Hypertension Management in Transition: From

CKD to ESRD
Aziz Valika and Aldo J. Peixoto

Hypertension is present in
90% of patients in late-stage CKD. There are scarce data focusing on the transition period between
CKD Stages 4 and 5 (end-stage kidney disease) as it relates to hypertension evaluation and management. Here, we propose that
a combination of the principles used in the management of patients with CKD Stages 4 and 5 be applied to patients in this
transition. These include the use of out-of-office blood pressure (BP) monitoring (eg, home BP), avoidance of excessively tight
BP goals, emphasis of sodium restriction, preferential use of blockers of the renin-angiotensin system and diuretics, and consid-
eration of the use of beta blockers.
Q 2016 by the National Kidney Foundation, Inc. All rights reserved.
Key Words: Hypertension, CKD

and colleagues8 found that HTN on ABPM predicted

T he prevalence of hypertension (HTN) in CKD Stages
4 and 5 is
90%, and most studies of the general
CKD population show that only a small fraction of these
patients have their pressure well controlled.1 Although
the average man or woman with CKD spends a relatively
short amount of time with Stage 5 disease (eg, 7.4 months
in a clinical trial environment2) before progressing to
dialysis or transplantation, it is a time where rates of
cardiovascular (CV) mortality and morbidity increase
and begin to mirror those of the dialysis population.3 It is
also a time of significant change for patients, as their
dialysis providers are often different from their usual clinic
providers, and medication adjustments are frequent
as contact with health care providers increases. This
“unstable” population has characteristically been
excluded from most clinical trials,4,5 thus, much of our
treatment strategy stems from conventional wisdom,
clinical experience, and extrapolation from populations
that have been studied more extensively (eg, early CKD,
ESRD, or subjects without any renal disease). Despite this
significant limitation, this review will describe an outline
for the assessment and treatment of HTN in patients who
are transitioning from advanced CKD to ESRD.
HYPERTENSION BURDEN AND BLOOD PRESSURE
ASSESSMENT
Before aggressive attempts at treatment, accurate assess-
ment of blood pressure (BP) is critical to appropriate
management of patients in transition. Isolated daytime
BP measurements at infrequent intervals during clinic
visits are often used to initiate and guide therapy. Discor-
dance between out-of-office and in-clinic readings is
highly prevalent in the CKD and dialysis population,
and studies using ambulatory blood pressure monitoring
(ABPM) have highlighted this difference. In a large study
of African Americans with hypertensive kidney disease,6
masked HTN (elevated readings at home but not at clinic)
was present in 43% of patients, whereas white coat HTN
occurred in 2.2%. In another cohort of white patients
with CKD due to various causes in which CKD stages
were reported, the rates of masked HTN and white coat
HTN in Stages 4 and 5 patients were 14% and 13%, respec-
tively.7
Out-of-office measurements were also useful and
accurate in prognostication of adverse events. Gabbai
both adverse renal and CV outcomes, independent of
clinic BP in the African American Study of Kidney
Disease. In a multicenter Italian study of CKD patients,
subjects with HTN on ABPM and normal clinic BP (ie,
“masked” uncontrolled HTN) had an increased risk of
CV and renal events and all-cause mortality (hazard ra-
tio (HR) 3.17, 3.93, 3.45, respectively), whereas the risk of
these events in those with in-clinic HTN only (ie, nor-
mal ABPM) was not statistically significant.7 A meta-
analysis of trials using ABPM in CKD patients showed
that 30% of patients who were thought to be uncon-
trolled on treatment in clinic were actually normotensive
at home, and 40% of those felt to be controlled were
hypertensive at home.9 Of note, only 1 of the trials re-
viewed actually enrolled patients with an average
glomerular filtration rate (GFR) in the CKD 4 range
(mean GFR 17.6).10 Similarly, in the dialysis population,
it seems that both ABPM and self-measurements at home
are more accurate in diagnosing HTN and more
predictive of adverse CV outcomes, when compared to
in-center measurements during dialysis sessions.11 In
addition, there are data showing that home BP is supe-
rior to clinic BP to achieve BP control in hemodialysis
patients.12 Therefore, in advanced CKD, relying on office
measurements alone seems to mischaracterize the BP
control of a significant proportion of patients with
CKD. Although there are practical difficulties in
routinely using out-of-clinic BP measurements to guide
antihypertensive therapy in all patients nearing dialysis,
the limitations and pitfalls of relying solely on in-clinic
measurements should be understood and taken into
account.
