Blood Pressure In Chronic Kidney Disease Research Articles

Hipertensión arterial en la enfermedad renal crónica

Chronic kidney disease (CKD) is increasingly prevalent worldwide, and it is associated with cardiovascular disease (CVD). Hypertension (HT) is therefore a cause as well as a consequence of CKD, and it affects the great majority of patients with CKD. It is highly important to control HT in individuals with CKD, as this slows down the progression of the disease and also reduces the risk of CVD. Existing treatment guidelines do not agree on the optimum target figures for blood pressure (BP) in this population. It is therefore crucially important to understand the mechanisms which contribute to the appearance of this pathology, to indicate the most suitable treatment to control it appropriately. Although non-pharmaceutical interventions are useful for reducing BP in CKD, they are rarely enough to achieve sufficient control of BP. Patients with CKD and HT often require a combination of antihypertensive drugs to achieve their target BP. Some pharmacological therapies have an action which protects the kidneys and/or the heart independently of their effect on BP, and this should be taken into account when prescribing a therapy. It is important to underline that a personalized and evidence-based management plan is still the key to achieve BP targets, reducing the risk of CVD and slowing down the progress of CKD.

KDOQI US Commentary on the 2021 KDIGO Clinical Practice Guideline for the Management of Blood Pressure in CKD

The Kidney Disease Outcomes Quality Initiative (KDOQI) convened a work group to review the 2021 KDIGO (Kidney Disease: Improving Global Outcomes) guideline for the management of blood pressure in chronic kidney disease (CKD). This commentary is the product of that work group and presents the recommendations and practice points from the KDIGO guideline in the context of US clinical practice. A critical addition to the KDIGO guideline is the recommendation for accurate assessment of blood pressure using standardized office blood pressure measurement. In the general adult population with CKD, KDIGO recommends a goal systolic blood pressureless than 120 mm Hg on the basis of results from the Systolic Blood Pressure Intervention Trial (SPRINT) and secondary analyses of the Action to Control Cardiovascular Risk in Diabetes-Blood Pressure (ACCORD-BP) trial. The KDOQI work group agreed with most of the recommendations while highlighting the weak evidence base especially for patients with diabetes and advanced CKD.

Novi pristup sagledavanju hipertenzije u hroničnoj bubrežnoj bolesti kroz prizmu poslednjeg KDIGO vodiča 2021

Hypertension associated with chronic kidney disease (CKD) is related with a high risk of cardiovascular disease (CVD), which is the most common cause of morbidity and mortality in patients with CKD. Control of hypertension is important primarily because it reduces the risk of CVD and all-cause mortality in patients with CKD. The new KDIGO (Kidney Disease: Improving Global Outcomes) guideline for the management of blood pressure in CKD were published in 2021 and represented an updated version of the original guideline from 2012. This guideline covers all topics contained in the original instructions, such as optimal blood pressure targets, lifestyle interventions, choice of antihypertensive drugs, and specific management in kidney transplant recipients and children. Some aspects of general and cardiovascular health, such as lipid control and smoking, are excluded. In addition, this guideline introduces a chapter dedicated to proper blood pressure measurement as all large randomized trials from which the evidence and recommendations of this guide emerged used standardized preparation and measurement protocols adhered to by patients and clinicians. The key recommendation of the KDIGO guideline refers to target systolic blood pressure under120 mmHg in most adults with CKD, provided that the standardized office blood pressure measurement is used. Despite recommendations for lowering target blood pressure, general lack of evidence, especially in patients with diabetes and advanced CKD, still suggests the need to individualize targets according to the characteristics, tolerances, and preferences of each patient. Larger randomized controlled trials are needed to examine the effects of blood pressure targets on major adverse events and mortality in patients with CKD, especially in subpopulations that were not adequately represented in previous studies.

The roles of sodium and volume overload on hypertension in chronic kidney disease.

