Management of CKD in Ischemic Heart Disease

Management of
CKD with Ischemic Heart Disease
DR. MD. ZAHIRUL ISLAM
PHASE A RESIDENT
BLUE UNIT, NIKDU

 CKD dramatically increases the risk of developing
cardiovascular disease(3-30 times depending on
CKD stage and study).Nearly half of all deaths in
CKD patients are from cardiovascular events, and
CKD patients are more likely to die from CVD than
progress to ESRD during their lifetime.

ISCHEMIC HEART DISEASE
 Acute Coronary Syndrome(ACS)
--ST elevation MI(STEMI)
--Non-ST elevation MI(NSTEMI
--Unstable angina(UA)
 Chronic Coronary Syndrome(CCS)
(previously called chronic stable angina)

CKD
 Abnormalities of kidney structure or function,present
for >3 months,with implications for health.
 Criteria for CKD(either of the following present for
>3months)
--Marker of kidney damage
--Decreased GFR

EPIDEMIOLOGY
Worldwide, CKD accounted for 2.9 million(1.1%)of disability
adjusted life years and 2.5 million(1.3%) of life years lost in 2012.A
meta-analysis of cohort studies involving >1.4 million individuals
yielded an association of not only low eGFR but also higher
albuminuria with cardiovascular disease. Thus,the risk of
developing CVD in patients with CKD surpasses the risk of reaching
end-stage kidney disease, and therefore, CKD must be considered
as one of the strongest risk factor for the development of CVD.

As glomerular
filtration
rate (GFR) declines
below - 60 to 75
ml/min/1.73 m2, the
probability of
developing
CAD increases
linearly
and patients with
CKD stages G3a to
G4
(15-60 ml/min/1.73 m2)
have approximately
double and triple the CVD
mortality risk,

 As GFR declines,
nonatherosclerotic
events assume a
higher proportion
of the CVD events

Traditional and Non traditional
Risk Factors of Vascular Disease in CKD
Traditional
 Hypertension
 Dyslipidemia
 Smoking
 Hyperglycemia
Non Traditional
• Vascular calcification
• Inflammation
• Increased Proteinuria

Myocardial Alterations in CKD
Patients with CKD exhibit characteristic changes in the
myocardium with pathological myocardial fibrosis with
collagen deposition between capillaries and
cardiomyocytes and cardiac hypertrophy the hallmarks of
uremic cardiomyopathy.

 LVH is present in about one-third of all patients with
CKD, increasing up to 70% to 80% in patients with
end-stage kidney disease. The presence of LVH is an
independent predictor of survival in patients with CKD,
even in those with early-stage CKD. Three main
mechanisms are considered to contribute to LVH in
CKD

Causes of LVH in CKD
(1) Afterload- and
abnormal arterial stiffness, increased systemic arterial resistance, and systolic hypertension
(2) Preload-related factors as well as
expansion of intravascular volume in CKD leading to volume overload, length extension of myocardial cells,
and eccentric or asymmetrical left ventricular remodeling
(3) Nonafterload, non preload-related factors.
intracellular mediators and pathways contributing to progressive LVH which is
activation of peroxisome proliferator-activated receptors, stimulation of small G-proteins or the mechanistic
target of rapamycin pathway, as well as metabolic changes such as decreased fatty acid oxidation

Pathogenesis of CVD in CKD
Three important mechanisms contribute to CVD progression in CKD:
Autonomic dysfunction:Autonomic function is impaired in
CKD patients,with a relative dominance of sympathetic over
parasympathetic activity.Increased sympathetic tone promotes smooth
muscle cells and fibroblast proliferation in blood vessels and activates
the RAAS pathway. Hence,autonomic dysfuction contributes to
cardiovascular pathological remodelling.
Vascular pathology:The mechanism leading to arterial
pathology and endothelial dysfuction in CKD are incompletely
understood,but increased oxidative stress,low grade inflammation,
uremic toxins, increased wall stress(associated with arterial
hypertension), and impaired calcium/phosphorous homeostasis likely
contribute.

 Cardiac Pathology:
LVH is present in 40% of CKD patients,and the prevalence increases
with declining GFR.LVH is likely promoted by chronic
hypertension,anemia,sympathetic and RAAS overactivity,and volume
overload.Cardiomyocyte hypertrophy is not accompanied by a
similar degree of neovascularisation.Hence,the cardiomyocyte -to-
capillary ratio increases,leading to relative ischemia of the
myocardium.
Heart failure is common in CKD,with a prevalence > 50%
among ESRD patients. The etiologies of heart failure in CKD
patients include pathological left ventricular remodelling seondary
to sympathetic and RAAS overstimulation,LVH,valvular heart
disease, and ischemic heart disease.

