Influence of prebiotic and probiotic supplementation on the progression of chronic kidney disease. Synbiotic Supplementations for Azotemia in Patients With Chronic Kidney Disease: a Randomized Controlled Trial. Uric acid and chronic kidney disease: new understanding of an old problem. SYNbiotics Easing Renal failure by improving Gut microbiologY (SYNERGY): a protocol of placebo-controlled randomised cross-over trial Uric acid as a risk factor for progression of non-diabetic chronic kidney disease? The Mild to Moderate Kidney Disease (MMKD) Study Predictors of heart rate variability and its prognostic significance in chronic kidney disease. Long-term outcomes of survivors of ICU acute kidney injury requiring renal replacement therapy: a 10-year prospective cohort study Evolution of chronic kidney disease in patients with systemic lupus erythematosus over a long-period follow-up: a single-center inception cohort study Medicare patients with cardiovascular disease have a high prevalence of chronic kidney disease and a high rate of progression to end-stage renal disease. Dietary nitrate load lowers blood pressure and renal resistive index in patients with chronic kidney disease: A pilot study. The exclusion of patients with chronic kidney disease from clinical trials in coronary artery disease. Efficacy of Folic Acid Therapy on the Progression of Chronic Kidney Disease: The Renal Substudy of the China Stroke Primary Prevention Trial. Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease Serum phosphate but not pulse wave velocity predicts decline in renal function in patients with early chronic kidney disease. Natural history of older adults with impaired kidney function: the InCHIANTI study. Should nephrologists use beta-blockers? A perspective. p-Cresyl sulphate and indoxyl sulphate predict progression of chronic kidney disease Dietary Changes Involving Bifidobacterium longum and Other Nutrients Delays Chronic Kidney Disease Progression An analysis of chronic kidney disease risk factors in a Louisiana nursing home population: a cross-sectional study. Renoprotective effects of febuxostat in hyperuricemic patients with chronic kidney disease: a parallel-group, randomized, controlled trial Pravastatin and cardiovascular risk in moderate chronic kidney disease. The use of an anti-inflammatory supplement in patients with chronic kidney disease Reduced cortical oxygenation predicts a progressive decline of renal function in patients with chronic kidney disease.
BACKGROUND One of the main goals in chronic kidney disease ( CKD ) patients is to diminish the accumulation of uremic toxins and to slow the progression of renal failure . We investigated whether prebiotic and probiotic supplementation along with low protein diet retards the progression of CKD . METHODS This is a 12-month prospect i ve observation study with a r and omized control and open-label design . A total of 24 stable CKD stage III to V patients , who are not on renal replacement therapy , were enrolled in this study . Patients were r and omly assigned to 2 groups : low protein diet + prebiotic + probiotic supplementation ( N.=12 ) , receiving 3 tablets of prebiotic + probiotic supplementation daily for 6 months , and the control group receiving low protein diet only ( N.=12 ) . We examined the effects of prebiotic and probiotic supplementation on estimated glomerular filtration rate ( eGFR ) in CKD . RESULTS The declining GFR  during prebiotic and probiotic supplementation were significantly lower ( -11.6±8.6 vs. -3.4±4.6 mL/min per 1.73 m2 per year , 95 % CI -6.45 - -9.86 , P<0.001 ) than those with low protein diet alone . CONCLUSIONS Prebiotic and probiotic supplementation along with low protein diet delayed the progression of CKD INTRODUCTION Chronic kidney disease ( CKD ) is a progressive and irreversible impairment of kidney function ; if it progresses to the end-stage of CKD , dialysis or kidney transplant is needed . In general , there are no definitive treatment to slow the progression of CKD . This study aim ed to determine the effect of synbiotic supplementations on azotemia in patients with CKD . MATERIAL S AND METHODS A r and omized controlled trial was conducted on 66 patients with CKD ( stages 3 and 4 ) . The participants were r and omly divided into 2 groups to receive synbiotic supplement , 1000 mg/d , and placebo ( 2 capsules a day ) for 6 weeks . At the beginning and end of the study , blood parameters and kidney function were evaluated . RESULTS Of the 66 patients studied , 16 patients ( 24.2 % ) were women and 50 ( 75.8 % ) were men . The mean age and body mass index of the participants were 61 ± 7.65 years and 28.52 ± 4.06 kg/m2 , respectively .  