Chronic kidney disease (CKD) is associated with increased risk of cardiovascular (CV) events, and the disease burden is rising rapidly. An important contributor to CV events and CKD progression is high blood pressure (BP). The main mechanisms of hypertension in early and advanced CKD are renin-angiotensin system activation and volume overload, respectively. Sodium retention is well known as a factor for high BP in CKD. However, a BP increase in response to total body sodium or volume overload can be limited by neurohormonal modulation. Recent clinical trial data favoring intensive BP lowering in CKD imply that the balance between volume and neurohormonal control could be revisited with respect to the safety and efficacy of strict volume control when using antihypertensive medications. In hemodialysis patients, the role of more liberal use of antihypertensive medications with the concept of functional dry weight for intensive BP control must be studied.

Commentary on the KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in CKD.

Purpose of ReviewTo summarize and explain the new guideline on blood pressure (BP) management in chronic kidney disease (CKD) published by Kidney Disease: Improving Global Outcomes (KDIGO), an independent global nonprofit organization which develops and implements evidence-based clinical practice guidelines in kidney disease. KDIGO issued its first clinical practice guideline for the Management of Blood Pressure (BP) in Chronic Kidney Disease (CKD) for patients not receiving dialysis in 2012 and now updated the guideline in 2021.Recent FindingsRecommendations in this update were developed based on systematic literature reviews and appraisal of the quality of the evidence and strength of recommendation following the “Grading of Recommendations Assessment, Development and Evaluation” (GRADE) approach. The updated guideline includes five chapters covering BP measurement techniques, lifestyle interventions for lowering BP, and management of BP in three target populations, namely adults (with and without diabetes), kidney transplant recipients, and children. A dedicated chapter on BP measurement emphasizing standardized preparation and measurement protocols for office BP measurement is a new addition, following protocols used in large randomized trials of BP targets with pivotal clinical outcomes.SummaryBased on the available evidence, and in particular in the CKD subgroup of the SPRINT trial, the 2021 guideline suggests a systolic BP target of <120 mm Hg, based on standardized measurements, for most individuals with CKD not receiving dialysis, with the exception of kidney transplant recipients and children. This recommendation is strictly contingent on the measurement of BP using standardized office readings and not routine office readings.

TaleNeprilysin and Neprilysin inhibition in chronic kidney disease.

Chronic kidney disease (CKD) is associated with increased risk of progression to end-stage kidney disease and cardiovascular events. There is limited evidence that available treatments have beneficial effects on cardiorenal outcomes in all people with nondiabetic CKD. Neprilysin inhibition (NEPi) is a new therapeutic strategy with potential to improve outcomes for patients with CKD. NEPi enhances the activity of the natriuretic peptide system producing natriuresis, diuresis and inhibition of the renin-angiotensin system and sympathetic nervous system. Sacubitril/valsartan is the first Angiotensin receptor-neprilysin inhibitor (ARNI) to be produced and has been shown to substantially improve cardiovascular outcomes in heart failure and delay progression of kidney disease in this population. Although ARNIs have not shown similar effects on kidney function in the short-to-medium term in people with CKD, they are associated with substantial reductions in cardiac biomarkers and blood pressure in CKD. These data suggest that NEPi with an ARNI could benefit patients with CKD by reducing the risk of cardiovascular disease and have the possibility of retarding the progression of CKD (hence delaying the need for renal replacement therapy).

Urinary Sodium-to-Potassium Ratio and Blood Pressure in CKD

IntroductionIn the general population, urinary sodium-to-potassium (uNa/K) ratio associates more strongly with high blood pressure (BP) than either urinary sodium or potassium alone. Whether this is also the case among patients with chronic kidney disease (CKD) is unknown.MethodsWe studied the associations of spot urine sodium-to-creatinine (uNa/Cr), potassium-to-creatinine (uK/Cr), and uNa/K ratios with a single office BP reading in 1660 patients with moderate to severe CKD at inclusion in the CKD-REIN cohort.ResultsPatients' median age was 68 (interquartile range [IQR], 59–76) years; most were men (65%), had moderate CKD (57%), and albuminuria (72%). Mean systolic and diastolic BP was 142/78 mm Hg. Spot uNa/Cr and uNa/K ratios were positively associated with systolic, mean arterial, and pulse pressures. The mean adjusted difference in systolic BP between the highest and the lowest quartile (Q4 vs. Q1) was 4.24 (95% confidence interval [CI], 1.53–6.96) mm Hg for uNa/Cr and 4.79 (95% CI, 2.18–7.39) mm Hg for uNa/K. Quartiles of spot uK/Cr were not associated with any BP index. The higher the quartile of uNa/K, the higher the prevalence ratio of uncontrolled (Q4 vs. Q1, 1.43; 95% CI, 1.19–1.72) or apparently treatment-resistant hypertension (Q4 vs. Q1, 1.35; 95% CI, 1.14–1.60). Findings were consistent in a subset of 803 individuals with 2 BP readings.ConclusionIn patients with CKD, higher urinary sodium excretion is associated with higher BP, but unlike in general population, lower potassium excretion is not. Urinary Na/K does not add significant value in assessing high BP risk, except perhaps for hypertension control assessment.

