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Effect of an Intensive Weight-Loss Lifestyle Intervention on Kidney Function: A Randomized Controlled Trial.
Díaz-López, A, Becerra-Tomás, N, Ruiz, V, Toledo, E, Babio, N, Corella, D, Fitó, M, Romaguera, D, Vioque, J, Alonso-Gómez, ÁM, et al
American journal of nephrology. 2021;(1):45-58
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Abstract
INTRODUCTION Large randomized trials testing the effect of a multifactorial weight-loss lifestyle intervention including Mediterranean diet (MedDiet) on renal function are lacking. Here, we evaluated the 1-year efficacy of an intensive weight-loss intervention with an energy-reduced MedDiet (erMedDiet) plus increased physical activity (PA) on renal function. METHODS Randomized controlled "PREvención con DIeta MEDiterránea-Plus" (PREDIMED-Plus) trial is conducted in 23 Spanish centers comprising 208 primary care clinics. Overweight/obese (n = 6,719) adults aged 55-75 years with metabolic syndrome were randomly assigned (1:1) to an intensive weight-loss lifestyle intervention with an erMedDiet, PA promotion, and behavioral support (intervention) or usual-care advice to adhere to an energy-unrestricted MedDiet (control) between September 2013 and December 2016. The primary outcome was 1-year change in estimated glomerular filtration rate (eGFR). Secondary outcomes were changes in urine albumin-to-creatinine ratio (UACR), incidence of moderately/severely impaired eGFR (<60 mL/min/1.73 m2) and micro- to macroalbuminuria (UACR ≥30 mg/g), and reversion of moderately (45 to <60 mL/min/1.73 m2) to mildly impaired GFR (60 to <90 mL/min/1.73 m2) or micro- to macroalbuminuria. RESULTS After 1 year, eGFR declined by 0.66 and 1.25 mL/min/1.73 m2 in the intervention and control groups, respectively (mean difference, 0.58 mL/min/1.73 m2; 95% CI: 0.15-1.02). There were no between-group differences in mean UACR or micro- to macroalbuminuria changes. Moderately/severely impaired eGFR incidence and reversion of moderately to mildly impaired GFR were 40% lower (HR 0.60; 0.44-0.82) and 92% higher (HR 1.92; 1.35-2.73), respectively, in the intervention group. CONCLUSIONS The PREDIMED-Plus lifestyle intervention approach may preserve renal function and delay CKD progression in overweight/obese adults.
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Uric acid and the cardio-renal effects of SGLT2 inhibitors.
Bailey, CJ
Diabetes, obesity & metabolism. 2019;(6):1291-1298
Abstract
Sodium/glucose co-transporter-2 (SGLT2) inhibitors, which lower blood glucose by increasing renal glucose elimination, have been shown to reduce the risk of adverse cardiovascular (CV) and renal events in type 2 diabetes. This has been ascribed, in part, to haemodynamic changes, body weight reduction and several possible effects on myocardial, endothelial and tubulo-glomerular functions, as well as to reduced glucotoxicity. This review evaluates evidence that an effect of SGLT2 inhibitors to lower uric acid may also contribute to reduced cardio-renal risk. Chronically elevated circulating uric acid concentrations are associated with increased risk of hypertension, CV disease and chronic kidney disease (CKD). The extent to which uric acid contributes to these conditions, either as a cause or an aggravating factor, remains unclear, but interventions that reduce urate production or increase urate excretion in hyperuricaemic patients have consistently improved cardio-renal prognoses. Uric acid concentrations are often elevated in type 2 diabetes, contributing to the "metabolic syndrome" of CV risk. Treating type 2 diabetes with an SGLT2 inhibitor increases uric acid excretion, reduces circulating uric acid and improves parameters of CV and renal function. This raises the possibility that the lowering of uric acid by SGLT2 inhibition may assist in reducing adverse CV events and slowing progression of CKD in type 2 diabetes. SGLT2 inhibition might also be useful in the treatment of gout and gouty arthritis, especially when co-existent with diabetes.
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Metabolic syndrome but not obesity measures are risk factors for accelerated age-related glomerular filtration rate decline in the general population.