The level of blood urea nitrogen showed a significant reduction following the intake of synbiotic supplement ( from 40.80 ± 22.11 mg/dL to 36.14 ± 20.52 mg/dL , P = .01 ) . Serum creatinine , uric acid , and other indicators of kidney function showed no significant change . CONCLUSIONS The intake of synbiotic supplement could reduce blood urea nitrogen in patients with CKD in stages 3 and 4 ; however , it had no effect on the other markers of kidney function Although an elevation of serum uric acid level is often associated with chronic kidney disease ( CKD ) , it remains controversial whether hyperuricemia per se is a true risk factor for the development or aggravation of CKD . Recent epidemiologic studies in healthy population s or in subjects with established kidney disease have reported the independent role of uric acid in lowering glomerular filtration rate and increasing the risk for new-onset kidney disease . Furthermore , lowering uric acid in patients with established renal disease has been reported to stabilize renal function independent of other confounders , suggesting a causative role of elevated uric acid in progression of CKD , rather than as an incidental finding related to CKD severity . In this manuscript we will discuss the potential role of uric acid in the development and aggravation of CKD based on epidemiologic , clinical and experimental studies . Given the worldwide epidemic of CKD , the importance of identifying modifiable risk factors of CKD , and the clinical implication of hyperuricemia in CKD , we propose large r and omized clinical trials to investigate whether uric acid-lowering therapy can slow the progression of CKD Background Emerging evidence suggests modulating the microbiota in the large bowel of patients with chronic kidney disease ( CKD ) through pre- and /probiotic supplementation may inhibit the development of key nephrovascular toxins . To date , quality intervention trials investigating this novel treatment in CKD are lacking . The aim of SYNERGY is to assess the effectiveness of synbiotics ( co-administration of pre- and probiotics ) as a potential treatment targeting the synthesis of uremic toxins , specifically , indoxyl sulphate ( IS ) and p-cresyl sulphate ( PCS ) . Methods / design Thirty-seven patients with moderate to severe CKD ( Stage IV and V , pre-dialysis ) will be recruited to a double-blind , placebo-controlled , r and omised cross-over trial . Patients will be provided with synbiotic therapy or placebo for 6 weeks , with a 4 week washout before cross-over . The primary outcome is serum IS , total and free ( unbound ) concentrations , measured using ultra-performance liquid chromatography . Secondary outcomes include serum PCS , total and free ( unbound ) concentrations ; cardiovascular risk , measured by serum lipopolysaccharides , serum trimethylamine-N-oxide ( TMAO ) and inflammation and oxidative stress markers ; kidney damage , measured by 24 hour proteinuria and albuminuria , estimated glomerular filtration rate and renal tubule damage ( urinary kidney injury molecule-1 ) ; patients ’ self assessed quality of life ; and gastrointestinal symptoms . In addition , the effects on the community structure of the stool microbiota will be explored in a subset of patients to vali date the mechanistic rationale underpinning the synbiotic therapy . Discussion IS and PCS are two novel uremic toxins implicated in both cardiovascular disease ( CVD ) and progression of CKD . Preliminary studies indicate that synbiotic therapy maybe a promising strategy when considering a targeted , tolerable and cost-efficient therapy for lowering serum IS and PCS concentrations . This trial will provide high quality ‘ proof-of-concept ’ data to eluci date both the efficacy of synbiotic therapy for lowering the toxins and whether reductions in serum IS and PCS translate into clinical benefits . Considering the potential of pre- and probiotics to not only shift toxin levels , but to also impede CVD and CKD progression , SYNERGY will provide vital insight into the effectiveness of this innocuous nutritional therapy . Trial Registration Universal Trial Number : U1111 - 1142 - 4363 . Australian New Zeal and Clinical Trials Registry Number : ACTRN12613000493741 , date registered : 2nd May 2013 The kidney is one of the organs most prominently affected by aging . This can be seen by a loss of renal mass which is caused by a decrease in the number of nephrons result ing in hyperfiltration , hypertrophy and elevations in glomerular pressure . The factors influencing aging of the kidney are not fully eluci date d. Epidemiological , experimental and interventional studies result ed in inconsistent results and have not firmly established whether uric acid levels affect progression of Chronic Kidney Disease ( CKD ) . Therefore , we analyzed whether uric acid levels predict the progression of CKD in the Mild to Moderate Kidney Disease Study comprising at baseline 227 Caucasian patients aged 18 - 65 years with primary non-diabetic CKD of various degrees of renal impairment . Of them , 177 completed a prospect i ve follow-up of 7 years . Primary endpoint was progression of CKD defined as doubling of baseline serum creatinine and /or terminal renal failure . Patients who reached a progression endpoint ( n = 6 5 ) were significantly older , had higher baseline serum creatinine and protein excretion rates as well as lower Glomerular Filtration Rate ( GFR ) . Uric acid levels were only higher in patients with progression of disease when patients with uric acid-lowering drugs were excluded from the analysis . Cox regression analysis revealed that increasing uric acid levels predict disease progression only when the analysis was not adjusted for baseline kidney function parameters . As soon as we adjusted the analysis for GFR and proteinuria this association completely vanished . In summary , our prospect i ve 7 year follow-up study in patients with non-diabetic primary CKD did not support uric acid as an independent predictor for CKD progression BACKGROUND Heart rate variability ( HRV ) , a noninvasive measure of autonomic dysfunction and a risk factor for cardiovascular disease ( CVD ) , has not been systematic ally studied in nondialysis chronic kidney disease ( CKD ) . METHODS HRV was assessed using 24-h Holter monitoring in 305 subjects from the Renal Research Institute-CKD Study , a four-center prospect i ve cohort of CKD ( Stages 3 - 5 ) .  