CHALLENGES IN CKD
 CKD patients with ACS are less likely to present with chest pain.
 Also more likely to have pre-existing ST segment depressions and/or
Q waves on resting ECG which considerably decreases the specificity
of ECG for diagonosing ongoing ACS.
 Furthermore,plasma biomarkers of cardiac damage,including
creatinine kinase(CK) AND Troponins, are often elevated at baseline.
 It is recommended to focus on temporal trends in troponin levels
and ST segment depressions and on angina equivalent symptoms
such as worsening dyspnoea.

www.escardio.org/guidelines
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
©ESC
ESC Classes of recommendations
Definition Wording to use
Class I Evidence and/or general agreement that a given
treatment or procedure is beneficial, useful,
effective.
Isrecommended
or isindicated
Class II Conflicting evidence and/or a divergence of opinion about the
usefulness/efficacy of the given treatment orprocedure.
ClassIIa Weight of evidence/opinion isin favour
of usefulness/efficacy.
Should be considered
ClassIIb Usefulness/efficacy is less well
established byevidence/opinion.
May be considered
Class III Evidence or general agreement that the given
treatment or procedureis not useful/effective,
and in some casesmay be harmful.
Is not recommended

©ESC
ESC Levels of evidence
Level of
evidenceA
Data derived from multiple randomized clinicaltrials or meta-analyses.
Level of
evidenceB
Data derived from a single randomized clinicaltrial or large non-
randomized studies.
Level of
evidenceC
Consensus of opinion of the experts and/or small studies, retrospective
studies, registries.

©ESC
Recommendations for patients with chronic kidney disease and
non-ST-segment elevation acute coronary syndrome (1)
Recommendations Class Level
Risk stratification in CKD
It is recommended to apply the same diagnostic and therapeutic strategies in
patients with CKD (dose adjustment may be necessary) as for patients with
normal renal function.
I C
It is recommended to assess kidney function by eGFR in all patients. I C

©ESC
Recommendations for patients with chronic kidney disease and
non-ST-segment elevation acute coronary syndrome (2)
Myocardial revascularization in patients with CKD
Use of low- or iso-osmolar contrast media (at lowest possible volume) are
recommended in invasive strategies.
I A
Pre- and post-hydration with isotonic saline should be considered if the
expected contrast volume is >100 mL in invasive strategies.
IIa C
As an alternative to the pre- and post-hydration regimen, tailored hydration
regimens may be considered.
IIb B
CABG should be considered over PCI in patients with multivessel CAD whose
surgical risk profile is acceptable and life expectancy is >1 year.
IIa B

©ESC
Figure 1
Diagnostic algorithm
and triage in acute
coronary syndrome.

©ESC
Table 1 Clinical implications of high-sensitivity cardiac troponin
assays (1)
Compared with standard cardiac troponin assays, hs-cTn assays:
• Have higher NPV for AMI.
• Reduce the 'troponin-blind' interval leading to earlier detection of AMI.
• Result in ~4% absolute and ~20% relative increases in the detection of type 1 MI
and a corresponding decrease in the diagnosis of unstable angina.
• Are associated with a 2-fold increase in the detection of type 2 MI.

©ESC
Table 1 Clinical implications of high-sensitivity cardiac troponin
assays (cTn) (2)
Levels of hs-cTn should be interpreted as quantitative markers of cardiomyocyte damage
(i.e. the higher the level, the greater the likelihood of MI):
• Elevations beyond 5-fold the upper reference limit have high (>90%) PPV for
acute type 1 MI.
• Elevations up to 3-fold the upper reference limit have only limited (50–60%) PPV
for AMI and may be associated with a broad spectrum of conditions.
• It is common to detect circulating levels of cTn in healthy individuals.
Rising and/or falling cTn levels differentiate acute (as in MI) from chronic cardiomyocyte
damage (the more pronounced the change, the higher the likelihood of AMI).

©ESC
Figure 2 Value of high-sensitivity cardiac troponin.
aThe limit of detection varies among the different hs-cTn assays
between 1 ng/L and 5 ng/L. Similarly, the 99th percentile varies
among the different hs-cTn assays, mainly being between 10 ng/L
and 20 ng/L.
hs-cTn assays (right) are reported in ng/L and provide identical
information as conventional assays (left, reported in μg/L) if the
concentration is substantially elevated, e.g. above 100 ng/L. In
contrast, only hs-cTn allows a precise differentiation between
‘normal’ and mildly elevated. Therefore, hs-cTn detects a relevant
proportion of patients with previously undetectable cardiac
troponin concentrations with the conventional assay who have hs-
cTn concentrations above the 99th percentile possibly related to
AMI.
??? = unknown due to the inability of the assay to measure in the
normal range