Stefansson, VTN, Schei, J, Solbu, MD, Jenssen, TG, Melsom, T, Eriksen, BO
Kidney international. 2018;(5):1183-1190
Abstract
Rapid age-related glomerular filtration rate (GFR) decline increases the risk of end-stage renal disease, and a low GFR increases the risk of mortality and cardiovascular disease. High body mass index and the metabolic syndrome are well-known risk factors for patients with advanced chronic kidney disease, but their role in accelerating age-related GFR decline independent of cardiovascular disease, hypertension and diabetes is not adequately understood. We studied body mass index, waist circumference, waist-hip ratio and metabolic syndrome as risk factors for accelerated GFR decline in 1261 middle-aged people representative of the general population without diabetes, cardiovascular disease or kidney disease. GFR was measured as iohexol clearance at baseline and repeated after a median of 5.6 years. Metabolic syndrome was defined as fulfilling three out of five criteria, based on waist circumference, blood pressure, glucose, high-density lipoprotein cholesterol and triglycerides. The mean GFR decline rate was 0.95 ml/min/year. Neither the body mass index, waist circumference nor waist-hip ratio predicted statistically significant changes in age-related GFR decline, but individuals with baseline metabolic syndrome had a significant mean of 0.30 ml/min/year faster decline than individuals without metabolic syndrome in a multivariable adjusted linear regression model. This association was mainly driven by the triglyceride criterion of metabolic syndrome, which was associated with a significant 0.36 ml/min/year faster decline when analyzed separately. Results differed significantly when GFR was estimated using creatinine and/or cystatin C. Thus, metabolic syndrome, but not the body mass index, waist circumference or waist-hip ratio, is an independent risk factor for accelerated age-related GFR decline in the general population.
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The comorbidity of increased arterial stiffness and microalbuminuria in a survey of middle-aged adults in China.
Miao, R, Wu, L, Ni, P, Zeng, Y, Chen, Z
BMC cardiovascular disorders. 2018;(1):83
Abstract
BACKGROUND Increased arterial stiffness (iAS) and microalbuminuria (MAU), which may occur simultaneously or separately in the general population and share similar risk factors, are markers of macro- and microvascular injuries. Our research investigated the comorbidity of iAS and MAU in the middle-aged population and examined the heterogeneous effects of metabolic risk factors on iAS and MAU. METHODS We selected 11,911 individuals aged 45 to 60 years who underwent a health examination at the 3rd Xiangya Hospital between 2010 and 2014. Metabolic syndrome (MetS) was determined according to IDF/NHLBI/AHA-2009 criteria. Multinomial logistic regression was applied to evaluate the influence of MetS, components of MetS and clusters of MetS on the co-occurrence (MAU(+)/iAS(+)) or non-co-occurrence (MAU(+)/iAS(-) and MAU(-)/iAS(+)) of MAU and iAS. RESULTS Reference group was MAU(-)/iAS(-). A positive effect of MetS on the presence of MAU(+)/iAS(-), MAU(-)/iAS(+), or MAU(+)/iAS(+) is listed in ascending order based on odds ratios (ORs = 2.11, 2.41, 4.61, respectively; P < 0.05). Compared with MAU(+)/iAS(-), Elevated blood pressure (BP) (OR = 1.62 vs. 4.83, P < 0.05), triglycerides(TG) (OR = 1.20 vs. 1.37, P < 0.05) were more strongly associated with MAU(-)/iAS(+), whereas fasting blood glucose (FBG) was less associated (OR = 1.37 vs. 1.31, P < 0.05). Decreased high-density lipoprotein cholesterol(HDL-c) (OR = 1.84, P < 0.01) and elevated waist circumference(WC) (OR = 1.28 P < 0.01) were the most strongly associated with MAU(+)/iAS(-). Compared with the individuals without MetS, individuals with the elevated BP, FBG, TG and decreased HDL-c cluster had the greatest likelihood of presenting a MAU(-)/iAS(+) (OR = 5.98, P < 0.01) and MAU(+)/iAS(+) (OR = 13.17, P < 0.01), these likelihood was even greater than the cluster with simultaneous alteration in all five MetS components (OR = 3.89 and 10.77, respectively, P < 0.01), which showed the most strongly association with MAU(+)/iAS(+) (OR = 5.22, P < 0.01). CONCLUSION Based on the heterogeneous influences of MetS-related risk factors on MAU and iAS, these influences could be selectively targeted to identify different types of vascular injuries.