Multiple linear regression was used to assess predictors of HRV ( both time and frequency domain ) and Cox regression used to predict outcomes of CVD , composite of CVD/death and end-stage renal disease ( ESRD ) . RESULTS A total of 47 CVD , 67 ESRD and 24 death events occurred over a median follow-up of 2.7 years . Lower HRV was significantly associated with older age , female gender , diabetes , higher heart rate , C-reactive protein and phosphorus , lower serum albumin and Stage 5 CKD . Lower HRV ( mostly frequency domain ) was significantly associated with higher risk of CVD and the composite end point of CVD or death . Significantly , lower HRV ( frequency domain ) was associated with higher risk of progression to ESRD , although this effect was relatively weaker . CONCLUSIONS This study draws attention to the importance of HRV as a relatively under recognized predictor of adverse cardiovascular and renal outcomes in patients with nondialysis CKD . Whether interventions that improve HRV will improve these outcomes in this high-risk population deserves further study Background Acute kidney injury ( AKI ) requiring renal replacement therapy ( RRT ) is associated with high in-hospital morbidity and mortality in critically ill patients . Long-term outcomes have received little attention . Methods The aim of this study was to characterize AKI – chronic kidney disease ( CKD ) nexus in critically ill patients with AKI ( RIFLE class F ) . We performed a single-centre prospect i ve observational study of 425 consecutive critically ill patients with AKI requiring RRT . None of these patients had pre-existing kidney disease . Primary outcomes were vital status and renal function at hospital discharge and at 5 and 10 years of follow-up . Results The overall in-hospital mortality of the study cohort was 47 % , the mortality rates at 1 , 5 and 10 years were 65 , 75 and 80 % , respectively . At hospital discharge , recovery of renal function was complete in 56 % of survivors . None of these patients developed CKD during follow-up . Ninety percent of the 100 survivors with partial recovery of renal function had ongoing CKD during long-term follow-up . CKD progressed to end-stage renal disease ( ESRD ) in 12 patients ( 3 % of the cohort or 5 % of survivors ) . The patients with post-AKICKD had a higher prevalence of hypertension , a higher rate of fatal cardiac diseases and a higher all-cause death rate . Conclusion Long-term survival of critically ill patients with AKI requiring RRT is poor and determined by the development of de novo CKD . There is a need for close follow-up of patients surviving AKI to prevent progressive CKD and to reduce associated lethal cardiac events The objective is to investigate the accrual rate and risk factors of chronic kidney disease ( CKD ) in an inception cohort of patients with systemic lupus erythematosus ( SLE ) followed at a single tertiary center . A prospect ively collected data base of 256 consecutive patients with SLE followed over a 25-year period was systematic ally interrogated for demographic , disease manifestations , co-morbidities , and outcome . St and ardized SLE activity and damage scores were determined for the first and last study visits , and estimated glomerular filtration rate ( eGFR ; MDRD formula ) was calculated at the time of diagnosis and at each year of the follow-up . CKD was defined as eGFR < 60 ml/min/1.73 m2 . Results were analyzed with univariate and multivariate models and Kaplan-Meier curves , as appropriate . The cohort was predominantly female ( 90 % ) and Jewish ( 91.1 % ) . Mean age at diagnosis was 38 ± 15.5 years , mean SLE activity score 6.4 ± 3.8 , mean disease duration 8.8 ± 6.6 years , and mean damage score 0.2 ± 0.6 . Seventy-five patients ( 30.8 % ) were diagnosed with American College of Rheumatology (ACR)-defined lupus renal disease during the study period . There was a progressive decrease in eGFR over time . The prevalence of CKD was 46.7 % in patients with ACR-defined renal lupus disease and 16.4 % in those without . The hazards ratio for CKD was significantly higher in patients with lupus nephritis ( LN ) than without ( p < 0.001 ) . Earlier CKD was positively associated with hypertension ( p = 0.01 ) , older age at diagnosis ( p = 0.01 ) , and LN ( p < 0.001 ) , and negatively associated  with  hydroxychloroquine treatment ( p < 0.001 ) . The prevalence of CKD increases cumulatively in patients with SLE , also in those without overt lupus renal disease . Lupus renal disease poses a significant hazard for earlier development of CKD , and hypertension is a major risk factor for patients with and without nephritis . Antimalarial treatment is associated with renal preservation only in patients with lupus nephritis The risk of progression to ESRD among individuals with cardiovascular disease and chronic kidney disease ( CKD ) is not well defined . The purpose of this study was to describe the risk of ESRD among patients with cardiovascular disease . Charts were abstract ed for r and omly selected hospitalized Medicare beneficiaries with a diagnosis of either congestive heart failure ( CHF ) or acute myocardial infa rct ion ( AMI ) . The prevalence of CKD , based on the estimated modified diet in renal disease GFR of < 60 ml/min per m2 , was 60.4 % of CHF patients and 51.7 % of AMI patients . When compared with patients without CKD , the 30-d readmission rate was higher for CHF patients with CKD ( odds ratio [ OR ] , 1.70 ; 95 % confidence interval [ CI ] , 1.18 to 2.44 ) and for AMI patients with CKD ( OR , 1.78 ; 95 % CI , 1.17 to 2.70 ) . CHF patients ( OR , 1.62 ; 95 % CI , 1.15 to 2.30 ) and AMI patients ( OR , 3.10 ; 95 % CI , 1.98 to 4.84 ) with CKD were more likely to die during the year after discharge from the hospital . ESRD after discharge occurred in nine of 517 patients with AMI and 24 of 640 patients with CHF . CKD increased the risk of ESRD among CHF patients ( OR , 34.5 ; 95 % CI , 4.23 to 279.43 ) and AMI patients ( 0 and 3 % for those without and with CKD , respectively ) . At discharge , 18 % of AMI patients and 21 % of CHF patients with CKD were discharged with a diagnosis of renal disease .  