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Hypertension as a Risk Factor for Chronic Kidney Disease
  JOHTN
REVIEW ARTICLE
Hypertension as a Risk Factor for Chronic Kidney Disease
Sabarinath. S, Dharmendra Bhadauria
Department of Nephrology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
Address for correspondence: Dharmendra Bhadauria, Department of Nephrology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of MedicalSciences, Lucknow - 226 014, Uttar Pradesh, India.
Phone: +91-9919737544.
Fax- 91-522-2668017.
E-mail: drdharm1@rediffmail.com
Received: 16-11-2017; Accepted: 27-12-2017
 
ABSTRACT
Five decades back, high blood pressure (BP) was considered as an essential malady and not a treatable condition. Gradually,evidences started accumulating through major trials and now hypertension is the most common comorbidity and a powerful riskfactor for chronic kidney disease (CKD) and coronary artery disease (CAD) and an independent risk factor for CKD progression.Although hypertension is the second most common cause of end-stage renal disease, next to diabetes mellitus, only few patients ofprimary hypertension develop renal dysfunction. The risk of hypertensive nephrosclerosis is high in African americans, independentof age, sex, and prevalence of hypertension. The clear-cut benefits of lowering BP in CKD patients are renoprotection and reducingthe risk of CV complications. The less clear is the optimal BP targets and the best method for measuring and achieving the targets.Recent evidences suggest a BP goal of < 130/80 mmHg irrespective of age and proteinuria, despite controversies. Home BPmonitoring is gaining importance and it should be emphasized in all hypertensive patients.
Keywords: Nephrosclerosis, hypertension, ESRD, BP goals, SPRINT
How to cite this article: Sabarinath S, Bhadauria D.Hypertension as a risk factor for chronic kidney disease.Hypertens 2018;4(1): 48-54.
Source of support: Nil
Conflict of interest: None
 
 

Introduction

Hypertension is one of the leading risk factors for death anddisability, including stroke, accelerated coronary and systemicatherosclerosis, heart failure, and chronic kidney disease (CKD).The kidney is a major site of target end organ damage, and itis the second most common cause of end-stage renal disease(ESRD) next to diabetes mellitus. The threshold for diagnosinghypertension has declined over time, on the basis of major trialsshowing cardiovascular benefits of lowering blood pressure(BP) targets. Previously, hypertension has been defined as a BPof 140/90 mmHg or more, the 2017 ACC-AHA hypertensionguideline adopted a lower threshold, in which hypertensionis defined as a systolic blood pressure (SBP) of 130 mmHg ormore or a diastolic BP of 80 mmHg or more.[1] It has been shownthat the risk ratio for CKD was 2.8 for a pre-treatment SBP of166-180 mmHg and 7.6 for pre-treatment BP >180 mmHg.Lowering SBP by more than 2 mmHg was associated with amarked decrease in the relative risk (RR) of developing ESRD.[2]Although hypertension was associated with an increased risk of developing ESRD, the overall rates of developing ESRD werelow; approximately 15 cases per 100,000 person-years in themultiple risk factor intervention trial (MRFIT) study. Althoughhypertensive nephrosclerosis is the second most commoncause of ESRD, the risk of developing ESRD in a hypertensivepatient is < 0.5%.[3] In this paper, we review the epidemiology,pathophysiology of hypertensive CKD, and various trials onintensive BP control and renal outcomes, and controversiesregarding the target BP goal.

 
Hypertension - cause and Consequence of CKD

High BP can be either a cause or a consequence of CKD.Estimating the prevalence of CKD attributable to hypertensionalone is difficult as individuals with presumed hypertensivenephrosclerosis are rarely biopsied, and strict clinical criteriaare not routinely followed to make a diagnosis. The reportedincidence and prevalence of ESRD owing to hypertensionis, therefore, likely an overestimate because of alternativediseases that are undiagnosed or overlooked. However, a strong relationship was observed between both SBP and diastolic bloodpressure (DBP) and ESRD. In men who were recruited in theMRFIT, the RR for ESRD was 20-fold higher for patients withStage 4 hypertension (SBP 210 mmHg or DBP 120 mmHg)than for patients with optimal BP levels (SBP 120 mmHg andDBP 80 mmHg).[4] The recent study by the Okinawa GeneralHealth Maintenance Association confirmed these results inwomen as well.[5] A 17-year follow-up study by Tozawa et al.have demonstrated that high normal BP and mild, moderate,or severe hypertension, when compared to optimal BP,are independent risk factors for ESRD in men and women.The study, which included 46,881 men and 51,878 womenundergoing dialysis, categorized BP as optimal (110 ± 6/68 ±6 mmHg), normal (121 ± 4/-75 ± 6 mmHg), high normal (131± 4/79 ± 6 mmHg), mild hypertension (142 ± 8/86 ± 7 mmHg),moderate hypertension (160 ± 11/94 ± 9 mmHg), and severehypertension (181±16/105±12 mmHg). Age, body mass index,and adjusted relative risk for systolic and diastolic blood pressurefor both men and women were measured. When these resultswere compared with an optimal blood pressure, the relative riskof development of end-stage renal disease for those with highnormalblood pressure and hypertension were significant inboth men and women. Despite many studies, the level of bloodpressure control that slows the progression and time course forthe development of CKD remains disputed.