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SGLT2 inhibitors and the kidney: Effects and mechanisms.
Tsimihodimos, V, Filippatos, TD, Elisaf, MS
Diabetes & metabolic syndrome. 2018;(6):1117-1123
Abstract
AIMS: Numerous clinical trials have shown that sodium glucose cotransporter 2 (SGLT2) inhibitors exert a favorable effect on the indices of renal function (albuminuria, glomerular filtration rate decline over time) and the incidence of hard renal endpoints such as renal death or time to initiation of renal replacement therapy. MATERIALS AND METHODS In this review, we describe in detail the evidence regarding the nephroprotective mechanisms of SGLT2 inhibitors and describe the risk factors that may predispose to the development of acute kidney injury in patients receiving these drugs. RESULTS Although the impact of these drugs on renal hemodynamics seems to represent the most important renoprotective mechanism of action, many other effects of these compounds, including beneficial effects on metabolism and blood pressure, have been proposed to contribute to the observed clinical benefit. CONCLUSIONS SGLT2 inhibitors clearly act beneficially in terms of kidney function with many proposed mechanisms.
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Prevalence and risk factors of chronic kidney disease in an african semi-urban area: Results from a cross-sectional survey in Gueoul, Senegal.
Faye, M, Lemrabott, AT, Cissé, MM, Fall, K, Keita, Y, Ngaide, AA, Mbaye, A, Fary Ka, EH, Niang, A, Kane, A, et al
Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia. 2017;(6):1389-1396
Abstract
Chronic kidney disease (CKD) is a public health priority worldwide; however, its prevalence and incidence are difficult to assess. In Africa, few studies have been conducted on the prevalence of CKD. This study sought to describe the epidemiological characteristics and profile of CKD, as well as the related risk factors in Guéoul, a semi-urban zone in Senegal. An observational, cross-sectional, and descriptive study was conducted in Guéoul city in Senegal from November 1, 2012, to December 10, 2012, according to the WHO STEPS approach. People older than 35 years living in Guéoul city were included in the study. Cardiovascular and renal disease risk factor screening was conducted for this population. Data were analyzed using the 3.5.1 version of Epi Info software. The significance level was a P <0.05. One thousand four hundred and eleven participants with a mean age of 48 ± 12.68 years and a sex ratio of 0.34 were included in the study (359 men/1052 women). The prevalence of renal disease was 36.5%. Sixty-eight people showed proteinuria greater than two cross with urinary dipsticks. Two hundred and six people had a glomerular filtration rate <60 mL/min, and among them, 201 were in stage III, two in stage IV, and three in stage V according to the modification of diet in renal disease formula. Ninety-eight participants had morphological abnormalities. Cardiovascular risk factors found among participants with renal disease were obesity (25.2%), hypertension (55.5%), diabetes (2.3%), and renal and metabolic syndrome (32.43%). Those that statistically significantly correlated with renal disease were obesity (P = 0.0001), hypertension (P = 0.0001), and diabetes (P = 0.021). This study assessed the extent of renal disease in the population of Guéoul city. Being aware of the prevalence of CKD in the general population of Senegal is mandatory for defining appropriate strategies for the management of these risk factors and progression of renal diseases.
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Fabry's disease: an example of cardiorenal syndrome type 5.