CKD is highly prevalent among patients with cardiovascular disease and is associated with increased risk of adverse outcomes , including progression to ESRD . This study suggests that opportunities may exist to improve the detection of CKD in these patients who are hospitalized with cardiovascular disease Beetroot has a high concentration of inorganic nitrate , which can serially reduced to form nitrite and nitric oxide ( NO ) after oral ingestion . Increased renal resistive index ( RRI ) measured by Doppler ultrasonography is associated with higher cardiovascular mortality in hypertensive patients with reduced renal function over time defined as chronic kidney disease ( CKD ) . Our aim was to investigate whether the supplementation of dietary nitrate by administration of beetroot juice is able to reduce blood pressure and renal resistive index ( RRI ) as prognostic markers for cardiovascular mortality in CKD patients . In a cross-over study design , 17 CKD patients were r and omized to either a dietary nitrate load ( 300 mg ) by highly concentrated beetroot juice ( BJ ) or placebo ( water ) . Hemodynamic parameters as well as plasma nitrate concentration and RRI were measured before and 4 h after treatment . In this cohort , CKD was mainly caused by hypertensive or diabetic nephropathy . The mean eGFR was 41.6 ± 12.0 ml/min/m2  . Plasma nitrate concentrations were significantly increased after ingestion of BJ compared to control . Peripheral systolic and diastolic blood pressure as well as mean arterial pressure ( MAP ) were significantly reduced secondary to the dietary nitrate load compared to control ( e.g. ΔMAPBJ = -8.2 ± 7.6 mmHg vs. ΔMAPcontrol = -2.2 ± 6.0 mmHg , p = 0.012 ) . BJ also led to significantly reduced RRI values ( ΔRRIBJ = -0.03 ± 0.04 versus ΔRRIcontrol = 0.01 ± 0.04 ; p = 0.017 ) . Serum potassium levels were not altered secondary to the treatment . In this study , administration of the nitrate donor BJ led to significantly reduced RRI values and peripheral blood pressure which might be explained by release of the vasodilatator NO after oral intake . Whether supplementation of dietary nitrate in addition to routine pharmacologic therapy is able to decelerate progression of cardiovascular and renal disease in CKD , remains to be investigated Chronic kidney disease ( CKD ) is associated with a high risk of death from coronary artery disease and may modify the response to st and ard cardiovascular therapies . Treatment of subjects with CKD should ideally be based on evidence from r and omized , clinical trials , but how often subjects with CKD have been excluded from these trials is uncertain . We undertook this study in order to quantify how often subjects with moderate to advanced CKD were excluded from large cardiovascular trials . MEDLINE and the reference list of selected articles were search ed in order to identify large , r and omized , controlled trials of five different coronary artery disease therapies  published between 1998 and 2005 . Exclusion criteria and reported clinical characteristics of subjects were abstract ed . Rates of exclusion and reporting of baseline characteristics of study participants were compared for CKD , diabetes , history of smoking , and hypertension . Eighty-six trials r and omizing 411 653 patients were identified . More than 80 % of trials excluded subjects with end-stage renal disease and 75.0 % excluded patients with CKD . Subjects with diabetes , hypertension , or a history of smoking  were excluded less than 4 % of the time . Baseline renal function of study participant was reported in only 7 % of trials . Patients with CKD are frequently excluded from coronary artery disease trials and renal function of r and omized subjects is rarely reported . These findings reinforce the notion that available data on the treatment of coronary artery disease in subjects with CKD have significant limitations and should be generalized to the treatment of subjects with CKD cautiously Importance The efficacy of folic acid therapy on renal outcomes has not been previously investigated in population s without folic acid fortification . Objective To test whether treatment with enalapril and folic acid is more effective in slowing renal function decline than enalapril alone across a spectrum of renal function at baseline from normal to moderate chronic kidney disease ( CKD ) among Chinese adults with hypertension . Design , Setting , and Participants In this sub study of eligible China Stroke Primary Prevention Trial ( CSPPT ) , 15 104 participants with an estimated glomerular filtration rate ( eGFR ) 30 mL/min/1.73 m2 or greater , including 1671 patients with CKD , were recruited