Management of Hypertension in Chronic Kidney Disease.

Chronic kidney disease (CKD) is an increasingly prevalent condition globally and is strongly associated with incident cardiovascular disease (CVD). Hypertension is both a cause and effect of CKD and affects the vast majority of CKD patients. Control of hypertension is important in those with CKD as it leads to slowing of disease progression as well as reduced CVD risk. Existing guidelines do not offer a consensus on optimal blood pressure (BP) targets. Therefore, an understanding of the evidence used to create these guidelines is vital when considering how best to manage individual patients. Non-pharmacological interventions are useful in reducing BP in CKD but are rarely sufficient to control BP adequately. Patients with CKD and hypertension will often require a combination of antihypertensive medications to achieve target BP. Certain pharmacological therapies provide additional BP-independent renoprotective and/or cardioprotective action and this must be considered when instituting therapy. Managing hypertension in the context of haemodialysis and following kidney transplantation presents further challenges. Novel therapies may enhance treatment in the near future. Importantly, a personalised and evidence-based management plan remains key to achieving BP targets, reducing CVD risk and slowing progression of CKD.

The effect of exercise on blood pressure in chronic kidney disease: A systematic review and meta-analysis of randomized controlled trials

Background and objectivesManagement of hypertension in chronic kidney disease (CKD) remains a major challenge. We conducted a systematic review to assess whether exercise is an effective strategy for lowering blood pressure in this population.Design, setting, participants, and measurementsWe searched MEDLINE, EMBASE, the Cochrane Library, CINAHL and Web of Science for randomized controlled trials (RCTs) that examined the effect of exercise on blood pressure in adults with non-dialysis CKD, stages 3–5. Outcomes were non-ambulatory systolic blood pressure (primary), other blood pressure parameters, 24-hour ambulatory blood pressure, pulse-wave velocity, and flow-mediated dilatation. Results were summarized using random effects models.ResultsTwelve studies with 505 participants were included. Ten trials (335 participants) reporting non-ambulatory systolic blood pressure were meta-analysed. All included studies were a high risk of bias. Using the last available time point, exercise was not associated with an effect on systolic blood pressure (mean difference, MD -4.33 mmHg, 95% confidence interval, CI -9.04, 0.38). The MD after 12–16 and 24–26 weeks of exercise was significant (-4.93 mmHg, 95% CI -8.83, -1.03 and -10.94 mmHg, 95% CI -15.83, -6.05, respectively) but not at 48–52 weeks (1.07 mmHg, 95% CI -6.62, 8.77). Overall, exercise did not have an effect on 24-hour ambulatory blood pressure (-5.40 mmHg, 95% CI -12.67, 1.87) or after 48–52 weeks (-7.50 mmHg 95% CI -20.21, 5.21) while an effect was seen at 24 weeks (-18.00 mmHg, 95% CI -29.92, -6.08). Exercise did not have a significant effect on measures of arterial stiffness or endothelial function.ConclusionLimited evidence from shorter term studies suggests that exercise is a potential strategy to lower blood pressure in CKD. However, to recommend exercise for blood pressure control in this population, high quality, longer term studies specifically designed to evaluate hypertension are needed.