hs Troponin I
In - ng/ml
At 99th percentile
By - Access 2

©ESC
Table 2 Conditions other than acute type 1 myocardial infarction
associated with cardiomyocyte injury (= cardiac troponin
elevation) (1)
Tachyarrhythmias
Heart failure
Hypertensive emergencies
Critical illness (e.g. shock/ sepsis/ burns)
Myocarditisa
Takotsubo syndrome
Valvular heart disease (e.g. aortic stenosis)
Aortic dissection
Pulmonary embolism, pulmonary hypertension
Renal dysfunction and associated cardiac disease
Bold = most frequent conditions. aIncludes myocardial extension of endocarditis or pericarditis.

©ESC
Table 2 Conditions other than acute type 1 myocardial infarction
associated with cardiomyocyte injury (= cardiac troponin
elevation) (2)
Acute neurological event (e.g. stroke or subarachnoid haemorrhage)
Cardiac contusion or cardiac procedures (CABG, PCI, ablation, pacing, cardioversion, or
endomyocardial biopsy)
Hypo- and hyperthyroidism
Infiltrative diseases (e.g. amyloidosis, haemochromatosis, sarcoidosis, scleroderma)
Myocardial drug toxicity or poisoning (e.g. doxorubicin, 5-fluorouracil, herceptin, snake
venoms)
Extreme endurance efforts
Rhabdomyolysis
Bold = most frequent conditions. aIncludes myocardial extension of endocarditis or pericarditis.

For patients with CKD in whom all troponin levels are at or above the
99th percentile, a greater than 20 percent rise or fall in serially
measured troponins is probably an acceptable threshold change for a
positive AMI diagnosis, although there are no data available to support
this approach –
UptoDate 2023
 Use of serial troponin levels – Among patients with CKD who present with
signs and symptoms suspicious for AMI, a change in troponin concentration (ie,
rise or fall over three to six hours after presentation) should be used to define
AMI, rather than a single value obtained on presentation or even a rapid change
over a period of one hour.

©ESC
Figure 3 (1)
0 h/1 h rule-out and
rule-in algorithm using
high-sensitivity cardiac
troponin assays in
haemodynamically stable
patients presenting with
suspected non-ST-
segment elevation acute
coronary syndrome to the
emergency department.
aOnly applicable if CPO >3 h.

©ESC
Figure 3 (2) 0 h/1 h rule-out and rule-in algorithm using high-sensitivity
cardiac troponin assays in haemodynamically stable patients presenting
with suspected non-ST-segment elevation acute coronary syndrome to
the emergency department.
aOnly applicable if CPO >3 h.
0 h and 1 h refer to the time from first blood test. NSTEMI can be ruled out at presentation if
the hs-cTn concentration is very low. NSTEMI can also be ruled out by the combination of
low baseline levels and the lack of a relevant increase within 1 h (no 1h∆). Patients have a
high likelihood of NSTEMI if the hs-cTn concentration at presentation is at least moderately
elevated or hs-cTn concentrations show a clear rise within the first hour (1h∆). Cut-offs are
assay specific (see Table 3) and derived to meet predefined criteria for sensitivity and
specificity for NSTEMI.

©ESC
Table 3 Assay specific cut-off levels in ng/l within the 0 h/1 h
and 0 h/2 h algorithms (1)
0 h/1 h algorithm Very low Low No 1h ∆ High 1h ∆
hs-cTn T (Elecsys; Roche) <5 <12 <3 ≥52 ≥5
hs-cTn I (Architect; Abbott) <4 <5 <2 ≥64 ≥6
hs-cTn I (Centaur; Siemens) <3 <6 <3 ≥120 ≥12
hs-cTn I (Access; Beckman Coulter) <4 <5 <4 ≥50 ≥15
hs-cTn I (Clarity; Singulex) <1 <2 <1 ≥30 ≥6
hs-cTn I (Vitros; ClinicalDiagnostics) <1 <2 <1 ≥40 ≥4
hs-cTn I (Pathfast; LSI Medience) <3 <4 <3 ≥90 ≥20
hs-cTn I (TriageTrue; Quidel) <4 <5 <3 ≥60 ≥8
These cut-offs apply irrespective of age and renal function. Optimized cut-offs for patients above 75 years of age and patients with renal dysfunction have been
evaluated, but not consistently shown to provide better balance between safety and efficacy as compared to these universal cut-offs. The algorithms for additional
assays are in development.
hs-cTn = high-sensitivity cardiac troponin; TBD = to be determined.

