***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Despite evidence implicating dietary sodium in the pathogenesis of cardiovascular disease ( CVD ) in chronic kidney disease ( CKD ) , quality intervention trials in CKD patients are lacking . This study aims to investigate the effect of reducing sodium intake on blood pressure , risk factors for progression of CKD and other cardiovascular risk factors in CKD . Methods / design The LowSALT CKD study is a six week r and omized-crossover trial assessing the effect of a moderate ( 180 mmol/day ) compared with a low ( 60 mmol/day ) sodium intake on cardiovascular risk factors and risk factors for kidney function decline in mild-moderate CKD ( stage III-IV ) . The primary outcome of interest is 24-hour ambulatory blood pressure , with secondary outcomes including arterial stiffness ( pulse wave velocity ) , proteinuria and fluid status . The r and omized crossover trial ( Phase 1 ) is supported by an ancillary trial ( Phase 2 ) of longitudinal-observational design to assess the longer term effectiveness of sodium restriction . Phase 2 will continue measurement of outcomes as per Phase 1 , with the addition of patient-centered outcomes , such as dietary adherence to sodium restriction ( degree of adherence and barriers/enablers ) , quality of life and taste assessment . Discussion The LowSALT CKD study is an investigator-initiated study specifically design ed to assess the proof-of-concept and efficacy of sodium restriction in patients with established CKD . Phase 2 will assess the longer term effectiveness of sodium restriction in the same participants , enhancing the translation of Phase 1 results into practice . This trial will provide much-needed insight into sodium restriction as a treatment option to reduce risk of CVD and CKD progression in CKD patients .Trial registration Universal Trial Number : U1111 - 1125 - 2149 . Australian New Zeal and Clinical Trials Registry Number : Background The effectiveness of salt restriction to lower blood pressure ( BP ) in Bangladeshi patients with chronic kidney disease ( CKD ) is uncertain . Objective To test the hypothesis that a tailored intervention intended to reduce salt intake in addition to st and ard care will achieve a greater reduction in BP in UK Bangladeshi patients with CKD than st and ard care alone . Design A r and omised parallel-group controlled trial conducted over a 6 month period . Setting A tertiary renal unit based in acute care hospital in East London . Participants 56 adult participants of Bangladeshi origin with CKD and BP > 130/80 mm Hg or on antihypertensive medication . Intervention Participants were r and omly allocated to receive a tailored low-salt diet or the st and ard low-salt advice .  BP medication , physical activity and weight were monitored . Main outcome measures The primary outcome was change in ambulatory BP . Adherence to dietary advice was assessed by measurement of 24 h urinary salt excretion . Results Of 56 participants r and omised , six withdrew at the start of the study . During the study , one intervention group participant died , one control group participant moved to Bangladesh . Data were available for the primary endpoint on 48 participants . Compared with control group the intervention urinary sodium excretion fell from 260 mmol/d to 103 mmol/d ( −131 to −76 , p<0.001 ) at 6 months and result ed in mean ( 95 % CI ) falls in 24 h systolic/diastolic BP of −8 mm Hg ( −11 to −5)/2 ( −4 to −2 ) both p<0.001 . Conclusions A tailored intervention can achieve moderate salt restriction in patients with CKD , result ing in clinical ly meaningful falls in BP independent of hypertensive medication . Trial Registration Clinical Trials.gov NCT00702312 Background —Aortic pulse wave velocity ( PWV ) is a predictor of mortality in patients with end-stage renal failure ( ESRF ) . The PWV is partly dependent on blood pressure ( BP ) , and a decrease in BP can attenuate the stiffness . Whether the changes in PWV in response to decreases in BP can predict mortality in ESRF patients has never been investigated . Methods and Results —One hundred fifty ESRF patients ( aged 52±16 years ) were monitored for 51±38 months . From entry until the end of follow-up , the changes of PWV in response to decreased BP were measured ultrasonographically . BP was controlled by adjustment of “ dry weight ” and , when necessary , with ACE inhibitors , calcium antagonists , and /or & bgr;-blockers , in combination if necessary . Fifty-nine deaths occurred , including 40 cardiovascular and 19 noncardiovascular events . Cox analyses demonstrated that independent of BP changes , the predictors of all-cause and cardiovascular mortality were as follows : absence of PWV decrease in response to BP decrease , increased left ventricular mass , age , and preexisting cardiovascular disease . Survival was positively associated with ACE inhibitor use . After adjustment for all confounding factors , the risk ratio for the absence of PWV decrease was 2.59 ( 95 % CI 1.51 to 4.43 ) for all-cause mortality and 2.35 ( 95 % CI 1.23 to 4.41 ) for cardiovascular mortality . The risk ratio for ACE inhibitor use was 0.19 ( 95 % CI 0.14 to 0.43 ) for all-cause mortality and 0.18 ( 95 % CI 0.06 to 0.55 ) for cardiovascular mortality . Conclusions —These results indicate that in ESRF patients , the insensitivity of PWV to decreased BP is an independent predictor of mortality and that use of ACE inhibitors has a favorable effect on survival that is independent of BP changes BACKGROUND AND OBJECTIVES Connective tissue growth factor ( CTGF/CCN-2 ) is a key player in fibrosis . Plasma CTGF levels predict end-stage renal disease and mortality in diabetic chronic kidney disease ( CKD ) , supporting roles in intra- and extrarenal fibrosis . Few data are available on CTGF in nondiabetic CKD . We investigated CTGF levels and effects of antiproteinuric interventions in nondiabetic proteinuric CKD . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS In a crossover r and omized controlled trial , 33 nondiabetic CKD patients ( 3.2 [ 2.5 to 4.0 ] g/24 h proteinuria ) were treated during 6-week periods with placebo , ARB ( 100 mg/d losartan ) , and ARB plus diuretics ( 100 mg/d losartan plus 25 mg/d hydrochlorothiazide ) combined with consecutively regular and low sodium diets ( 193 ± 62 versus 93 ± 52 mmol Na(+)/d ) . RESULTS CTGF was elevated in plasma ( 464 [ 387 to 556 ] pmol/L ) and urine ( 205 [ 135 to 311 ] pmol/24 h ) of patients compared with healthy controls ( n = 21 ; 96 [ 86 to 108 ] pmol/L and 73 [ 55 to 98 ] pmol/24 h ) . Urinary CTGF was lowered by antiproteinuric intervention , in proportion to the reduction of proteinuria , with normalization during triple therapy ( CTGF 99 [ 67 to 146 ] in CKD versus 73 [ 55 to 98 ] pmol/24 h in controls ) . In contrast , plasma CTGF was not affected . CONCLUSIONS Urinary and plasma CTGF are elevated in nondiabetic CKD . Only urinary CTGF is normalized by antiproteinuric intervention , consistent with amelioration of tubular dysfunction . The lack of effect on plasma CTGF suggests that its driving force might be independent of proteinuria and that short-term antiproteinuric interventions are not sufficient to correct the systemic profibrotic state in CKD BACKGROUND AND OBJECTIVES The antiproteinuric effect of a renin-angiotensin-aldosterone system blockade can be magnified by dietary salt restriction . This study sought to determine the effect of intensive low-salt diet education on BP and urine albumin excretion in nondiabetic patients with hypertension and albuminuria . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS This study was conducted between March of 2012 and March of 2013 as an open-label , r and omized , controlled trial . After a run-in period of 8 weeks , all patients received the angiotensin II receptor blocker olmesartan ( 40 mg daily ) . Patients were then divided into two groups . One group was treated for another 8 weeks with angiotensin II receptor blocker plus conventional low-salt diet education , and the other group was treated for 8 weeks with angiotensin II receptor blocker plus intensive low-salt diet education . The final analyses was performed with 245 completed patients . RESULTS The amount of daily albuminuria was significantly decreased from 0 ( 566.0 [ 