Hypertension Journal

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Management of Hypertension in Patients with Chronic Kidney Diseaseand End-stage Renal Disease
  JOHTN
REVIEW ARTICLE
Management of Hypertension in Patients with Chronic Kidney Disease
and End-stage Renal Disease
Manas R. Patel, Amit Gupta
Department of Nephrology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
Address for correspondence: Prof. Amit Gupta, Professor, Department of Nephrology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of MedicalSciences, Lucknow, Uttar Pradesh - 226014, India.
E-mail: dramitguptanephropgi@gmail.com
Received: 08-11-2017; Accepted: 17-12-2017
 
ABSTRACT
Elevated blood pressures (BP) are common in patients with impaired kidney function. Hypertension (HTN) not only can be aconsequence of chronic kidney disease (CKD) but it is also the most important risk factor for progressive decline of renal function inCKD leading to end-stage renal disease (ESRD). Hence, identification and management of HTN is essential for reducing morbidityand mortality resulting from both, i.e., cardiovascular events and renal failure. A combination of healthy lifestyle measures, dietarysodium restriction, and appropriate fluid management along with individualized antihypertensive regimen can achieve BP targets.Patients on renal replacement therapy also require optimized dialysis prescriptions in addition to the above measures. Finally, homemeasurement of BP and adherence to treatment is central for having a successful outcome. In this review, we discuss the benefits ofBP control, measurement techniques, controversies regarding target pressures, rationale of current guidelines, and specific issues inmanagement in patients with CKD and ESRD.
Keywords: Hyperfilteration, renin-angiotensin, endothelial dysfunction
How to cite this article: Patel MR, Gupta A. Management ofhypertension in patients with chronic kidney disease and endstagerenal disease. Hypertens 2018;4(1): 55-63.
Source of support: Nil
Conflict of interest: None
 
 

Introduction

There is plenty of evidence in scientific literature that clearlydemonstrates that elevated blood pressure (BP) levels reduce lifeexpectancy. Hypertension (HTN) is a major contributor to oneor more target organ damage, including of the heart, brain, eyes,and kidneys. Historically, major focus of HTN management wasto prevent morbidity and mortality resulting from cardiovascularand cerebrovascular diseases. In the recent past multiple factors,i.e., role of the kidney in pathophysiology of HTN, increasedprevalence of HTN in kidney diseases, and rapid deteriorationof renal function in patients with uncontrolled HTN has led toincreased awareness of benefits of BP management.

About 10% of world population have some form of renaldysfunction and HTN is the most common comorbidity affecting65-95% of patients with chronic kidney disease (CKD).[1]Prevalence and severity of HTN and hence the incidence of endorgandamage increases with declining renal function.[2] ElevatedBP can occur as a consequence of CKD but is also a risk factor for CKD progression. Interaction between HTN and CKD iscomplex and pathophysiologically it is difficult to determinewhich process precedes the other. Age, race, obesity, diabetesmellitus, and cardiovascular disease are common risk factors forboth HTN and CKD.[3] Coexistence of both is known to greatlyincrease the risk of cardiovascular and cerebrovascular events.Therefore, control of HTN is the first priority in the managementof CKD both to slow CKD progression and prevent other targetorgan(s) damage.

 
HTN accelerates kidney injury as impaired renalautoregulation allows transmission of high systemic pressuresto the glomeruli, leading to hyperfiltration and acceleratedglomerulosclerosis.[4] On the other hand, renal injury cancause HTN, by multiple mechanisms including decreasedsodium excretion, poor volume control, enhanced activity ofthe sympathetic nervous system (SNS) and renin-angiotensinaldosterone system (RAAS), and endothelial dysfunction, etc.[5]HTN in this population is usually resistant or refractory requiringmultiple antihypertensive agents of different mechanism of actions. Detailed discussion of pathogenesis can be foundelsewhere.

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This article reviews various issues, i.e., importance of homeand ambulatory BP monitoring (ABPM), controversies andvarious recommendations regarding BP target levels, andimplications of a most recent trial in relation to patients withCKD. Finally, we conclude by discussing current practice andsuggestions in the management of high BP in patients with CKDand in patients with end-stage renal disease (ESRD) undergoingdialysis.