 
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The debate on kidney being a cause of essential hypertensionwas resolved, after the proof-of-principle experiment, whichdemonstrated remission of essential hypertension in sixAfrican- American hypertensives with ESRD after they receivedsuccessful kidney transplants from a normotensive donor.Hypertension develops early in the course of CKD and can beassociated with worsening renal function and developmentof cardiovascular disease. Based on a national survey ofrepresentative sample of non-institutionalized adults in the USA,it is estimated that hypertension occurs in 23.3% of individualswithout CKD, and 35.8% of Stage 1, 48.1% of Stage 2, 59.9% ofStage 3, and 84.1% of Stage 4-5 CKD patients.[6]

Pathogenesis

The renal pathology typically observed in majority of individualswith essential hypertension is benign nephrosclerosis, describedas an accelerated aging of the renal vasculature, which ischaracterized by a very slow progressive thickening andsclerosis of the renal resistance vessels, whereas the glomerularcapillaries are largely spared.[7] Some ischemic glomerular lossdoes occur, but it is limited and happens slowly over decades.Thus, significant reduction in renal function and ESRD developsonly after large losses of glomerular filtration surface area;hence, it is not too surprising that incidence of ESRD occursinfrequently in essential hypertension. In fact, except for somegenetically susceptible groups such as African americans, theonly individuals with essential hypertension who developsufficient hypertension-induced renal damage (HIRD) to causeESRD are those in whom the hypertension becomes very severeand results in the development of malignant nephrosclerosis. In contrast to the relative resistance to HIRD in individuals withessential hypertension in the absence of genetic predispositionand malignant nephrosclerosis, individuals with CKD anddiabetes mellitus seem to exhibit a much greater susceptibilityto the adverse renal effects of even moderate hypertension.[8]Moreover, in contradistinction to the largely vascular pathologyof benign and malignant nephrosclerosis, the site of HIRD inCKD is predominantly glomerular, with a pattern of acceleratedsegmental or global glomerulosclerosis often superimposed onthe intrinsic phenotype of the underlying renal disease.[9]

 
Normally, episodic or sustained increases in BP result inproportionate autoregulatory vasoconstriction of the afferentarteriole (preglomerular vasculature) such that renal blood flow ismaintained relatively constant within the autoregulatory range.[10]The glomerular capillaries are protected from barotraumas aslong as autoregulation is intact [Figure 2]. Hence, vast majorityof cases with essential hypertension usually do not exhibitglomerular injury and proteinuria. However, the resistancearterioles are exposed to chronic hypertension and slowly developthe pathology of benign nephrosclerosis. If the hypertensionbecomes very severe and exceeds the threshold for autoregulation,disruptive vascular injury occurs and malignant nephrosclerosisdevelops. The impairment of renal autoregulation associated withsevere reductions in renal mass, as in established CKD, allowseven moderate hypertension to be more freely transmitted to theglomerular capillaries with resultant barotraumas and progressiveglomerulosclerosis [Figure 1]. Vasodilatation alone withpreserved autoregulation, observed after uninephrectomy onlymodestly increases the susceptibility to hypertensive injury.[11]

The discovery of an association between MYH9polymorphisms and kidney disease added insight into theunderlying etiology of hypertensive nephrosclerosis.[12] MYH9polymorphisms result in podocyte dysfunction, leading toglomerulosclerosis. This might explain why BP control alonecannot reverse existing kidney damage or stop progression inAASK population[13] (The African American study of kidneydisease and hypertension).