From the Section of Nephrology, Department of Medicine, Yale University
School of Medicine, New Haven, CT.
Financial Disclosure: The authors declare that they have no relevant finan-
cial interests.
Address correspondence to Aldo J. Peixoto, MD, Section of Nephrology, Yale
University School of Medicine, Boardman 114, 330 Cedar Street, New Haven,
CT 06520. E-mail: aldo.peixoto@yale.edu
Ó 2016 by the National Kidney Foundation, Inc. All rights reserved.
1548-5595/$36.00
http://dx.doi.org/10.1053/j.ackd.2016.02.002

Advances in Chronic Kidney Disease, Vol 23, No 4 (July), 2016: pp 255-261 255
256 Valika and Peixoto

Despite the lack of data showing the superiority of home
BP or ABPM to guide the treatment of HTN, we believe
there may be value based on prognostic studies and data
on the increased patient engagement with use of home
BP.13 This is in agreement with the recent recommenda-
tions of the US Preventive Services Task Force released in
October 2015 (http://www.uspreventiveservicestaskforce.
org/Page/Document/UpdateSummaryFinal/high-blood-
pressure-in-adults-screening?ds¼1&s¼hypertension).
We use home BP routinely and follow the European
protocol for data acquisition and collection14; that is,
7 days of twice daily readings, preferably in duplicate at
each time. We use the outcome-based reference value of
130/85 mm Hg15 as equivalent to a clinic BP target of
140/90 mm Hg. In patients in whom home BP is
not possible or unreliable, we perform 24-hour ABPM
(Table 1).
TARGET BP
The Irbesartan in Diabetic Nephropathy Trial and
long-term follow-up analyses of the Modification of Diet
in Renal Disease and African American Study of Kidney
Disease (AASK) trials all suggest that targeting goal BPs
of less than 125 to 130/75 to 80 mm Hg is beneficial in
patients with proteinuric
CKD, both diabetic and
nondiabetic.16-18 It is CLINICAL SUMMARY
relatively well established
that achieving these targets
1. Out-of-office BP is helpful to better assess the overall
leads to a slower decline in hypertension burden and improve treatment decisions.
GFR, although without a
significant effect on 2. Salt restriction and diuretics are essential to adequate BP
mortality or CV outcomes. control.
However, none of the 3 3. RAS blockers and beta-blockers, if well tolerated, are the
clinical trials that proposed preferred antihypertensive drugs.
lower targets for BP control
was able to demonstrate a
difference when compared to the conventional target
of 140/90 mm Hg.19 Recent major guidelines have differed
in their recommendations. The Kidney Disease Improving
Global Outcomes recommends a goal of 130/80 mm Hg in
the presence of albuminuria, whereas the evidence-based
guidelines (also known as, “JNC 8”), and the European
guidelines propose 140/90 mm Hg.20,21 Multiple
epidemiological studies of subjects with ESRD have
shown a J-shaped association between BP and survival,
noting that patients with lower BPs (below
120/80 mm
Hg) have higher mortality than those with higher
levels.22 Some studies find systolic blood pressures
(SBPs) as high as 180 mm Hg to be protective in compari-
son. Similar data are available for patients with earlier
stages of CKD.23 However, an interesting recent long-
term follow-up (19.3 years) report of the Modification of
Diet in Renal Disease study indicates that randomization
to a lower BP target (125/75 mm Hg during the trial)
resulted in a 28% lower risk of death after ESRD was
reached (HR 0.72, P ¼ .003) and significant reductions in
the development of heart failure and coronary disease at
24
the time of reaching ESRD, thus suggesting value of BP
control during CKD that is only realized after very long
follow-up. The exciting results of the recently published
Systolic Blood Pressure Intervention Trial (SPRINT)
showing significant reductions in mortality and CV events
among patients randomized to a SBP target of 120 mm Hg
(compared with 140 mm Hg) have, unfortunately, limited
applicability to the CKD 5 population.
However, these associative studies do not prove causa-
tion; no prospective studies have been performed that
evaluate varying target BPs in dialysis or predialysis
patients, and few have assessed the effect of antihyperten-
sive medications. Patients progressing to dialysis are often
volume-overloaded, and HTN is nearly universal; most of
the subset of patients with lower or “controlled” BPs may
represent those with comorbidities that carry a high risk of
mortality, such as congestive heart failure or cirrhosis.
