Role of Altered Intestinal Microbiota in Systemic Inflammation and Cardiovascular Disease in Chronic Kidney Disease

Mafra, Denise; Lobo, Julie Calixto; Barros, Amanda F.; Koppe, Laetitia; Vaziri, Nosratola D.; Fouque, Denis

doi:10.2217/fmb.13.165

Cited by 133 publications

(92 citation statements)

References 85 publications

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“…Furthermore, in a cohort of people with normal renal function but on a high meat diet, the risk of microalbuminuria has been clearly demon strated. [31,32] TMAO metabolites comprise choline, phosphatidylcholine (lecithin) and L-carnitine, and the levels are particularly high in red meat, liver, other meats and egg yolk. Lower levels are found in poultry.…”

Section: Acidosismentioning

confidence: 99%

Recent important strategies in the management of chronic kidney disease

Meyers

Davies

2017

S Afr Med J

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The burden of chronic kidney disease (CKD) is considerably higher in low-and middle-income countries, which are less able than the developed world to cope with treating advanced renal failure owing to financial constraints. Prevention, early diagnosis and implementation of existing knowledge can improve outcomes. This review presents several recent advances to assist with avoiding and slowing down CKD progression and reducing common comorbid complications. The following are discussed: the possible use of metformin in patients with type 2 diabetes-related CKD; recent inexpensive important developments in the treatment of autosomal-dominant polycystic kidney disease; prevention of acidosis and the early dietary reduction of red meat consumption; and the therapeutic lowering of uric acid in persistent hyperuricaemia. Finally, an active and monitored exercise programme should be undertaken whenever possible. All of these recommendations have been shown to significantly slow the progression of CKD and increase cardiovascular protection. CME 731September 2017, Vol. 107, No. 9 CME addition to the multiple cardiovascular and renal complications of DM, renal dysfunction in the elderly is further compounded by the slow but progressive fall in glomerular filtration rate (GFR) in persons >45 years of age (i.e. ±1 mL/min/year) and also because people live longer. For many years the US Food and Drug Administration (FDA), the Regulatory Cooperation Council (RCC) in Canada and other regulatory bodies have indicated that the use of MF is contraindicated in patients with mild and moderate CKD (stages 3a and 3b) owing to the rarely reported but life-threatening complication of lactic acidosis (LA) (serum lactate levels ≥15 mmol/L).That LA does not occur in patients who receive MF, with an estimated GFR (eGFR) of 50 -30 mL/min., has been indicated in studies conducted by Inzucchi et al. [13] They showed that MF can be safely used in these patients, provided that certain guidelines are always followed. A Coch rane meta-analysis conducted on 47 096 patients with a follow-up of 86 067 patient-years compared the incidence of LA in patients who received MF with those who did not, irrespective of the eGFR.[14] They found that for the upper limit of 95% confidence the true incidence of LA was 6.3/100 000 patient-years for the MF group and 7.8/100 000 patient-years for the non-MF group.It is important to remember that before prescribing MF for any degree of renal function, certain rules are essential and must be fully adhered to. As many practitioners are either unaware or uncertain of the predisposing conditions, these are set out in Table 4.Mechanisms of MF-associated LA are not well elucidated, but include conversion of glucose to lactate in the splanchnic bed and inhibition of hepatic gluconeogenesis (i.e. from lactate, pyruvate and adenine). [15,16] It is essential that any patient with the abovementioned precipi ta ting disorders is instructed to immediately but temporarily withdraw the use of MF and present to a doctor. Patients h...

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Section: Acidosismentioning

confidence: 99%

Recent important strategies in the management of chronic kidney disease

Meyers

Davies

2017

S Afr Med J

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“…Toksik gazlar, indoxyl sülfat, p-cresol sülfat, aminler, amonyak ve trimetil amin N-oksit (TMAO), lipopolisakkaritler kan dolaşımına geçerek sistemik inflamasyondan sorumlu olabilmektedirler (32). Bu bileşenler sitotoksik olup kardiyovasküler ve immün değişikliklere yol açmaktadır.…”

Section: Di̇yet-bağirsak-böbrek Aksiunclassified

Kronik Böbrek Hastalığında Bağırsak Mikrobiyotası ve Diyet Posasının Rolü

Melekoğlu¹,

Samur²

2017

Turk Neph Dial Transpl

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“…Klotho protein is a β-glucuronidase. Reduced klotho expression in chronically diseased kidneys is associated with chronic inflammatory cell infiltrate, sclerosis of intrarenal small sized arteries, interstitial fibrosis and renal tubular atrophy [16] . Decreased klotho expression underlies excessive fibroblast emergence as a consequence of EMT following acute insults posed on renal tubular epithelium [12] .…”

Section: Sharaf El Din Uaa Et Al Stop Chronic Kidney Disease Progrementioning

confidence: 99%

“…[10] , cardiac hypertrophy [11] , renal tubular epithelial-mesenchymal cell transformation [12] , and increased interstitial fibrosis [13] . The last decade also witnessed the role of the gut in the pathogenesis of systemic inflammation in CKD patients [14][15][16] . This chronic inflammatory status might add directly, through absorbed toxins or through its interaction with Klotho gene to the risk of V.C.…”

Section: Introductionmentioning

confidence: 99%

Stop chronic kidney disease progression: Time is approaching

Din¹,

Salem²,

Abdulazim³

2016

WJN

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Progression of chronic kidney disease (CKD) is inevitable. However, the last decade has witnessed tremendous achievements in this field. Today we are optimistic; the dream of withholding this progression is about to be realistic. The recent discoveries in the field of CKD management involved most of the individual diseases leading the patients to end-stage renal disease. Most of these advances involved patients suffering diabetic kidney disease, chronic glomerulonephritis, polycystic kidney disease, renal amyloidosis and chronic tubulointerstitial disease. The chronic systemic inflammatory status and increased oxidative stress were also investigated. This inflammatory status influences the antisenescence Klotho gene expression. The role of Klotho in CKD progression together with its therapeutic value are explored. The role of gut as a major source of inflammation, the pathogenesis of intestinal mucosal barrier damage, the role of intestinal alkaline phosphatase and the dietary and therapeutic implications add a novel therapeutic tool to delay CKD progression.

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Role of Altered Intestinal Microbiota in Systemic Inflammation and Cardiovascular Disease in Chronic Kidney Disease

Cited by 133 publications

References 85 publications

Recent important strategies in the management of chronic kidney disease

Recent important strategies in the management of chronic kidney disease

Kronik Böbrek Hastalığında Bağırsak Mikrobiyotası ve Diyet Posasının Rolü

Stop chronic kidney disease progression: Time is approaching

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