Sharma, A, Sartori, M, Zaragoza, JJ, Villa, G, Lu, R, Faggiana, E, Brocca, A, Di Lullo, L, Feriozzi, S, Ronco, C
Heart failure reviews. 2015;(6):689-708
Abstract
Cardiorenal syndrome type 5 (CRS-5) includes conditions where there is a simultaneous involvement of the heart and kidney from a systemic disorder. This is a bilateral organ cross talk. Fabry's disease (FD) is a devastating progressive inborn error of metabolism with lysosomal glycosphingolipid deposition in variety of cell types, capillary endothelial cells, renal, cardiac and nerve cells. Basic effect is absent or deficient activity of lysosomal exoglycohydrolase a-galactosidase A. Renal involvement consists of proteinuria, isosthenuria, altered tubular function, presenting in second or third decade leading to azotemia and end-stage renal disease in third to fifth decade mainly due to irreversible changes to glomerular, tubular and vascular structures, especially highlighted by podocytes foot process effacement. Cardiac involvement consists of left ventricular hypertrophy, right ventricular hypertrophy, arrhythmias (sinus node and conduction system impairment), diastolic dysfunction, myocardial ischemia, infarction, transmural replacement fibrosis, congestive heart failure and cardiac death. Management of FD is based on enzymatic replacement therapy and control of renal (with anti-proteinuric agents such as angiotensin-converting enzyme inhibitors-and/or angiotensin II receptor blockers), brain (coated aspirin, clopidogrel and statin to prevent strokes) and heart complications (calcium channel blockers for ischemic cardiomyopathy, warfarin and amiodarone or cardioverter device for arrhythmias).
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Cardiorenal syndrome: pathophysiology and potential targets for clinical management.
Hatamizadeh, P, Fonarow, GC, Budoff, MJ, Darabian, S, Kovesdy, CP, Kalantar-Zadeh, K
Nature reviews. Nephrology. 2013;(2):99-111
Abstract
Combined dysfunction of the heart and the kidneys, which can be associated with haemodynamic impairment, is classically referred to as cardiorenal syndrome (CRS). Cardiac pump failure with resulting volume retention by the kidneys, once thought to be the major pathophysiologic mechanism of CRS, is now considered to be only a part of a much more complicated phenomenon. Multiple body systems may contribute to the development of this pathologic constellation in an interconnected network of events. These events include heart failure (systolic or diastolic), atherosclerosis and endothelial cell dysfunction, uraemia and kidney failure, neurohormonal dysregulation, anaemia and iron disorders, mineral metabolic derangements including fibroblast growth factor 23, phosphorus and vitamin D disorders, and inflammatory pathways that may lead to malnutrition-inflammation-cachexia complex and protein-energy wasting. Hence, a pathophysiologically and clinically relevant classification of CRS based on the above components would be prudent. With the existing medical knowledge, it is almost impossible to identify where the process has started in any given patient. Rather, the events involved are closely interrelated, so that once the process starts at a particular point, other pathways of the network are potentially activated. Current therapies for CRS as well as ongoing studies are mostly focused on haemodynamic adjustments. The timely targeting of different components of this complex network, which may eventually lead to haemodynamic and vascular compromise and cause refractoriness to conventional treatments, seems necessary. Future studies should focus on interventions targeting these components.
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[Pharmacological nephroprotection in chronic kidney disease: current opportunities and perspectives (review of foreign literature)].
Nikolaev, AIu
Terapevticheskii arkhiv. 2012;(6):77-80
Abstract
A brief literature review analyses pharmacoprotective strategy in most widespread forms of chronic kidney disease: metabolic syndrome, hypertensive angionephrosclerosis. diabetic and non-diabetic nephropathy Nephroprotective properties of the blockers of rennin-angiotensin-aldosteron system and other antiadrenergic drugs, diuretics, hypolipidemic, antianemic and hypouricemic drugs, active metabolites of vitamin D, metphormine and glytasones are reviewed. The highest efficacy of combined pharmaconephroprotection is demonstrated.
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Advances in WNK signaling of salt and potassium metabolism: clinical implications.
Arroyo, JP, Gamba, G
American journal of nephrology. 2012;(4):379-86
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Abstract
Recent evidence due to the discovery of a family of kinases implicated in arterial hypertension now points to the underlying molecular mechanisms that dictate Na(+), K(+) and water handling in the nephron. These new key players need to be understood in order to fully comprehend the pathophysiology, manifestations, and treatment of common clinical entities such as hypovolemic shock, congestive heart failure, primary hyperaldosteronism, nephrotic syndrome and hypertension. It is through the analysis of the volume status and electrolyte abnormalities that commonly present with these diseases that we can begin to create a link between the abstract concept of a kinase regulation and how a patient will respond to a particular treatment. This review is an attempt to bridge that gap.