from 20 communities in Jiangsu province in China . Interventions Participants were r and omized to receive a single tablet daily containing 10 mg enalapril and 0.8 mg folic acid ( n = 7545 ) or 10 mg enalapril alone ( n = 7559 ) . Main Outcomes and Measures The primary outcome was the progression of CKD , defined as a decrease in eGFR of 30 % or more and to a level of less than 60 mL/min/1.73 m2 if the baseline eGFR was 60 mL/min/1.73 m2 or more , or a decrease in eGFR of 50 % or more if the baseline eGFR was less than 60 mL/min/1.73 m2 ; or end-stage renal disease . Secondary outcomes included a composite of the primary outcome and all-cause death , rapid decline in renal function , and rate of eGFR decline . Results Overall , 15 104 Chinese adults with a mean ( range ) age of 60 ( 45 - 75 ) years were recruited ; median follow-up was 4.4 years . There were 164 and 132 primary events in the enalapril group and the enalapril-folic acid group , respectively . Compared with the enalapril group , the enalapril-folic acid group had a 21 % reduction in the odds of the primary event ( odds ratio [ OR ] , 0.79 ; 95 % CI , 0.62 - 1.00 ) and a slower rate of eGFR decline ( 1.28 % vs 1.42 % per year ; P = .02 ) . Among the participants with CKD at baseline , folic acid therapy result ed in a significant reduction in the risks for the primary event ( OR , 0.44 ; 95 % CI , 0.26 - 0.75 ) , rapid decline in renal function ( OR , 0.67 ; 95 % CI , 0.47 - 0.96 ) and the composite event ( OR , 0.62 ; 95 % CI , 0.43 - 0.90 ) , and a 44 % slower decline in renal function ( 0.96 % vs 1.72 % per year , P < .001 ) . Among those without CKD at baseline , there was no between-group difference in the primary end point . Conclusions and Relevance Enalapril-folic acid therapy , compared with enalapril alone , can significantly delay the progression of CKD among patients with mild-to-moderate CKD . Trial Registration clinical trials.gov Identifier : NCT00794885 Introduction Uremic syndrome consists of nitrogenous waste retention , deficiency in kidney-derived hormones , and reduced acid excretion , and , if untreated , may progress to coma and eventual death . Previous experience suggests that oral administration of a probiotic formulation of selected microbial strains may extend renoprotection via intraintestinal extraction of toxic waste solutes in patients with chronic kidney disease (CKD)stages 3 and 4 . This report presents preliminary data from a pilot study . Methods This was a 6-month prospect i ve , r and omized , double-blind , placebo-controlled crossover trial of a probiotic bacterial formulation conducted in four countries , at five institutions , on 46 out patients with CKD stages 3 an nd 4 : USA ( n=10 ) , Canada ( n=113 ) , Nigeria ( n=115 ) , and Argentina ( n=8 ) . Outcomes were compared using biochemical parameters : blood urea nitrogen ( BUN ) , serum creatinine , and uric acid . General well-being was assessed as a secondary parameter by a quality of life ( QQOL ) question naire on a subjective scale of 1–10 . Results Oral ingestion of probiotics ( 90 billion colony forming units [CFUs]/day ) was well tolerated and safe during the entire trial period at all sites . BUN levels decreased in 29 patients ( 63 % , P<0.05 ) , creatinine levels decreased in 20 patients ( 43 % , no statistical significance ) , and uric acid levels decreased in 15 patients ( 33 % , no statistical significance ) . Almost all subjects expressed a perceived substantial overall improvement in QOL ( 86 % , P<0.05 ) . Conclusion The main outcomes of this preliminary trial include a significant reduction of BUN , enhanced well-being , and absence of serious adverse effects , thus supporting the use of the chosen probiotic formulation for bowel-based toxic solute extraction . QOL and BUN levels showed statistically significant differences in outcome ( P<0.05 ) between placebo and probiotic treatment periods at all four sites ( 46 patients ) . A major limitation of this trial is the small sample size nd elated inconsistencies BACKGROUND The rate of decline in kidney function is a powerful predictor of cardiovascular risk in patients with chronic kidney disease ( CKD ) . Serum phosphate and increased arterial stiffness are associated with elevated cardiovascular risk in CKD and the general population . We sought to determine whether serum phosphate and markers of arterial stiffness predict progression of renal dysfunction in patients with early CKD . METHODS Two hundred and twenty-five patients with Stage II-IV CKD were prospect ively followed up at University Hospital Birmingham .  Serum phosphate was measured at baseline and arterial stiffness was determined through measurement of aortic pulse wave velocity ( PWV ) and augmentation index ( AIx ) . Progression of renal dysfunction was defined as the slope of estimated glomerular filtration rate ( eGFR ) against time . We determined the associations between possible predictors and rate of progression and also examined a combined end point of start of dialysis or ≥ 25 % decline in eGFR . RESULTS Mean baseline eGFR was 43 ± 19 mL/min/1.73 m(2 ) and serum phosphate 1.22 ± 0.27 mmol/L. Median follow-up was 924 days . Serum phosphate independently predicted a greater decline in eGFR ; a 1 mmol/L increment in serum phosphate was associated with a 0.34 mL/min/month steeper decline ( P = 0.02 ) . Brachial and aortic systolic pressure independently predicted the rate of renal function decline but aortic PWV and AIx had no