The effects of oral sodium bicarbonate on extracellular water in patients with chronic kidney disease

Background: Metabolic acidosis in chronic kidney disease (CKD) is often treated with oral sodium bicarbonate. There is limited evidence around the effects of sodium bicarbonate on extracellular fluid and blood pressure in CKD. Methods: In a double blind randomised comparison patients with stage 3-5 CKD were randomised to either oral sodium bicarbonate 1.5 g three times a day (n=18) or placebo (n=21) for 4 weeks. Assessments performed at 0 and 4 weeks included: body weight, office blood pressure and assessment for peripheral/pulmonary oedema; serum creatinine, electrolytes and venous bicarbonate; 24-hour urine for sodium excretion; extracellular fluid volume and total body water determined by sodium bromide and deuterium oxide dilution respectively; extracellular fluid volume and total body water by bioimpedance. Differences between the active and placebo groups at week 4 were analysed by ANCOVA. Results: At week 4, serum bicarbonate was higher (25.6±2.4 vs 23.3±3.1 mmol/l) and blood urea lower (14.2±5.6 vs 17.0±5.8 mmol/l) in the active treatment group. Urine sodium concentration was also higher (82.7±25.3 vs 59.0±21.9 mmol/l). Extracellular fluid volume (20.0±4.3 vs 18.0±2.9) and total body water (42.3±9.6 vs 39.0±6.8) measured by bioimpedance and total body water by deuterium dilution (41.7±8.3 vs 39.4±6.2) were significantly greater in the treatment arm at week 4. Differences in systolic and diastolic blood pressure did not reach statistical significance. Conclusions: Oral sodium bicarbonate has a biological effect and increases body water content, without evidence of a clinical consequence. This may reflect the fact that some of the ingested sodium is excreted in the urine.

Aortic Calcification Affects Noninvasive Estimates of Central Blood Pressure in Patients with Severe Chronic Kidney Disease

Background: Central blood pressure (BP) assessed noninvasively considerably underestimates true invasively measured aortic BP in chronic kidney disease (CKD) patients. The difference between the estimated and the true aortic BP increases with decreasing estimated glomerular filtration rates (eGFR). The present study investigated whether aortic calcification affects noninvasive estimates of central BP. Methods: Twenty-four patients with CKD stage 4–5 undergoing coronary angiography and an aortic computed tomography scan were included (63% males, age [mean ± SD ] 53 ± 11 years, and eGFR 9 ± 5 mL/min/1.73 m²). Invasive aortic BP was measured through the angiography catheter, while non-invasive central BP was obtained using radial artery tonometry with a SphygmoCor® device. The Agatston calcium score (CS) in the aorta was quantified on CT scans using the CS on CT scans. Results: The invasive aortic systolic BP (SBP) was 152 ± 23 mm Hg, while the estimated central SBP was 133 ± 20 mm Hg. Ten patients had a CS of 0 in the aorta, while 14 patients had a CS >0 in the aorta. The estimated central SBP was lower than the invasive aortic SBP in patients with aortic calcification compared to patients without (mean difference 8 mm Hg, 95% CI 0.3–16; p = 0.04). The brachial SBP was lower than the aortic SBP in patients with aortic calcification compared to patients without (mean difference 10 mm Hg, 95% CI 2–19; p = 0.02). Conclusion: In patients with advanced CKD the presence of aortic calcification is associated with a higher difference between invasively measured central aortic BP and non-invasive estimates of central BP as compared to patients without calcifications.

Hypertension in patients on dialysis: diagnosis, mechanisms, and management.

Hypertension (blood pressure > 140/90 mm Hg) is very common in patients undergoing regular dialysis, with a prevalence of 70-80%, and only the minority has adequate blood pressure (BP) control. In contrast to the unclear association of predialytic BP recordings with cardiovascular mortality, prospective studies showed that interdialytic BP, recorded as home BP or by ambulatory blood pressure monitoring in hemodialysis patients, associates more closely with mortality and cardiovascular events. Although BP is measured frequently in the dialysis treatment environment, aspects related to the measurement technique traditionally employed may be unsatisfactory. Several other tools are now available and being used in clinical trials and in clinical practice to evaluate and treat elevated BP in chronic kidney disease (CKD) patients. While we wait for the ongoing review of the CKD Blood Pressure KIDGO guidelines, there is no guideline for the dialysis population addressing this important issue. Thus, the objective of this review is to provide a critical analysis of the information available on the epidemiology, pathogenic mechanisms, and the main pillars involved in the management of blood pressure in stage 5-D CKD, based on current knowledge.