BP Measurement

In-Office Versus Home BP Monitoring

In-office measurements should be accurate if done in astandardized manner by a trained clinical staff even though it ismore time-consuming than single conventional BP measurementdone routinely. Out-of-office measurements may not be alwaysavailable; consequently, most treatment decisions must still bebased primarily on in-office readings. Recent reports indicatethat home BP monitoring is superior to in-office BP readings inpredicting adverse clinical outcomes in CKD patients, more soin patients undergoing dialysis.[6,7] Patients who use home BPmonitoring are more likely to have target BP levels as well ashaving a near-dry weight as compared to those who are treatedbased only on in-office measurements.[8] This may be due toimproved self-motivation and better adherence to salt water andantihypertensive regimens.[9]

Manual versus Automated BP Measurements

Evidence now supports that home and ABPM can betterpredict the risk of cardiovascular events both in generalpopulation and in patients with CKD as compared to in-officemeasurements.[10,11] However, there remains a question ofconsistency and accuracy of these measurements. Adequatepatient training and a standardized approach with the useof validated automated oscillometric device might be morereliable than manual auscultatory methods and may providereproducible measurements when done repeatedly.[12,13]

ABPM

24-h ABPM provides additional information about nocturnalmeasurements and BP variability.[14] Normal circadian BPrhythm and nocturnal BP is often abnormal in CKD and isusually characterized by either loss of the normal nocturnal fall(10-20%) in systolic BP (SBP) and diastolic BPs (DPBs) (nondippers)or even a paradoxical rise in nocturnal BP (risers).[15,16]Exact underlying mechanism is not known, but high nocturnalBP is associated with reduced diuresis in day and enhancedpressure natriuresis at night.[17] The average level of nocturnalBP has been linked to both cardiovascular disease and CKDprogression; however, evidence supporting that a reductionin BP variability leads to improved outcomes is currently lacking.[18,19] In addition, ABPM is diagnostic for white-coatHTN and masked HTN, the later appears to be remarkablyprevalent in CKD.[20]

 
Target BP in CKD

Optimal goals of BP therapy for individuals with CKD havebeen controversial. In addition to prevention of cardiovascularand cerebrovascular events as in general population, therationale for treatment of HTN in CKD is to slow on-goingrenal injury and to delay progression to ESRD.[21,22] Anotherimportant factor is the presence of proteinuria. Patientswith proteinuria have poorer outcomes.[23] These patientsmay require more aggressive BP management to preventmorbidity and mortality as compared to those withoutproteinuria.[24] The relationship between BP and cardiovascularevents in patients with CKD is complex. Large observationalstudies have identified U- or J-curve phenomena with increasein mortality in patients with CKD at SBP < 120 mmHg and/or DBP < 60 mmHg.[25,26] Guidelines that have proposedrecommendations for CKD population are based on dataobtained mainly from two randomized controlled trials, e.g.,the modification of diet in renal disease study and the AfricanAmerican Study of Kidney Disease and HTN.[27,28] Both trialswere negative, failing to show benefit from lower BP targets of125-130/75-80 mmHg compared to < 140/90 mmHg eitherin reducing cardiovascular events or slowing progression ofCKD to ESRD. Post hoc analyses of both studies, however,suggested a benefit of intensive BP treatment in the subgroupwith significant proteinuria. None of these studies includedpatients with diabetes mellitus. Subsequent meta-analysesyielded conflicting results regarding the potential effect of BPreduction on the development of ESRD.[29,30] The Action toControl Cardiovascular Risk in Diabetes trial of patients withtype 2 diabetes mellitus and normal renal function failed toshow cardiovascular or mortality benefit of a lower BP target(i.e., SBP of < 120 vs. < 140 mmHg).[31] Intensive controlgroup had greater number of serious adverse effects such ashypotension and acute kidney injury.

The 2012 KDIGO guideline target of < 140/90 mmHg inpatients with CKD without proteinuria was based on limitedclinical trial evidence.[32] For patients with proteinuria, they seta target of < 130/80 mmHg but acknowledged that this decisionwas based solely on expert opinion. While disagreement remainsmost consensus guidelines for CKD, set SBP targets mostly to< 140 mmHg and DBP between 80 and 90 mmHg [Table 1].[32-40]The 2014 NICE CKD guideline recommends drug therapy forBPs of ≥140/90 mmHg in patients without proteinuria and≥130/80 mmHg in patients with proteinuria to target of 120-139/< 90 mmHg and 120-129/< 80 mmHg in patients withoutand with proteinuria, respectively.[39]