significant influence . Forty-one patients ( 18 % ) reached the combined end point ; serum phosphate was significantly higher in this group ( 1.32 ± 0.36 versus 1.19 ± 0.24 mmol/L , P = 0.04 ) and was an independent predictor for the combined end point . CONCLUSIONS Serum phosphate independently predicts decline in renal function in early CKD . Further studies are required to determine the mechanisms involved and to investigate the potential benefits of phosphate lowering on preserving kidney function The aim of this study was to assess the kidney function of an older community-dwelling population at baseline and appraise its evolution after 3 years of follow-up in terms of chronic kidney disease ( CKD ) stage progression , magnitude of glomerular filtration rate ( GFR ) changes , and value of serum creatinine . This was a prospect i ve population -based study of 676 Italian participants , aged 65 years and older . GFR was estimated using the Cockcroft-Gault equation and the Modification of Diet in Renal Disease Study equation . Using the Cockcroft-Gault equation . A total of 33 % of participants had criteria of CKD ( GFR < 60 mL/min ) at baseline ; among them , the majority remained stable , 10 % improved , and 7 % progressed to more severe CKD stages at follow-up . Loss of GFR in participants with GFR < 60 mL/min was significantly lower ( 1.4 mL/min per year ) than in participants with GFR ≥ 60 mL/min ( 3.3 mL/min per year ) at baseline . Most participants classified with CKD stage 2 ( GFR 60 - 89 mL/min ) or stage 3 ( GFR 30 - 59 mL/min ) at baseline did not change stage , whereas 55 % of people with CKD stage 1 ( GFR > 90 mL/min ) at baseline worsened to stage 2 and 10 % worsened to stage 3 . An abnormal high level of serum creatinine at baseline did not help to predict who might worsen at follow-up . Older people with CKD displayed a low progression of renal disease and therefore are at higher risk for co-morbidities related to CKD than for progression to end-stage renal disease Given the high prevalence of cardiovascular disease in people with chronic kidney disease ( CKD ) and the clear benefits of mortality reduction observed for most β−blockers in clinical trials , they are relatively underused in CKD patients [ 1,2 ] . The rationale for use of β-blockers in patients with CKD is review ed in detail elsewhere [ 2,3 ] but is summarized in this editorial . Alterations in β- and α-receptor responsiveness are associated with sympathetic over-activity in CKD . This increased sympathetic activity is involved in the genesis of hypertension , and contributes to cardiac complications seen in CKD [ 2,3 ] . The contribution of the sympathetic nervous system to nephropathy progression is documented in sub-totally nephrectomized rats where non-hypotensive doses of β-blockers ameliorate development of glomerulosclerosis and cardiac injury [ 4 ] . In men ,  sympathetic over-activity  , as assessed by sural nerve microneurography , was present in patients on haemodialysis [ 5 ] , stage 4 nephropathy [ 6 ] and in early stage 2 nephropathy among patients with polycystic kidney disease [ 7 ] . The role of the damaged kidney in causing sympathetic over-activity is illustrated by normalization of sympathetic over-activity in haemodialysis patients following bilateral nephrectomy [ 5 ] and in renal allograft recipients when their shrunken native kidneys are removed [ 8 ] . The most common cause of death in stage 3 and higher CKD results from complications of cardiovascular disease . This may be due , in part , to inadequate treatment of blood pressure , where blood pressure goals were not attained and agents known to reduce mortality secondary to cardiovascular causes , i.e. aspirin , ACE inhibitors and β-blockers were not used [ 9 ] . In a separate study , β-blockers were used in fewer than 30 % of haemodialysis patients [ 10 ] . This is surprising , since β-blockers are well-established , evidence -based therapy for reducing cardiovascular risk in hypertension associated with diabetes and after myocardial infa rct ion [ 11,12 ] . Observational studies support definite survival benefits derived from β-blocker use in patients with advanced CKD [ 13,14 ] . Furthermore , a prospect i ve Background . Indoxyl sulphate ( IS ) and p-cresyl sulphate ( PCS ) are uraemic toxins that have similar protein binding , dialytic clearance and proinflammatory features . However , only a few prospect i ve studies have evaluated possible associations between these two retained solutes and renal disease progression in chronic kidney disease ( CKD ) patients . Methods . This prospect i ve observational study evaluated independent associations between serum total IS and PCS with renal progression in a selected cohort of patients having different stages of CKD .  