population alone, DKD-related expenditures among this mostly older group were nearly $25 billion in 2011. Due to the high human and societal costs, the Consensus Conference on Chronic Kidney Disease and Diabetes was convened by the American Diabetes Association in collaboration with the American Society of Nephrology and the National Kidney Foundation to appraise issues regarding patient management, highlighting current practices and new directions. Major topic areas in DKD included 1) identification and monitoring, 2) cardiovascular disease and management of dyslipidemia, 3) hypertension and use of renin-angiotensin-aldosterone system blockade and mineralocorticoid receptor blockade, 4) glycemia measurement, hypoglycemia, and drug therapies, 5) nutrition and general care in advanced-stage chronic kidney disease, 6) children and adolescents, and 7) multidisciplinary approaches and medical home models for health care delivery. This current state summary and research recommendations are designed to guide advances in care and the generation of new knowledge that will meaningfully improve life for people with DKD.

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Section: Sodium-glucose Cotransporter 2 Inhibitorsmentioning

confidence: 99%

Diabetic Kidney Disease: A Report From an ADA Consensus Conference

Tuttle

Bakris

Bilous

et al. 2014

American Journal of Kidney Diseases

648

616

View full text Add to dashboard Cite

show abstract

“…30 A subsequent meta-analysis, however, failed to demonstrate any significant effect of a low protein diet on GFR decline in 585 type 1 and type 2 diabetic patients included in 12 controlled studies. 31 On the other hand, evidence that glomerular capillary hypertension is often maintained by angiotensin-dependent mechanisms fueled a series of experimental studies aimed to test the long-term renoprotective effects of inhibitors of the RAS such as ACE inhibitors and ARBs. 32 At comparable systemic BP control, ACE inhibitors more effectively than combined therapy with hydralazine, reserpine, and a diuretic reduced glomerular capillary pressure and slowed disease progression in experimental models of CKD characterized by glomerular capillary hypertension such as reduced nephron mass 33 and streptozotocin-induced diabetes, 34 an effect that, again, was invariably associated with a consistent reduction in proteinuria.…”

Section: Therapeutic Advantages Of Ras Inhibitorsmentioning

confidence: 99%

Mechanisms and Treatment of CKD

Ruggenenti

Cravedi

Remuzzi

2012

Journal of the American Society of Nephrology

238

183

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As CKD continues to increase worldwide, along with the demand for related lifesaving therapies, the financial burden of CKD will place an increasing drain on health care systems. Experimental studies showed that glomerular capillary hypertension and impaired sieving function with consequent protein overload play a pathogenic role in the progression of CKD. Consistently, human studies show that proteinuria is an independent predictor of progression and that its reduction is renoprotective. At comparable BP control, inhibitors of the renin-angiotensin system (RAS), including angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), more effectively than non-RAS inhibitor therapy reduce proteinuria, slow progression to ESRD, and even improve the kidney function achieving disease regression in some cases. In participants with diabetes, RAS inhibitors delay the onset of microalbuminuria and its progression to macroalbuminuria, and ACE inhibitors may reduce the excess cardiovascular mortality associated with diabetic renal disease. In addition to RAS inhibitors, however, multimodal approaches including lifestyle modifications and multidrug therapy will be required in most cases to optimize control of the several risk factors for CKD and related cardiovascular morbidity. Whether novel medications may help further improve the cost-effectiveness of renoprotective interventions is a matter of investigation.

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“…Regarding diet therapy, the efficacy of a low-protein diet (LPD) for advanced diabetic nephropathy remains controversial [2]. Previous clinical studies have not consistently shown beneficial effects of an LPD for the preservation of renal function in diabetic nephropathy [3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity

et al. 2016

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Aims/hypothesis The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity. Methods Diabetic male Wistar fatty (fa/fa) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1). Results Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA 1c levels in WFRs, and no differences in mean BP were observed among any of the groups. Conclusions/interpretation A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway.

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Protein restriction for diabetic renal disease

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Cited by 155 publications

References 64 publications

Diabetic Kidney Disease: A Report From an ADA Consensus Conference

Diabetic Kidney Disease: A Report From an ADA Consensus Conference

Mechanisms and Treatment of CKD

A very-low-protein diet ameliorates advanced diabetic nephropathy through autophagy induction by suppression of the mTORC1 pathway in Wistar fatty rats, an animal model of type 2 diabetes and obesity

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