Most recent data comes from analysis of CKD subset(n = 2646 patients with estimated glomerular filtration rate[eGFR] of 20-59 ml/min per 1.73 m2) of SBP InterventionTrial (SPRINT).[41,42] Till date, this is the largest randomized study assessing different BP targets (SBP target of 140 mmHgin the standard group and 120 mmHg in the intensive group)on the cardiovascular and renal outcomes in patients withCKD. Multiple BP readings were obtained by automatedmachine at 1-min intervals and averaged at each visit. Meanage of patients was 72 years. At the end of 1 year, SBP valuesof 136.9 ± 0.2 and 123.0 ± 0.2 mmHg were achieved instandard and intensive group, respectively. On an average oftwo in the standard group and three antihypertensive agentsin the intensive group were required. The trial was stoppedprematurely because of the significantly reduced (25% relativerisk reduction) overall and cardiovascular mortality andcomposite end points in the intensive group. This observedmortality benefit was also seen in the whole CKD cohortand was even more pronounced in older patients with CKD.Intensive group had higher risk of a 30% fall in eGFR but nota 50% fall in eGFR. The fall in eGFR occurred early in theintensive group, but annual decrement in renal function wassimilar in both the groups. Few cases of progressive CKD and/or ESRD occurred in this cohort over the 3.3-year durationof the study. More intensive antihypertensive drug therapywas associated with increases in specific adverse events likehypo and/or hyperkalemia and acute kidney injury but notserious ones such as hypotension, syncope, and injurious falls.However, patients with diabetes, proteinuria more than 1 g/day, and autosomal dominant polycystic kidney disease wereexcluded from the study.

 
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Table 1: Guidelines for BP targets and treatment recommendations in patients with CKD
Management of Hypertension in Patients with Chronic Kidney Diseaseand End-stage Renal Disease
*Proteinuria is defined as either+1 (by dipstick); >500 mg protein per 24 h; or>200 mg albumin per 24 h. ACEI: Angiotensin-converting enzymeinhibitor, ADA: American Diabetes Association, ARB: Angiotensin receptor blocker, ASH/ISH: American Society of HTN/International Society ofHTN, CHEP: Canadian HTN Education Program, CKD: Chronic kidney disease, ESC/ESH: European Society of Cardiology/European Society of HTN,ISHIB: International Society of HTN in Blacks, KDIGO: Kidney Disease Improving Global Outcomes, NICE: National Institute for Health and CareExcellence, JNC: Joint National Committee. HTN: Hypertension, DPB: Diastolic blood pressure

Taken together, data show probably a large number ofuncomplicated CKD patients need to be treated intensivelyto achieve a moderate reduction in cardiovascular events andmortality that too at increased risk of adverse effects.[43,44]This goal might be challenging in clinical practice, especiallywith advanced CKD, diabetes, proteinuria, and with othercomorbidities; who are more likely to have resistant HTN. Suchindividuals are likely to require more medications than the study participants even for liberal BP targets and hence will have higherrisk of serious side effects. Ultimately, the net gain may be offsetby adverse symptoms in many patients.

Till definitive clinical trial data are available, it is prudent toadhere to the current guidelines of target 130-140/< 90 mmHgin patients with CKD without proteinuria and < 130/80 mmHgin patients with proteinuria. There may be a tendency to maintainlower BP targets for those with more severe proteinuria providedpatients are able to tolerate lower BP levels without developingsymptoms. Conversely, targets may be loosened for those whoare likely to develop symptoms of hypoperfusion, i.e., elderly orfrail patients.

 
Treatment of HTN in CKD

Non-pharmacologic Therapy

As in general population, modifiable lifestyle factors includingdietary salt restriction, weight loss, regular exercise, cessationof smoking, and alcohol ingestion are first steps in themanagement of HTN in CKD.[45] Sodium intake contributesto drug resistance, more so in patients with a reducedGFR. Accordingly, dietary sodium restriction of < 100 mEq(2300 mg)/24 h is recommended in advanced CKD and ESRDand is particularly effective in patients with higher degree ofproteinuria.[46,47]Pharmacologic TherapyIndividualization of treatment should be based on CKDstage, age, gender, existing comorbidities such as diabetesand cardiovascular risk status [Table 2].[48] Combination oflong-acting drugs of different class that increases the renalsodium excretion and inhibit both RAAS and SNS activityprovide synergistic effect with minimal side effects.[49,50] Most antihypertensive agents can be used alone or in combinationafter consideration of their metabolism and dosing requirementsaccording to the level of renal function. Avoidance of complexdosing regimens, use of combination pills, and consideration oncost improve compliance and adherence to therapy.[51] Bedtimeadministration of at least one of the drugs is associated with abetter 24-h mean BP control and could induce the desirednocturnal dip in non-dippers.[52]