Abstract 053: Dietary Sodium Restriction versus Diuretics for Salt-Sensitive Hypertension in Chronic Kidney Disease

Fluid overload and salt-sensitive hypertension are hallmarks of advanced chronic kidney disease (CKD) and associated with worse outcomes. Dietary sodium (Na + ) restriction is an accepted intervention, but long-term adherence remains a challenge. Distal diuretics could provide an alternative approach, but they are considered less effective in advanced CKD. Here, we compared both approaches head-to-head. Methods: Twenty-six patients with CKD stage 3 or 4 and hypertension were included in this single-center, open-label, randomized cross-over trial (baseline eGFR 39 ± 13 ml/min/1.73 m 2 ). Renin-angiotensin inhibitors and diuretics were discontinued 2 weeks prior to interventions and during study period. Subsequently, we compared dietary Na + restriction (60 mmol/day) versus amiloride/hydrochlorothiazide (5/50 mg once daily). Both interventions lasted for two weeks and were separated by a 2-week wash-out period. The primary endpoint was 24h systolic blood pressure (SBP). Results: Urinary Na + excretion was successfully lowered with dietary Na + restriction (160 ± 66 to 64 ± 37 mmol/day, p &lt; 0.01), and remained similar with diuretics (154 ± 47 to 153 ± 63 mmol/day, p = 0.95). Dietary Na + restriction lowered 24-hour SBP (134 ± 12 to 129 ± 14 mmHg, p &lt; 0.05), while diuretics had a greater effect (138 ± 12 to 124 ± 13 mmHg, p &lt; 0.01 for within and between interventions). Both maneuvers significantly lowered indices of fluid overload, including body weight (-1.6 ± 1.1 kg with dietary Na + restriction and -1.9 ± 1.5 kg with diuretics), NT-pro-BNP (median -10 and -7 pmol/L), and overhydration as assessed by bioimpedance (-0.6 ± 0.6 and -1.3 ± 0.7 L). Both interventions also lowered eGFR (-2 ± 4 and -5 ± 5 ml/min/1.73 m 2 , p&lt;0.05 for both) and showed a trend towards albuminuria reduction (median -5 mg/day and -20 mg/day). The reduction in overhydration and eGFR was greater with diuretics than with dietary Na + restriction ( p &lt; 0.05). Conclusions: Distal diuretics and dietary Na + restriction effectively lower blood pressure in CKD 3 and 4 in the absence of renin-angiotensin inhibitors. Both interventions also lower indices of fluid overload. Diuretics produce greater effects than dietary Na + restriction. These beneficial effects may outweigh the (hemodynamic) reduction in eGFR.

A comprehensive characterization of myocardial and vascular phenotype in pediatric chronic kidney disease using cardiovascular magnetic resonance imaging

BackgroundChildren with chronic kidney disease (CKD) have increased cardiovascular mortality. Identifying high-risk children who may benefit from further therapeutic intervention is difficult as cardiovascular abnormalities are subtle. Although transthoracic echocardiography may be used to detect sub-clinical abnormalities, it has well-known problems with reproducibility that limit its ability to accurately detect these changes. Cardiovascular magnetic resonance (CMR) is the reference standard method for assessing blood flow, cardiac structure and function. Furthermore, recent innovations enable the assessment of radial and longitudinal myocardial velocity, such that detection of sub-clinical changes is now possible. Thus, CMR may be ideal for cardiovascular assessment in pediatric CKD. This study aims to comprehensively assess cardiovascular function in pediatric CKD using CMR and determine its relationship with CKD severity.MethodsA total of 120 children (40 mild, 40 moderate, 20 severe pre-dialysis CKD subjects and 20 healthy controls) underwent CMR with non-invasive blood pressure (BP) measurements. Cardiovascular parameters measured included systemic vascular resistance (SVR), total arterial compliance (TAC), left ventricular (LV) structure, ejection fraction (EF), cardiac timings, radial and longitudinal systolic and diastolic myocardial velocities. Between group comparisons and regression modelling were used to identify abnormalities in CKD and determine the effects of renal severity on myocardial function.ResultsThe elevation in mean BP in CKD was accompanied by significantly increased afterload (SVR), without evidence of arterial stiffness (TAC) or increased fluid overload. Left ventricular volumes and global function were not abnormal in CKD. However, there was evidence of LV remodelling, prolongation of isovolumic relaxation time and reduced systolic and diastolic myocardial velocities.ConclusionAbnormal cardiovascular function is evident in pre-dialysis pediatric CKD. Novel CMR biomarkers may be useful for the detection of subtle abnormalities in this population. Further studies are needed to determine to prognostic value of these biomarkers.