Baseline PCS and IS were correlated with renal progression [ defined as decrements in estimated glomerular filtration rate ( eGFR ) > 50 % from baseline or progression to end-stage renal disease ( ESRD ) ] and death during a follow-up period of 24 months . Results . Of 268 patients , 35 ( 13.1 % ) had renal progression and 14 ( 5.2 % ) died  after a mean follow-up of 21 ± 3 months . Univariate Cox regression analysis followed by multivariate analysis showed that high-serum PCS levels were associated with renal progression and all-cause mortality independent of age , gender , diabetes status , albumin levels , serum IS , serum creatinine , Ca × P product , intact parathyroid hormone , haemoglobin or high-sensitivity C-reactive protein level . Serum IS was only associated with renal progression ; however , the predictive power of serum IS was weakened when serum PCS was also present in the analytical model . Conclusions . In addition to traditional and uraemia-related risk factors such as renal function , serum IS and PCS levels may help in predicting the risk of renal progression in patients having different stages of CKD Background : Recent studies suggest that prebiotic and /or probiotic treatments ameliorate kidney function in humans and animals by improving the gut environment . However , the gut microbiota and kidney disease interactions remain to be determined . This study investigated whether synbiotics modulate the gut microbiota and ameliorate kidney function using a rat model of chronic kidney disease ( CKD ) . As uremic toxins are associated with CKD-related mineral and bone disorder , the secondary aim was to evaluate the relationship between synbiotics and secondary hyperparathyroidism ( SHPT ) . Methods : 5/6 nephrectomy ( Nx ) rats were developed as the CKD model . Sham-operated ( sham ) rats were used as the control . To investigate the effectiveness of prebiotics ( glutamine , dietary fiber , and oligosaccharide ) and probiotics ( Bifidobacterium longum strain ; GFOB diet ) , rats were r and omly assigned to 4 groups : Nx group fed the GFOB diet ( n = 10 ) ; Nx group fed the control ( CON ) diet ( n = 10 ) ; sham group fed the GFOB diet ( n = 5 ) ; and sham group fed the control diet ( n = 5 ) . Blood , feces , and kidney sample s were collected and analyzed . Results : Serum creatinine ( Cre ) and blood urea nitrogen in the Nx GFOB group were significantly lower than those in the Nx CON group . Serum indoxyl sulfate in the Nx GFOB group was lower than that in the Nx CON group , and significantly correlated with serum Cre . Inorganic phosphorus and intact parathyroid hormone in the Nx GFOB group were significantly lower than those in the Nx CON group . Conclusion : Improving the gut environment using synbiotics ameliorated kidney function and might be a pharmacological treatment for SHPT without any serious adverse events BACKGROUND Chronic Kidney Disease ( CKD ) and its progression are associated with multiple risk factors . CKD is prevalent in nursing homes residents , but factors related to CKD in this setting have not been defined . METHODS A cross-sectional study was conducted ( n=103 ) . Data was abstract ed using st and ardized forms and analyzed ( SAS 9.2 ) . Chi square and t-test statistics were used to compare proportions and means ; correlation coefficients were used to describe associations . Logistic models were fit to the data to determine multivariate associations . Modification of Diet in Renal Disease ( MDRD ) formula was used to estimate GFR . CKD was defined according to established st and ards . A cutoff point of 60 was chosen for further analysis . RESULTS Twenty-three percent of subjects had CKD . Mean age for eGFR < 60 was 70.8 + /- 13 and for eGFR > 60 was 61.7 + /-14 . Frequent co-morbidities were hypertension ( 75 % ) , GERD ( 40 % ) , obesity ( 39 % ) , dyslipidemia ( 35 % ) , depression ( 34 % ) , anemia ( 32 % ) , and diabetes ( 32 % ) . CONCLUSIONS Our population is unique in terms of its age and reasons for nursing home admission . Factors associated with CKD in our study include age > 65 years old , being male , having a positive history of cardiovascular disease ( including congestive heart failure and coronary artery disease , ) anemia , polypharmacy , and being obese ( BMI > 30 ) . Further analysis showed that age and anemia are the strongest factors associated with CKD in our population . Management targeted at CKD risk factor reduction may play a vital role in controlling the magnitude of this disease . Prospect i ve studies to investigate the relationship between gender , a BMI greater than 30 , cardiovascular disease , and CKD and its complications are warranted Background Hyperuricemia is associated with the onset of chronic kidney disease ( CKD ) and renal disease progression . Febuxostat , a novel , non-purine , selective xanthine oxidase inhibitor , has been reported to have a stronger effect on hyperuricemia than conventional therapy with allopurinol . However , few data are available regarding the clinical effect of febuxostat in patients with CKD . Methods A prospect i ve , r and omized , open-label , parallel-group trial was conducted in hyperuricemic patients with stage 3 CKD . Patients were r and omly assigned to treatment with febuxostat  ( n = 21 ) or to continue conventional therapy  ( n = 19 ) . Treatment was continued for 12 weeks . The efficacy of febuxostat was determined by monitoring serum uric acid ( UA ) levels , blood pressures , renal function , and urinary protein levels . In addition , urinary liver-type fatty acid-binding protein ( L-FABP ) , urinary albumin , urinary beta 2 microglobulin ( β2MG ) , and serum high sensitivity C-reactive protein were measured before and 12 weeks after febuxostat was added to the treatment . Results Febuxostat result ed in a significantly greater reduction in serum UA ( −2.2 mg/dL ) than conventional therapy ( −0.3 mg/dL , P < 0.001 ) . Serum creatinine and estimated glomerular filtration rate changed little during the study period in each group . However , treatment with febuxostat for 12 weeks reduced the urinary levels of L-FABP , albumin , and β2MG , whereas the levels of these markers did not change in