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Most guidelines for patients with CKD recommendangiotensin-converting enzyme inhibitors (ACEI) orangiotensin receptor blockers (ARB) as initial treatment oradd-on to the current regimen.[53-55] RAAS blockade reducesintraglomerular pressure and thereby reduces hyperfiltrationand proteinuria. A concurrent reduction in GFR results in anincrease in serum creatinine of up to 30%, however, greaterincreases in serum creatinine should be investigated forother causes, i.e., volume contraction, nephrotoxic agents,or bilateral renal artery stenosis.[56,57] Combination of ACEIand ARB is discouraged following increased adverse effectsof hyperkalemia and acute kidney injury in randomizedtrials as compared to use of ACEI or ARB therapy alone.[58-60] Similarly, combination of ACEI or ARB with analdosterone antagonist is also generally discouraged.[55]Frequent monitoring of serum potassium and creatininelevels must be performed if at all these combinations areused as hyperkalemia will be more severe as renal functiondeclines.[61] ACEIs and ARBs have been used in patientswith CKD to delay progression. However, discontinuingRAAS blockade in patients with low levels of renal functionmight delay initiation of dialysis.[62] Most patients with CKDshould have a diuretic as their first or second agent to managevolume and sodium retention.[63] In early CKD, a long-actingthiazide and in advanced CKD stages (i.e., eGFR of < 30 ml/min/1.73 m2), a loop diuretic may be effective in resistantHTN.[64,65] Addition of a diuretic might correct nocturnalnon-dipping and restore the circadian rhythm of BP in CKD.[66] Dihydropyridine calcium channel blockers (CCBs) aremore effective in lowering BP than non-dihydropyridineCCBs and can be used as monotherapy or in combination.[67] Long-acting CCB combined with ACEI or ARB might bemore effective in slowing the progression of nephropathy,particularly in black race.[68] CCB induced lower extremityedema due to pre-capillary arterial dilatation is refractory todiuretics but responds to addition of ACEI. Beta-blockersare often used, especially when there is a coexisting cardiacdisease.[69,70] Combined alpha and beta antagonists arethe more effective agents in patients with CKD.[71] Alphablockersdespite their possible favorable effect on BP andvascular remodeling have limited role due to common sideeffect of dizziness. Clonidine, a potent centrally actingagent but requires frequent dosing, has a significant sideeffect profile including rebound HTN which can be lifethreatening.Vasodilators such as di-hydralazine or minoxidilare less preferred drugs due to a higher incidence of adverseeffects and are usually reserved for refractory cases.

 
Device Interventions

Renal denervation by radiofrequency ablation has resulted insignificant reductions in BP in some but not all patients withCKD.[72,73] Similarly, baroreflex activation therapy using a pacinggenerator has been successful in limited uncontrolled studies inpatients with CKD.[74] Even though procedures are safe in thesepatients, their effectiveness and reproducibility remain to bedetermined.[75,76]

Treatment of HTN in ESRD

HTN in dialysis patients pose unique diagnostic, prognostic,and therapeutic challenges. Sodium and volume overload is theprominent mechanism of HTN in ESRD in addition to arterialstiffness, activation of RAAS and SNS, endothelial dysfunction,and the use of erythropoietin-stimulating agents.[77,78]

Due to the extreme variability of BP, diagnosis of HTNin ESRD is not straightforward. Recent recommendationssuggest that diagnosis of HTN in patients on dialysis shouldideally be made on the basis of either home BP measurements(≥135/85 mmHg) or 24/44-h ABPM (≥130/80 mmHg) butnot on the basis of pre- or post-dialysis BP.[79] When neitherABPM nor home BP measurements are available the diagnosiscan be made on the basis of average of interdialytic office BPmeasurements (≥140/90 mmHg) taken in a mid-week day freeof hemodialysis.[80]