Thiazide Diuretics in Chronic Kidney Disease.

Widely prevalent in the general population, chronic kidney disease (CKD) is frequently complicated with hypertension. Control of hypertension in this high-risk population is a major modifiable cardiovascular and renal risk factor but often requires multiple medications. Although thiazides are an attractive agent, guidelines have previously recommended against thiazide use in stage 4 CKD. We review the updated guidelines on thiazide use in advanced CKD, the antihypertensive mechanism of thiazides, and the clinical studies of thiazides in CKD. Older uncontrolled studies have shown that metolazone reduces blood pressure in CKD, but more recently small randomized controlled trials of hydrochlorothiazide in CKD have shown significant improvement in mean arterial pressure of 15mmHg. Two recent uncontrolled studies of chlorthalidone including one that used ambulatory blood pressure monitoring found significant improvements in blood pressure. These findings all suggest that thiazides may be efficacious even in advanced CKD; however, electrolyte abnormalities were common in the studies reviewed so close monitoring is necessary during use. Adequately powered randomized trials are now needed before the routine use of thiazide diuretics in advanced CKD can be recommended.

Canadian Society of Nephrology Commentary on the 2012 KDIGO Clinical Practice Guideline for the Management of Blood Pressure in CKD

The KDIGO (Kidney Disease: Improving Global Outcomes) 2012 clinical practice guideline for the management of blood pressure (BP) in chronic kidney disease (CKD) provides the structural and evidence base for the Canadian Society of Nephrology (CSN) commentary on this guideline's relevancy and application to the Canadian health care system. While in general agreement, we provide commentary on 13 of the 21 KDIGO guideline statements. Specifically, we agreed that nonpharmacological interventions should play a significant role in the management of hypertension in patients with CKD. We also agreed that the approach to the management of hypertension in elderly patients with CKD should be individualized and take into account comorbid conditions to avoid adverse outcomes from excessive BP lowering. In contrast to KDIGO, the CSN Work Group believes there is insufficient evidence to target a lower BP for nondiabetic CKD patients based on the presence and severity of albuminuria. The CSN Work Group concurs with the Canadian Hypertension Education Program (CHEP) recommendation of a target BP for all non-dialysis-dependent CKD patients without diabetes of ≤140 mm Hg systolic and ≤90 mm Hg diastolic. Similarly, it is our position that in diabetic patients with CKD and normal urinary albumin excretion, raising the threshold for treatment from <130 mm Hg systolic BP to <140 mm Hg systolic BP could increase stroke risk and the risk of worsening kidney disease. The CSN Work Group concurs with the CHEP and the Canadian Diabetic Association recommendation for diabetic patients with CKD with or without albuminuria to continue to be treated to a BP target similar to that of the overall diabetes population, aiming for BP levels < 130/80 mm Hg. Consistent with this, the CSN Work Group endorses a BP target of <130/80 mm Hg for diabetic patients with a kidney transplant. Finally, in the absence of evidence for a lower BP target, the CSN Work Group concurs with the CHEP recommendation to target BP<140/90 mm Hg for nondiabetic patients with a kidney transplant.

KDOQI US Commentary on the 2012 KDIGO Clinical Practice Guideline for Management of Blood Pressure in CKD

In response to the 2012 KDIGO (Kidney Disease: Improving Global Outcomes) guideline for blood pressure management in patients with chronic kidney disease not on dialysis, the National Kidney Foundation organized a group of US experts in hypertension and transplant nephrology to review the recommendations and comment on their relevancy in the context of current US clinical practice and concerns. The overriding message was the dearth of clinical trial evidence to provide strong evidence-based recommendations. For patients with CKD with normal to mildly increased albuminuria, goal blood pressure has been relaxed to ≤140/90 mm Hg for both diabetic and nondiabetic patients. In contrast, KDIGO continues to recommend goal blood pressure ≤130/80 mm Hg for patients with chronic kidney disease with moderately or severely increased albuminuria and for all renal transplant recipients regardless of the presence of proteinuria, without supporting data. The expert panel thought the KDIGO recommendations were generally reasonable but lacking in sufficient evidence support and that additional studies are greatly needed.