the control group . Conclusion Febuxostat  reduced serum UA levels more effectively than conventional therapy and might have a renoprotective effect in hyperuricemic patients with CKD . Further studies should clarify whether febuxostat prevents the progression of renal disease and improves the prognosis of CKD OBJECTIVES To investigate the relation between chronic kidney disease ( CKD ) and cardiovascular disease ( CVD ) and retrospectively to evaluate the effect of low dose of pravastatin in Japanese hypercholesterolemic patients with CKD enrolled in the large-scale r and omized MEGA Study . METHODS In this post hoc analysis , effect of low dose pravastatin treatment ( 10 - 20 mg daily ) on the primary prevention of the cardiovascular disease and renal function after 5 years was evaluated in 7196 patients with normal kidney function/mild CKD or moderate CKD . Patients were classified based on an estimated glomerular filtration rate ( eGFR ) > or=60 or 30-<60mL/min/1.73m(2 ) as having normal renal function/mild CKD or moderate CKD , respectively . Since Japanese guidelines do not allow statin use in patients with severe kidney disease , such individuals were excluded . RESULTS The incidence of CVD events was 35 - 49 % higher in patients with moderate CKD than in those with normal renal function/mild CKD . Notably , in the moderate CKD group pravastatin significantly reduced CHD by 48 % ( P=0.02 ) , stroke by 73 % ( P<0.01 ) , CVD by 55 % ( P<0.01 ) , and total mortality by 51 % ( P=0.02 ) . Moreover , the change in eGFR during follow-up in patients with moderate CKD was significantly ( P=0.03 ) higher in those assigned to receive diet plus pravastatin ( + 6.3 % ) compared with those on diet alone ( + 5.1 % ) . CONCLUSIONS Risk of CVD is higher in patients with moderate CKD compared with those with normal renal function/mild CKD , and was significantly reduced by treatment with pravastatin . Pravastatin also exerted beneficial effects on renal function in patients with moderate CKD Abstract Chronic kidney disease ( CKD ) is characterized by a continuous reduction in kidney function , increased inflammation , and reduced antioxidant capacity . The objective of this study was to assess the effects of a herbal supplement on systemic inflammation and antioxidant status in non-dialysis CKD patients . Sixteen patients with CKD ( 56.0±16.0 yrs , 171.4±11.9 cm , 99.3±20.2 kg ) were r and omly chosen to receive a herbal supplement composed of Curcuma longa and Boswellia serrata , or placebo . Plasma levels of interleukin-6 ( IL-6 ) , tumor necrosis factor-α ( TNF-α ) , glutathione peroxidase ( GPx ) , and serum C-reactive protein ( CRP ) were measured at baseline and 8 weeks . Baseline data demonstrated elevated inflammation and low antioxidant levels . A significant time effect ( p=0.03 ) and time x compliance interaction effect ( p=0.04 ) were observed for IL-6 . No significant differences were observed for any other variables . This study demonstrates that mild and moderate CKD is associated with chronic inflammation and low antioxidant activity . Systemic inflammation and impaired antioxidant status may be greater in CKD population s with multiple comorbidities . Curcumin and Boswellia serrata are safe and tolerable and helped to improve the levels of an inflammatory cytokine Renal tissue hypoxia is a final pathway in the development and progression of chronic kidney disease ( CKD ) , but whether renal oxygenation predicts renal function decline in humans has not been proven . Therefore , we performed a prospect i ve study and measured renal tissue oxygenation by blood oxygenation level-dependent magnetic resonance imaging ( BOLD-MRI ) in 112 patients with CKD , 47 with hypertension without CKD , and 24 healthy control individuals . Images were analyzed with the twelve-layer concentric objects method that divided the renal parenchyma in 12 layers of equal thickness and reports the mean R2 * value of each layer ( a high R2 * corresponds to low oxygenation ) , along with the change in R2 * between layers called the R2 * slope . Serum creatinine values were collected to calculate the yearly change in estimated glomerular function rate ( MDRD eGFR ) . Follow up was three years . The  change in eGFR in CKD , hypertensive and control individuals was -2.0 , 0.5 and -0.2 ml/min/1.73m2/year , respectively . In multivariable regression analysis adjusted for age , sex , diabetes , RAS-blockers , eGFR , and proteinuria the yearly eGFR change correlated negatively with baseline 24 hour proteinuria and the mean R2 * value of the cortical layers , and positively with the R2 * slope , but not with the other covariates . Patients with CKD and high outer R2 * or a flat R2 * slope were three times more likely to develop an adverse renal outcome ( renal replacement therapy or over a 30 % increase in serum creatinine ) . Thus , low cortical oxygenation is an independent predictor of renal function decline . This finding should stimulate studies exploring the therapeutic impact of improving renal oxygenation on renal disease progression
Most of the included articles reported positive effects in renal function and decreased levels of urea , blood urea nitrogen , ammonia , plasma p-cresol , p-cresyl sulfate , and indoxyl sulfate
ABSTRACT Chronic kidney disease ( CKD ) is a syndrome caused by the progressive reduction of renal function .
This study aim ed to systematic ally examine the effects of supplementation with probiotics in the treatment of CKD .