The mechanisms of hypertension in CKD are multifactorial[Table 1]. Failure of pressure natriuresis is one of the dominantmechanisms causing hypertension in CKD. Defective efferentarteriolar NO production during endothelial dysfunctionstates, such as diabetes mellitus and obesity, may exaggerateglomerular capillary pressure and increased susceptibilityto glomerulosclerosis. Activation of the renin-angiotensinsystem (RAS) was proposed to be the mechanism in dialysispatients with uncontrolled hypertension despite optimizedultrafiltration.[14] Bilateral nephrectomy or RAS blockers insuch patients have been shown to control BP, suggesting failingkidneys as the source of excess renin.[15] RAS activation mayalso contribute to hypertension by stimulating the sympatheticnervous system.

BP Goals

Whether intensifying the BP control in the prehypertensive stagewill prevent the development of CKD and whether the use of antihypertensive therapy in patients with Stage 3 nephropathywill slow the rate of decline in kidney function to the same extentas in patients with normal kidney function is still a question. Thestudies to address them will be difficult to perform because oflow event rates, longer duration of follow-up, and higher cost.

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Hypertension as a Risk Factor for Chronic Kidney Disease
Figure 1: Illustrating differences in susceptibility to hypertensioninducedrenal damage

Hypertension as a Risk Factor for Chronic Kidney Disease
Figure 2: Depicting autoregulatory mechanisms in normalkidney, chronic kidney disease, and vasodilation vascular bed inuninephrectomy

Trials Evaluating BP Levels on Outcomes

Initial recommendation was a BP target of 130/80 mmHg,for all CKD patients, irrespective of proteinuria.[16] Thesewere primarily based on observational data from the generalpopulation showing that the presence of CKD, irrespective of thelevel of proteinuria, is associated with high risk of CVD [Table 2].

Non-proteinuric Nephropathy

Many recent RCTs have not shown a benefit of loweringBP targets in patients without proteinuria in retarding CKD progression. The best representation of natural history ofhypertensive nephrosclerosis was the AASK cohort, whichexcluded patients with diabetes and marked proteinuria oralternative etiologies of renal dysfunction. The AASK studyfollowed approximately 1100 individuals with baseline CKD(eGFR 20-60 ml/min/1.73 m2) and evaluated the effectof "strict" BP lowering on kidney disease progression. Theintensive group targeted a mean arterial pressure (MAP) of92 mmHg, whereas the control group targeted MAP of 102mmHg.[17] There was no significant difference in retardingCKD progression between the two groups on 10-year followup.[18] However, a subgroup analysis in AASK cohort foundthat, in those who had a proteinuria of more than 300 mg/day,they demonstrated a slower decline in GFR at lower BP levels.Thus, the renoprotective effect of lower BP is actually evidentin patients with higher proteinuria, thus providing additionalsupport for recommending lower BP targets for these patients.
 
Non-diabetic Proteinuric Nephropathy

RCTs have shown that BP of < 130/80 mmHg may reduceprogression of CKD in patients with urine albumin excretionof more than 300 mg per 24 h ("macroalbuminuria"). In asubgroup analysis of MDRD study, which consisted of nondiabeticpatients, showed that lowering mean BP to 92 mmHg(equivalent to 125/75 mmHg) preserved renal function inthose with proteinuria of >3 g/day or >1 g/day in a subset withglomerular filtration rate of 25-55 ml/min/1.73m2.[19] Thebenefit of lowering BP target in patients with a PCR of more than220 mg/g was also evident from the long-term follow-up data ofAASK population. Thus, there is sufficient evidence to suggesta BP target of < 130/80 mmHg for kidney protection in thosewith macroalbuminuria. KDIGO graded this suggestion as 2C,as the reported benefits in the AASK and the MDRD study werebased on post hoc and subgroup analyses. However, it should bekept in mind that in both the MDRD study and AASK, MAP wastargeted rather than systolic and diastolic BP, and a specific MAPmay translate into different systolic and diastolic BP, dependingon the individual patient.