25.0 - 5398.6 ] mg/d ) to 8 weeks ( 282.5 [ 16.1 - 4898.5 ] mg/d ; P<0.001 ) . From 8 to 16 weeks , the 24-hour urinary sodium excretion was decreased by 36.0±5.9 mmol/d in the intensive education group and 8.8±4.9 mmol/d in the conventional education group ( interaction P<0.001 ) . Patients who completed intensive low-salt diet education exhibited greater decreases in urinary albumin excretion than the control group ( change in albuminuria from 8 to 16 weeks , -154.0 versus 0.4 mg/d ; P=0.01 ) . Urinary albumin excretion tended to decrease as the 24-hour urinary sodium excretion amount decreased ( R=0.32 ; 95 % confidence interval , 0.20 to 0.43 ; P<0.001 ) . CONCLUSIONS The 24-hour urinary albumin excretion was decreased more in patients in the intensive low-salt diet education group than patients in the conventional education group . Weekly intensive education on a low-salt diet would be a suitable method for clinical practice Summary Information is limited regarding the efficacy of antihypertensive drugs in patients with hypertension associated with renal insufficiency . To address this question , a group of 14 out patients with essential hypertension and mild renal insufficiency received slow release verapamil 240 mg/day for 14 days after a 4-week washout period . Patients were r and omly assigned to a low ( 4 g/ day ) or high ( 11 g/day ) salt diet , and crossed over to the alternative diet after 7 days .  24-Hour blood pressure monitoring was performed at the end of the washout period and after 7 and 14 days during verapamil treatment . Verapamil induced a significant fall in mean 24-hour blood pressure that was similar for patients on both diets ( p < 0.01 ) . As expected , natriuresis increased significantly during high sodium intake ( p < 0.01 ) , and bodyweight fell significantly when sodium intake was reduced ( p < 0.05 ) . Meanwhile , serum creatinine and creatinine clearance remained stable . These results indicate that the antihypertensive effect of verapamil is independent of sodium intake even in the presence of mild renal insufficiency Objective To compare the effects on proteinuria and blood pressure of addition of dietary sodium restriction or angiotensin receptor blockade at maximum dose , or their combination , in patients with non-diabetic nephropathy receiving background treatment with angiotensin converting enzyme ( ACE ) inhibition at maximum dose . Design Multicentre crossover r and omised controlled trial . Setting Outpatient clinics in the Netherl and s. Participants 52 patients with non-diabetic nephropathy . Interventions All patients were treated during four 6 week periods , in r and om order , with angiotensin receptor blockade ( valsartan 320 mg/day ) or placebo , each combined with , consecutively , a low sodium diet ( target 50 mmol Na+/day ) and a regular sodium diet ( target 200 mmol Na+/day ) , with a background of ACE inhibition ( lisinopril 40 mg/day ) during the entire study . The drug interventions were double blind ; the dietary interventions were open label . Main outcome measures The primary outcome measure was proteinuria ; the secondary outcome measure was blood pressure . Results Mean urinary sodium excretion , a measure of dietary sodium intake , was 106 ( SE 5 ) mmol Na+/day during a low sodium diet and 184 ( 6 ) mmol Na+/day during a regular sodium diet ( P<0.001 ) . Geometric mean residual proteinuria was 1.68 ( 95 % confidence interval 1.31 to 2.14 ) g/day during ACE inhibition plus a regular sodium diet . Addition of angiotensin receptor blockade to ACE inhibition reduced proteinuria to 1.44 ( 
    Output:
    
We found a critical evidence gap in long-term effects of salt restriction in people with CKD that meant we were unable to determine the direct effects of sodium restriction on primary endpoints such as mortality and progression to end-stage kidney disease ( ESKD ) .
We found that salt reduction in people with CKD reduced blood pressure considerably and consistently reduced proteinuria .
If such reductions could be maintained long-term , this effect may translate to clinical ly significant reductions in ESKD incidence and cardiovascular events .