2016
DOI: 10.3109/0886022x.2015.1136874
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Erythropoiesis-stimulating agent slows the progression of chronic kidney disease: a possibility of a direct action of erythropoietin

Abstract: Background Controversy exists regarding the renoprotective effect of erythropoiesis-stimulating agent (ESA) in progressive chronic kidney disease (CKD) with renal anemia. In this study, we examined whether ESA therapy has a renoprotective effect in progressive CKD. Methods The subjects in this retrospective observational study were 68 non-dialysis dependent CKD patients with renal anemia. We compared the progression rate (PR), defined by the slope of the linear regression line of estimated glomerular filtratio… Show more

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Cited by 14 publications
(8 citation statements)
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“…Multivariate analysis of this study showed that anemia was an independent risk factor of CKD progression [30]. Some randomized controlled trials indicated that correcting anemia using erythropoiesisstimulating agents (ESAs) slows renal function deterioration [31][32][33][34]. On the other hand, anemia may be caused by the reduction of erythropoietin due to renal tubulointerstitial lesions [35].…”
Section: Discussionmentioning
confidence: 86%
“…Multivariate analysis of this study showed that anemia was an independent risk factor of CKD progression [30]. Some randomized controlled trials indicated that correcting anemia using erythropoiesisstimulating agents (ESAs) slows renal function deterioration [31][32][33][34]. On the other hand, anemia may be caused by the reduction of erythropoietin due to renal tubulointerstitial lesions [35].…”
Section: Discussionmentioning
confidence: 86%
“…Anemia is one of the most important complications of chronic renal failure (7).Anemia is also one of the mortality predictive factors in patients suffering from advanced chronic renal failure that leads to numerous pathophysiological disorders in these patients and brings about problems such as reduced tissue oxygenation, left ventricular hypertrophy, angina pectoris, heart failure, and immune system disorders.…”
Section: Discussionmentioning
confidence: 99%
“…The proposed mechanisms for the cardioprotective and nephroprotective effects of dapagliflozin include64,65 (i) the improvement of hyperglycemia and insulin sensitivity, along with other metabolic effects such as uric acid reduction, (ii) the reduced inflammation, oxidative stress and oxygen‐consuming transport workload owing to reduced sodium and glucose reabsorption in the proximal renal tubules (indeed, it has been demonstrated that dapagliflozin may reduce proximal tubular cell injury),66,67 (iii) the blood pressure lowering effect, (iv) the increase in fasting glucagon,68 (v) the reduction in intraglomerular pressure owing to SGLT2 inhibition-induced increased sodium delivery to the macula densa, leading to constriction of afferent renal arterioles, (vi) the reduction of kidney fat deposition, which is considered ectopic fat that promotes diabetic kidney disease progression,60 (vii) the reversal of hypomagnesemia, which is correlated with a more rapid decline of renal function,69,70 (viii) the increase in erythropoietin levels that exhibits direct renoprotective effects,71 (ix) the increase in the production of ketone bodies, since they can be used as a more efficient energy substrate leading to reduction in renal hypoxia 72…”
Section: Effects Of Dapagliflozinmentioning
confidence: 99%