Furthermore, a higher rate of mortality due to background
diagnoses (eg, diabetes or smoking) precludes obtaining
a beneficial signal from HTN control over relatively
short periods of time.25 A long-term study of a prevalent
cohort of dialysis patients in Uruguay showed that late
mortality (.5 years) was associated only with higher,
not lower BPs.26 Likewise, the association of mortality
with SBPs , 120 mm Hg disappeared in those who
survived greater than 2 years in a group of US-based
patients.27 Regardless of BP control or time on dialysis,
the use of antihypertensives
in ESRD is associated with
improved survival, and
meta-analyses of random-
ized controlled trials of
various different BP-
lowering drugs showed an
overall reduction in mortal-
ity and CV events from their
use.28,29
So, from a clinician’s
perspective, how should we
proceed during this CKD or
ESRD transition? Although many of these studies were
in incident dialysis cohorts, none apply directly to
advanced CKD. Given that many dialysis patients live
longer or are bridged to transplant, it is likely that
patients will still reap CV benefit from adequate BP con-
trol. Therefore, our opinion is that a target of 140/90 mm
Hg is justified in this transition phase.
DIETARY SALT RESTRICTION AND DIURETIC USE
Salt reduction is essential in the management of HTN in
CKD, and the more advanced the CKD, the more
salt-sensitive BP becomes. In anephric patients, classic
studies by Merril and colleagues30 demonstrated that
excess sodium accumulation was the primary cause of
HTN in the “renoprival state” and that HTN in subjects
with kidney disease was readily responsive to adequate
sodium and water removal during dialysis.31 A modest
but significant reduction of 5/3 mm Hg was shown in a
recent meta-analysis of a number of clinical trials for
dietary sodium restriction on BP control in the general
population.32 This effect has been described across many
populations with different characteristics, including age,
gender, and race, and the response is observed in normo-
tensive patients as well. Given this relatively mild effect
 Hypertension in Transition
and the near universal use of potent antihypertensives in
advanced CKD, is salt restriction still relevant? Some
data have pointed to the fact that lower sodium intake
seems to potentiate the effect of many antihypertensives,
and similarly, in dialysis patients, BP medications are often
ineffective when volume status is not controlled.
We are not aware of any clinical trials of sodium restric-
tion in CKD. In a small trial of resistant hypertensives,
a group similar to advanced CKD in that all were
uncontrolled on multiple antihypertensives at baseline, a
comparison between high salt diet (.250 meq) and low
salt diet (,50 meq) groups showed a marked difference
in BP of 22.7/9.1 mm Hg.33 In addition, in nondiabetic
Stage 3 CKD patients with residual proteinuria while on
lisinopril, a low sodium diet was more effective than the
addition of an angiotensin receptor blocker (ARB) in
reducing SBP (7 mm Hg vs 2 mm Hg) and was more
effective in reducing proteinuria as well (51% vs 21%).34
In dialysis patients, observational data indicate prominent
effects of strict dietary sodium restriction on BP control
and left ventricular mass reduction.35 Because there is
general agreement of the importance of sodium intake to
interdialytic weight gain and volume overload in hemodi-
alysis patients, both factors associated with increased
mortality in this population, it is unlikely that a clinical
trial will ever be conducted. We feel strongly that dietary
education is a key factor that needs enforcement and
education in patients with advanced CKD.
The use of objective measures of volume status (eg,
bioimpedance, inferior vena cava ultrasound, lung ultra-
sound, and blood volume monitoring) has documented
value in the evaluation and management of patients with
ESRD.36 In earlier stages of CKD37 and in resistant
HTN,38 these measures also have proven value in control-
ling BP. In a study using bioimpedance to assess fluid
compartment specifically in CKD patients (mean
estimated GFR 29 mL/min), hypervolemia was frequent
and correlated with a lower estimated GFR, higher SBPs,
and increased arterial stiffness. Twenty percent of the
CKD patients studied had expanded extracellular fluid
volume in the absence of appreciable edema, suggesting
that diuretics and sodium restriction would likely be
beneficial regardless of examination or historical findings,
and should not only be applied to those with clinically
apparent volume overload.39
Despite the significance of sodium to the HTN in CKD,40
diuretics are often misused and sometimes forgotten in
advanced CKD. Often patients are kept on the same dose
of a loop diuretic, without dose escalation as GFR
declines—or often with dose reductions due to concerns
that decreasing intravascular volume will further decrease
renal perfusion and hasten GFR decline. These concerns, in
the absence of obvious volume depletion are largely
unfounded.