Non-pharmacological measures to reduce sodium andvolume excess are fundamental for BP reduction in dialysispatients and individualized dialysis prescriptions should bestrictly followed along with pharmacological interventions.Main measures include gradual supervised achievement ofindividual patients' dry weight, avoidance of short (i.e., < 4 h)dialysis duration and minimization of inter- and intradialyticsodium gain by restriction of sodium intake to < 65 mmol(1.5 g of sodium or 4 g of sodium chloride) per day, decreasingdialysate sodium toward pre-dialysis sodium in selectedindividuals, and avoidance of sodium-containing or sodiumexchangingdrugs.[81-83]

Randomized trials clearly show that BP lowering is associatedwith reduced cardiovascular morbidity and mortality in dialysispatients.[84,85] All drug classes are useful except diuretics, whichare ineffective in patients with ESRD [Table 2]. Multiple studieshave supported efficacy of non-dialyzable long-acting betablockers,e.g., carvedilol and atenolol in lowering risk of suddendeath, improving LV systolic function, and reducing the risk ofall-cause hospitalization.[86,87] Dihydropyridine CCBs are potentagents even in volume-expanded state like in dialysis patients.In a study, amlodipine improved survival compared withplacebo and was equally effective as ACEIs or ARBs in reducingLV hypertrophy.[88,89] Of note, all CCBs are non-dialyzable.The first-line use of ACEIs and ARBs in dialysis populationis not supported by a meta-analysis of randomized trials.[90]However, ARBs, e.g., losartan, valsartan, and candesartan butnot olmesartan reduced cardiovascular events and mortality compared with treatment in dialysis patients and are preferredover ACEIs for sustained BP reduction.[91-93]

 
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Table 2: Treatment considerations in patients with CKD and ESRD
Management of Hypertension in Patients with Chronic Kidney Diseaseand End-stage Renal Disease
*Stages 1, 2, 3, 4, and 5 with GFR of≥90, 60-89, 30-59, 15-29, and< 15 ml/min/1.73 m2. CKD: Chronic kidney disease, ESRD: End-stage renal disease,GFR: glomerular filtration rate, ACEIs: Angiotensin-converting enzyme inhibitors, ARBs: Angiotensin receptor blockers, CCBS: Calcium channel blockers

Table 3: Pathophysiology and management of intradialytic HTN in patients with ESRD
Management of Hypertension in Patients with Chronic Kidney Diseaseand End-stage Renal Disease
ESRD: End-stage renal disease, HTN: Hypertension, RAAS: Renin-angiotensin aldosterone system, CCB: Calcium channel blockers

Intradialytic HTN is defined as an increase in mean arterialBP of 15 mmHg or more during hemodialysis that is resistant toultrafiltration.[94,95] It has a prevalence of 5-15% among patientson hemodialysis and is associated with adverse outcomesincluding higher mortality.[96,97] Mechanism remains elusive andhence management remains empiric and problematic as very fewguidelines addresses this issue.[98] Potential pathophysiologicmechanisms and possible interventions are shown in Table 3.[99]

Conclusions

HTN is a major risk factor for target organ damage, cardiovascularand cerebrovascular events, and hence a major contributor ofmorbidity and mortality both in patients with CKD and patientson dialysis. Elevated BP can be a consequence of a progressive decline in renal function. On the other hand, it is the mostimportant risk factor for CKD progression leading to ESRD.Standardized out-of-office BP measurements better predict therisk of cardiovascular events than the usual practice of in-officemeasurements. Automated home readings and ABPM bettercharacterize these patients, may help clinicians to optimizedisease management. Mostly, current guidelines recommendBP target of < 140/90 mmHg in most patients with CKD,with a suggestion based on expert opinion only to maintaina target of < 130/80 mmHg for patients with proteinuria.Recent randomized trial showed moderate reduction in thecardiovascular events with an intensive systolic target of< 120 mmHg in uncomplicated population, but no benefit wasobserved in relation to CKD progression to ESRD. Although themajor adverse effects such as hypotension and falls were similar,incidence of hyperkalemia and acute kidney injury increased inthe group with stricter target. Taken together, lowering of systolic target to < 120 mmHg should not be applied to patients withCKD, and it seems prudent to continue to adhere to the existingguidelines. Multiple pathophysiologic processes contribute andtheir individual contributions might differ in patients. Hence,medication regimens need to be individualized and optimized.Lifestyle measures, dietary recommendations, drug and dialysisregimen adherence, and home monitoring of BP are essentialcomponents for successful management of HTN in patients withCKD and in patients with ESRD on dialysis.

 

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