Diabetic Nephropathy

The antiproteinuric effect of lowering BP is one of the mostimportant mechanisms involved in the renoprotection,regardless of the type of drug administered, in both diabetic andnon-diabetic kidney disease. The secondary analysis of the IDNTstudy, in type 2 diabetics, showed an optimal renoprotectiveeffect when the SBP is between 120 and 130 mmHg, with nofurther benefits < 120 mmHg.[20] The normotensive ABCD trialcompared intensive with moderate BP lowering in normotensivetype 2 diabetic patients. BP attained in the intensive andmoderate treatment arms were 128/75 and 137/81 mmHg,respectively, and the corresponding rates of microalbuminuriawere 21% and 25%. There was no difference in the rate of decline of renal function; lesser degree of proteinuria was notedwith intensive therapy. This is especially true from the resultsof ACCORD BP trial.[21] This trial included a large number ofdiabetic patients, who had a mean serum creatinine of 0.9 mg/dl,with minimal proteinuria, with cardiovascular disease, or at leasttwo risk factors for cardiovascular disease and evaluated theimpact of lowering SBP < 120 or 140 mmHg. While the intensivegroup attained an average SBP of 119 mmHg, the standard groupattained an average SBP of 133 mmHg. There was no differencein the primary outcome between the two groups except for thereduction in non-fatal stroke in the intensive therapy group.The intensive control group had lower risk of stroke but at theexpense of higher rates of serious side effects. KDIGO suggeststhat in diabetic patients with microalbuminuria, a BP goalof < 130/80 mmHg and in those without microalbuminuria,KDIGO recommends a target of < 140/90 mmHg.

 
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BP Measurement - When and Where? Importance of
Home BP Monitoring


Home BP and ambulatory blood pressure (AMBP) monitoring isimportant because of its ability to identify masked and white coathypertension. White coat hypertension is diagnosed when the BPrecordings are persistently elevated (more than 140/90 mmHg)in the clinical setting and having a normal 24 h average bloodpressure (< 130/80 mmHg).[22] Although it was earlier thoughtto be benign, studies have shown that the cardiovascular risk issimilar to that of essential hypertension.[23] Masked hypertension,the opposite of white coat hypertension, carries a similar risk of cardiovascular complications. The (Self-measurement of BP atHome in the Elderly [SHEAF]: Assessment and Follow-up)study showed that the cardiovascular complications were higherin individuals with masked hypertension than in those withwhite coat and controlled hypertension. Agarwal and Andersenfound that elevated home blood pressure readings were thebest predictors of patient prognosis and composite outcome(ESRD or death) than office blood pressure readings.[24] Theyalso found that home BP monitoring correlated more closelywith AMBP monitoring.[25] The most important value of AMBPmonitoring in CKD patients is the evaluation of circadianvariations in BP. Normally during sleep, BP should decreaseby at least 10%, a nocturnal dipping. Non-dipping is associatedwith increased severity of kidney disease and cardiovasculardisease. The individuals with proteinuria were more likely tohave blunted circadian variations in BP than individuals withoutproteinuria.[26] Hence, in all CKD patients, home BP recordingshould be emphasized for better monitoring of BP control.

Table 1: Factors causing hypertension in CKD
Hypertension as a Risk Factor for Chronic Kidney Disease
CKD: Chronic kidney disease

Table 2: The change in BP goals before and after SPRINT trial
Hypertension as a Risk Factor for Chronic Kidney Disease

 
Has the Sprint Introduced New BP Goal?

Before the SPRINT trial, optimal blood pressure controlfell within the high-normal range (SBP/DBP 130-139/85-89 mmHg).[27] The subject of debate was whether patientswith prehypertension or mild hypertension need better BPcontrol? In prehypertensives, the 10-year absolute risk ofcardiovascular disease for middle-aged adults without diabetesis about 10%, and rises to 40% in the presence of diabetes and/or established cardiovascular disease. Use of antihypertensivesin prehypertensives for secondary prevention decreased the CVdisease and death by 15%.[28]

The SPRINT trial included approximately 9000 non-diabeticpatients, with an SBP of 130-180 mmHg, aged ≥50 years witha high CV risk, or an established CV disease (excluding stroke).Patients were randomly assigned to SBP targets of either< 120 mmHg (intensive treatment) or < 140 mmHg (standardtreatment). The mean SBP in the intensive BP control groupwas 121.4 mmHg compared to 136.2 mmHg in the standardtreatmentgroup. The trial was stopped prematurely after3.26 years of follow-up because of a significantly lower rate of thecomposite primary end point in the intensive-treatment groupcompared with the standard-treatment group. No benefit wasshown for secondary renal end points. Adverse effects were morewith the intensive treatment, but serious adverse events werecomparable in both groups. The generalization of the positivefindings of the SPRINT trial has to be still evaluated, as it excludeddiabetic and stroke patients, and the SPRINT cohort representsonly 20-30% of all patients with hypertension [Figure 3].