Moreover, although loop diuretics are more routinely
used in advanced CKD due to their increased potency,
thiazide diuretics should not be overlooked in the
predialysis population.41 Although guidelines have
recommended loop diuretics over thiazides in patients
with low GFR, the combination of a thiazide with a loop
diuretic, often used in diuretic-resistant heart failure
257
patients,42 has been shown to be an effective regimen in
CKD as well. This “sequential nephron blockade” has
a significant additive effect on natriuresis in both
mild43 and advanced CKD.44 Dussol and colleagues45,46
reported 2 randomized double-blind trials looking at the
combination of furosemide and hydrochlorothiazide vs
either agent alone in advanced CKD; in both, the greatest
reduction in BP and increase in natriuresis occurred with
combination of both diuretics. Corroborating these find-
ings, Agarwal and colleagues47 demonstrated sustained
effects of chlorthalidone on BP in a small group of patients
with GFR between 20 and 45 mL/min. We share this favor-
able impression and like to use thiazides and thiazide-like
diuretics in patients with advanced CKD with the goal of
improving volume status, reducing BP, and often allowing
patients to remain in better potassium balance, thus allow-
ing continued use of renin-angiotensin system (RAS)
blockers. Unfortunately, there are no data to substantiate
any favorable effects of any diuretic class on outcomes
in CKD.
CONSIDERATIONS ABOUT OTHER
ANTIHYPERTENSIVE DRUGS
ACE Inhibitors and Angiotensin Receptor Blockers
Ample data in CKD support the use of angiotensin-
converting enzyme inhibitors (ACE-I) and ARBs in
reducing proteinuria and slowing GFR decline. Treatment
in non-uremic patients with left ventricular systolic
dysfunction leads to a well-described reduction in mortal-
ity. However, very limited data exist in advanced CKD. In
an important study to address the often-asked question
about the safety of use of ACE inhibitors in advanced
CKD, Hou and colleagues48 evaluated the safety and
efficacy of benazepril in a study of 224 patients with
CKD (average creatinine clearance 26 mL/min) random-
ized to either placebo or benazepril. After 3 years of
follow-up, the group on benazepril had a 19% absolute
risk reduction of a composite end point of ESRD, doubling
of creatinine, or death. The ACE inhibitor was well toler-
ated, and hyperkalemia or other drug-related adverse
effects were not more common in either group.48
Further data come from the dialysis population. Residual
renal function inversely correlates with mortality in ESRD,
and given that the primary benefit of RAS inhibition in
CKD is with slowing GFR decline, one might expect these
agents to improve outcomes when continued into dialysis.
In patients on peritoneal dialysis, RAS inhibition decreases
the loss of residual renal function,49 and for that reason, it
is the preferred drug class despite lack of definitive
evidence of an impact on CV events or mortality.50,51 In
hemodialysis, randomized controlled trials including
anuric and oliguric subjects also have produced variable
results with respect to hard end points. Although some
studies with several different ARBs have shown
protective effects with respect to CV events and death,52-54
other studies with larger number of patients receiving
either ARBs (olmesartan) or an ACE inhibitor (fosinopril)
failed to show any benefit from these agents55,56
compared with placebo or “control” therapies that did
not include a blocker of the renin-angiotensin system.
258 Valika and Peixoto
Table 1. Practical Information on the Use of Home Blood Pressure
Monitoring
Technique
 Use only arm cuffs (not wrist or finger).
 Appropriately sized cuff to match arm size.
 At least 5 min of quiet rest before measurements.
 Obtain readings in duplicate, twice daily (morning before
medications and evening before dinner) for 7 d. Use the
average of 7 d to make clinical decisions.
 In patients with high blood pressure (BP) variability, there
may be value of measuring BP more frequently.
Interpretation
 If home BP , 125/76, continue to monitor (or continue same
treatment).
 If home BP . 135/85 mm Hg, start treatment (or escalate
therapy).
 If home BP between 125/76 and 135/85 mm Hg, obtain
ambulatory blood pressure monitoring (ABPM).