The QICKD study protocol: a cluster randomised trial to compare quality improvement interventions to lower systolic BP in chronic kidney disease (CKD) in primary care

BackgroundChronic kidney disease (CKD) is a relatively newly recognised but common long-term condition affecting 5 to 10% of the population. Effective management of CKD, with emphasis on strict blood pressure (BP) control, reduces cardiovascular risk and slows the progression of CKD. There is currently an unprecedented rise in referral to specialist renal services, which are often located in tertiary centres, inconvenient for patients, and wasteful of resources. National and international CKD guidelines include quality targets for primary care. However, there have been no rigorous evaluations of strategies to implement these guidelines. This study aims to test whether quality improvement interventions improve primary care management of elevated BP in CKD, reduce cardiovascular risk, and slow renal disease progressionDesignCluster randomised controlled trial (CRT)MethodsThis three-armed CRT compares two well-established quality improvement interventions with usual practice. The two interventions comprise: provision of clinical practice guidelines with prompts and audit-based education.The study population will be all individuals with CKD from general practices in eight localities across England. Randomisation will take place at the level of the general practices. The intended sample (three arms of 25 practices) powers the study to detect a 3 mmHg difference in systolic BP between the different quality improvement interventions. An additional 10 practices per arm will receive a questionnaire to measure any change in confidence in managing CKD. Follow up will take place over two years. Outcomes will be measured using anonymised routinely collected data extracted from practice computer systems. Our primary outcome measure will be reduction of systolic BP in people with CKD and hypertension at two years. Secondary outcomes will include biomedical outcomes and markers of quality, including practitioner confidence in managing CKD.A small group of practices (n = 4) will take part in an in-depth process evaluation. We will use time series data to examine the natural history of CKD in the community. Finally, we will conduct an economic evaluation based on a comparison of the cost effectiveness of each intervention.Clinical Trials RegistrationISRCTN56023731. ClinicalTrials.gov identifier.

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Changing the Timing of Antihypertensive Therapy to Reduce Nocturnal Blood Pressure in CKD: An 8-Week Uncontrolled Trial

Nondipping status is associated with greater cardiovascular morbidity and mortality and faster progression of chronic kidney disease (CKD). We examined whether shifting 1 antihypertensive drug from morning to evening restores the circadian rhythm of blood pressure in nondipper patients with CKD. 8-week clinical trial without a control group. We selected from our outpatient renal clinic 32 patients with CKD with estimated glomerular filtration rate less than 90 mL/min/1.73 m(2) and night-day ratio of mean ambulatory blood pressure (ABP) greater than 0.9, but with normal daytime ABP (<135/85 mm Hg) to avoid the required therapy intensification. Shifting 1 antihypertensive drug from morning to evening. Percentage of patients changing the night-day ratio of mean ABP from greater than 0.9 to 0.9 or less 8 weeks after the shift. Office blood pressure/ABP and proteinuria at baseline and after the shift. There were 55% men with a mean age of 67.4 +/- 11.3 years and estimated glomerular filtration rate of 46 +/- 12 mL/min/1.73 m(2). They were treated with 2.4 +/- 1.4 antihypertensive drugs. After the drug shift, the night-day ratio of mean ABP decreased in 93.7% of patients, with normal circadian rhythm restored in 87.5%. The nocturnal systolic and diastolic ABP decrease was not associated with an increase in diurnal ABP and was independent from number and class of shifted drug. Office blood pressure in the morning also decreased (from 136 +/- 16/77 +/- 10 to 131 +/- 13/75 +/- 8 mm Hg; P = 0.02). Urinary protein excretion decreased from 235 +/- 259 to 167 +/- 206 mg/d (P < 0.001). Absence of a control group and patients with severe proteinuria or uncontrolled daytime ABP. In nondipper patients with CKD, changing the timing of antihypertensive therapy decreases nocturnal blood pressure and proteinuria.