Caveats of the Sprint Trial

The method used for the measurement of BP in SPRINT trialwas different from the other studies. SPRINT used an automated,validated oscillometric device, and the BP was recorded thricein a quiet and isolated room. This automated office bloodpressure measurement (AOBP) was superior to conventional office BP measurement, and it correlated well with the AMBPmeasurement (ABPM substudy in SPRINT) and target endorgandamage. The Spanish ABMP study shows that with aBP of < 125 mmHg, the white coat hypertension and maskedhypertension are very low. The other point to note is, SBP whenassessed by AOBP was much lower than when measured with amanual BP instrument.[29] Some authors claim that the BP levelsattained in the SPRINT intensive control group correspondto office SBP values of 136 mmHg, which is recommended asadequate BP control. Hence, it is still unclear how to translatethe AOBP to conventional office BP. Whether that SPRINT trialhas overestimated that the result is yet an another question, as50% of the SPRINT population was in prehypertensive stage.ABPM registry showed that among patients with characteristicslike SPRINT, 42% of patients had daytime SBP < 130 and 21%had 24 h SBP values < 120 mmHg. Hence, many people receivingantihypertensive therapy are already within the SBP levelsattained in the intensive BP control in SPRINT.

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Hypertension as a Risk Factor for Chronic Kidney Disease
Figure 3: Potential influence of the SPRINT trial in blood pressuregoals in daily clinical practice


Why the difference compared to the HOPE 3 trial, whichalmost has a similar cohort like SPRINT? In HOPE trial, theintensively treated group did not benefit from lowering the BP,one major reason being, the population included was those withlower cardiovascular risk, in contrast to the SPRINT cohort.

Effect on the Guidelines

The SPRINT trial signaled the need for review of methodologyof BP measurement in future clinical trials, and the importanceof home AOBP to avoid masked and white coat hypertension.Although the New Australian hypertension guidelines[30] andlatest Canadian guidelines[31] accepted the lowering of BP< 120/80 mmHg, in patients with similar profile of SPRINT,the Latin American society of hypertension did not change theirguidelines, quoting the methodology for BP measurement usedin SPRINT trial.[32]

 
Does Intensive BP Lowering Increases the Incidence
of CKD? The Other Side of the Coin!!


A very recent secondary analysis of two major trialsACCORD and SPRINT showed that intensive control ofSBP increased the risk of incident CKD in patients with andwithout diabetes. as in established[33] This analysis included4311 individuals from ACCORD and 6715 individuals withSPRINT. All participants had a baseline eGFR of 60 ml/min per 1.73 m2 or higher (subgroup without CKD - 70%of SPRINT cohort and more than 90% of the ACCORDtrial cohort). Baseline characteristics were comparable forintensive and standard SBP interventions within ACCORDtrial and SPRINT trial. Compared with SPRINT populationwho did not have diabetes, ACCORD population was younger,having higher BMI, and higher eGFR and albuminuria. Bothin the intensive and standard interventions in the ACCORDtrial, an early steep in decline in eGFR was noted during thefirst 12 months, the decline being more pronounced withthe intensive intervention. Incident CKD were lower in bothintervention groups in SPRINT than in the ACCORD. At3 years the cumulative incidence of CKD in the ACCORDtrial was 10% with the intensive intervention and 4.1% withthe standard intervention, corresponding SPRINT valueswere 3.5% and 1.0%. The absolute risk difference was slightlyhigher in the ACCORD trial than in SPRINT. This was evenstronger in participants with a baseline urinary ACR of 3.4mg/mmol or higher. Hence, the positive SPRINT resultshave to be cautiously extrapolated to the patients who areexcluded, i.e., diabetic patients. Although ACCORD wasunderpowered to detect true difference in cardiovasculardisease outcomes, participant level pooled meta-analysisof SPRINT and ACCORD showed decreased risk ofcardiovascular disease events in the combined cohort. Thisstudy suggests the need for monitoring of renal functionduring intensive antihypertensive therapy, particularly inadults with diabetes. Hence, future studies are needed inthis area to understand the clinical implication of treatmentrelatedreductions in eGFR.

Conclusion

Hypertension is an important cause and a consequenceof CKD. Proteinuric CKD is the target for more intensiveintervention. Targeting to < 130/80 mmHg definitely hasbenefit in terms of cardiovascular disease and in proteinuriaCKD, but generalizing this statement to all hypertensivepopulation is still questionable, weighing benefit versus risk.Home BP monitoring should be emphasized in all hypertensivepatients. Additional studies characterizing the relationshipbetween mild hypertension and subsequent risk of renaldisease, standardizing the method of BP measurement isurgently needed.

 
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