 If 24-h ABPM average , 130/80 mm Hg, continue same
strategy. If higher, start or increase treatment.
Furthermore, another study showed that atenolol was
superior to lisinopril in reducing BP, left ventricular
hypertrophy (LVH) and CV events and mortality in
hemodialysis patients,57 findings that will certainly
warrant further investigation.
Given the aforementioned evidence, our opinion is that
blockers of the renin-angiotensin system should be
continued in advanced CKD if already in use and well
tolerated from the standpoint of potassium balance. Given
the favorable effects on residual kidney function, they
should be continued until the patient has no remaining
residual function (ie, urine output , 100 mL/d), especially
in patients starting on peritoneal dialysis. It should be
recognized that because these agents have an acute
reducing effect on GFR, there may be value in stopping
them in patients who need an acute “boost” in renal
function (eg, several weeks), such as those awaiting trans-
plantation from a live donor. Likewise, it is imperative that
potassium levels be monitored closely as these patients
with very low GFR are at an enhanced risk of hyperkale-
mia when exposed to RAS blockers.
Beta Blockers
Beta blockers are effective in lowering BP in patients with
renal disease. Despite their indication in patients with
heart failure accompanied by left ventricular dysfunction
and those with recent myocardial infarction, no specific
renal benefit has been shown in CKD patients with the
exception of a modest effect in the AASK trial, where
metoprolol performed better than amlodipine but was
inferior to ramipril in decreasing the composite end point
of halving of GFR, ESRD, or death.19 In dialysis patients,
Cice and colleagues compared carvedilol vs placebo in a
cohort of patients with dilated cardiomyopathy on digoxin
and some form of RAS inhibition. After 2 years of follow-
up, there was a reduction in all-cause mortality in the
carvedilol group (HR 0.51).58 In addition, in one of the
few head-to-head trials of BP medicines for patients on
dialysis (The Hypertension in Hemodialysis Patients
Treated with Atenolol or Lisinopril [HDPAL] trial), ateno-
lol was shown to be superior to lisinopril in reducing LVH
and major CV events.57 Notably, this cohort was largely
African American, and the lisinopril group had higher
overall BP and increased use of other antihypertensives
to achieve the same target BPs. It is unclear that either of
these trials provides firm evidence for the universal use
of beta blockers in predialysis or dialysis-dependent pa-
tients, but certainly provides encouraging results, espe-
cially given the known overactivity of the sympathetic
nervous system in CKD/ESRD.22
Beta blockers are quite different among each other,
but there is little evidence to guide choice in advanced
CKD. Given that diabetes is a leading cause of progressive
CKD, the effect of beta blockers on glycemic control
could be important. In the Glycemic Effects in Diabetes
Mellitus: Carvedilol-Metoprolol Comparison in Hyperten-
sives trial, investigators compared carvedilol with
metoprolol in diabetic, hypertensive patients all on ACE
or ARB monotherapy, and diabetes-related parameters
other than BP control were assessed. Metoprolol was asso-
ciated with decreased insulin sensitivity, a small increase
in glycosylated hemoglobin, mild weight gain, and a
higher tendency to develop increased albuminuria (urine
albumin . 30 mg/d) in patients previously without it.59
No difference in CV events or overall BP reduction was
noted. Notably, however, this trial excluded all patients
with an initial GFR of less than 60, so, our ability to
extrapolate this to patients with diabetic nephropathy,
and particularly those with advanced stages of CKD, is
quite limited.
Aside from lack of clear evidence to support any partic-
ular drug from the class, there are also pharmacokinetic
concerns regarding dosing of beta blockers, especially in
advanced CKD. Many beta blockers are renally cleared
to varying degrees, so as GFR declines, dosing strategies
require adjustment, sometimes in the form of dose reduc-
tion or increased dosing intervals. As an example, in the
HDPAL trial discussed previously,57 atenolol was dosed
after dialysis every 48 to 72 hours, a regimen shown to
be safe and effective in lowering BPs in dialysis patients60;
in those with GFR , 15 not on dialysis, dosing guidelines
suggest dose reduction by 75% or increasing the dosing
interval sometimes to every 96 hours. Conversely, others
have suggested that using highly dialyzable beta blockers
in ESRD may decrease their cardioprotective benefits. One
recent retrospective analysis of a large cohort of Canadian
patients on dialysis showed a higher risk of death in
patients initiating a highly dialyzable beta blocker vs a
poorly dialyzed one.61 The agents compared were limited
to atenolol, acebutolol, metoprolol (high dialyzability) and
bisopropolol or propranolol (low dialyzability). Carvedi-
lol (considered poorly dialyzed by the authors) was not
included due to its restricted use in the area where the
study was performed.
So, there may be a benefit of beta blocker therapy in
advanced CKD when transitioning to dialysis, carvedilol
may be favored over metoprolol in diabetic patients, and
perhaps over other highly dialyzed beta blockers as well,
unless using unique dosing schedules. Use in later stages
of CKD must be monitored with caution due to the
 Hypertension in Transition
accumulation of some agents at routine doses and their
potential for overdose and toxicity. However, we some-
times take advantage these changes in pharmacokinetics
to allow easier, less frequent dosing, especially in patients
with documented poor adherence to treatment.
Calcium Channel Blockers
Calcium channel blockers (CCBs) are useful agents in
the treatment of HTN in patients with kidney disease.
They have a good safety profile in advanced kidney
disease, but drug-specific renal or CV benefits are not
demonstrated, and data from the Irbesartan Diabetic
Nephropathy Trial showed that amlodipine was no
different from placebo in preventing the composite
outcome of doubling of serum creatinine, ESRD, or death
in patients with moderate to advanced diabetic nephropa-
thy.62 The non-dihydropyridine CCBs (diltiazem and
verapamil) have modest antiproteinuric effects in
CKD,63,64 although it is unclear whether this has
an impact on renal outcomes. From the perspective of
CV outcomes, there are no data in CKD 4. However,
in early Stage 3 CKD, data from the ACCOMPLISH
trial showed superiority of the benazepril/amlodipine
combination over benazepril/hydrochlorothiazide in the
subset of patients with CKD.65 In hemodialysis, Tepel
and colleagues66 compared the effects of amlodipine vs
placebo in 251 patients, showing a protective effect of
amlodipine on the composite secondary end point of death
or CV events, although the primary end point of all-cause
mortality did not differ between the groups.
Although there is weak evidence of benefit from CCBs in
renal patients, the class will remain commonly used due to
its lack of acute effects on kidney function or electrolytes, a
particularly appealing attribute to the nephrologist treat-
ing patients who are nearing renal replacement therapy.
Patients with proteinuric CKD need to be monitored
closely to detect worsening proteinuria in the presence of
a CCB, but in most patients, this effect will not be signifi-
cant if the CCB contributes to effective BP control.
Mineralocorticoid Receptor Antagonists (MRA)
Similar to the use of RAS inhibition, the nephrologist’s
ability to make use of MRAs in patients with severely
impaired GFRs is often limited by hyperkalemia. This
effect occurs in a significant proportion of individuals,
leading to drug discontinuation, hospitalization, or most
concerning, serious cardiac events.67 In mild to moderate
CKD, credible evidence has accumulated showing that
when added to ACE/ARB, spironolactone is noted to
have an additive effect on BP and proteinuria reduc-
tion.68,69 Despite this, outcome studies looking at
survival or kidney-related outcomes are lacking, and trials
of patients with advanced CKD are nonexistent.70
Recently, a randomized controlled trial in dialysis patients
showed that spironolactone was well tolerated and
resulted in a substantial reduction in mortality and CV
outcomes when compared to placebo.71 Another study
demonstrated a favorable effect on LVH in peritoneal
dialysis patients. However, the use of MRAs in advanced
CKD is strongly discouraged by some guidelines given
the risks of hyperkalemia.21 We agree with these concerns,
259
but, we also believe that these agents can be used as long as
closely monitored, especially given their benefit in the
management of resistant HTN,72 including in patients
with CKD.73,74
CONCLUSIONS
Management of HTN in advanced CKD is guided largely
by experience, common sense, and judicious use of infor-
mation derived from earlier CKD and ESRD studies.
A general BP target of 140/90 mm Hg seems appropriate,
and use of out-of-office monitoring is important. Sodium
restriction and diuretic use are important to allow volume
and BP control. Most patients require antihypertensive
agents, and blockers of the renin-angiotensin system
(ACE inhibitors or ARBs) are the most appropriate first
choice and are well tolerated even in this group of patients
with low kidney function.
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