©ESC
Table 3 Assay specific cut-off levels in ng/l within the 0 h/1 h
and 0 h/2 h algorithms (2)
0 h/2 h algorithm Very low Low No 2h ∆ High 2h ∆
hs-cTn T (Elecsys; Roche) <5 <14 <4 ≥52 ≥10
hs-cTn I (Architect; Abbott) <4 <6 <2 ≥64 ≥15
hs-cTn I (Centaur; Siemens) <3 <8 <7 ≥120 ≥20
hs-cTn I (Access; Beckman Coulter) <4 <5 <5 ≥50 ≥20
hs-cTn I (Clarity; Singulex) <1 Tbd Tbd ≥30 Tbd
hs-cTn I (Vitros; ClinicalDiagnostics) <1 Tbd Tbd ≥40 Tbd
hs-cTn I (Pathfast; LSI Medience) <3 Tbd Tbd ≥90 Tbd
hs-cTn I (TriageTrue; Quidel) <4 Tbd Tbd ≥60 Tbd
These cut-offs apply irrespective of age and renal function. Optimized cut-offs for patients above 75 years of age and patients with renal dysfunction have been
evaluated, but not consistently shown to provide better balance between safety and efficacy as compared to these universal cut-offs. The algorithms for additional
assays are in development.
hs-cTn = high-sensitivity cardiac troponin; TBD = to be determined.

©ESC
Figure 4 (1) Timing of the
blood draws and clinical
decisions when using
the European Society
of Cardiology
0 h/1 h algorithm.

©ESC
Figure 4 (2) Timing of the blood draws and clinical decisions when
using the European Society of Cardiology 0 h/1 h algorithm (2).
0 h and 1 h refer to the time points at which blood is taken. The turn-around time is the time
period from blood draw to reporting back the results to the clinician. It is usually about 1 h
using an automated platform in the central laboratory. It includes transport of the blood
tube to the lab, scanning of the probe, centrifugation, putting plasma on the automated
platform, the analysis itself, and the reporting of the test result to the hospital information
technology/electronic patient record. The turn-around time is identical whether using a hs-
cTn assay vs. a conventional assay, as long as both are run on an automated platform.
Adding the local turn-around time to the time of blood draw determines the earliest time
point for clinical decision making based on hs-cTn concentrations. e.g. for the 0 h time point,
time to decision is at 1 h if the local turn-around time is 1 h. For the blood drawn at 1 h, the
results are reported back at 2 h (1 h + 1 h) if the local turn-around time is 1 h. Relevant 1 h
changes are assay dependent and listed in Table 3.

©ESC
Recommendations for diagnosis, risk stratification, imaging, and
rhythm monitoring in patients with suspected non-ST-segment
elevation acute coronary syndrome (1)
Diagnosis and risk stratification
It is recommended to base diagnosis and initial short-term risk stratification
on a combination of clinical history, symptoms, vital signs, other physical
findings, ECG, and laboratory results including hs-cTn.
I B
It is recommended to measure cardiac troponins with high-sensitivity assays
immediately after admission and obtain the results within 60 min of blood
sampling.
I B
It is recommended to obtain a 12-lead ECG within 10 min after first medical
contact and to have it immediately interpreted by an experienced physician.
I B
0 h = time of first blood test; 1 h, 2 h, 3 h = 1, 2, or 3 h after the first blood test.

©ESC
Diagnosis and risk stratification (continued)
It is recommended to obtain an additional 12-lead ECG in case of recurrent
symptoms or diagnostic uncertainty.
I C
The ESC 0 h/1 h algorithm with blood sampling at 0 h and 1 h is
recommended if an hs-cTn test with a validated 0 h/1 h algorithm is
available.
I B
Additional testing after 3 h is recommended if the first two cardiac troponin
measurements of the 0 h/1 h algorithm are not conclusive and the clinical
condition is still suggestive of ACS.
I B

©ESC
As an alternative to the ESC 0 h/1 h algorithm, it is recommended to use the
ESC 0 h/2 h algorithm with blood sampling at 0 h and 2 h, if an hs-cTn test with
a validated 0 h/2 h algorithm is available.
I B
Additional ECG leads (V3R, V4R, V7–V9) are recommended if ongoing
ischaemia is suspected when standard leads are inconclusive.
I C
As an alternative to the ESC 0 h/1 h algorithm, a rapid rule-out and rule-in
protocol with blood sampling at 0 h and 3 h should be considered, if a high-
sensitivity (or sensitive) cardiac troponin test with a validated 0 h/3 h
algorithm is available.
IIa B

©ESC
The routine use of copeptin as an additional biomarker for the early rule-out of
MI should be considered where hs-cTn assays are not available.
IIa B
It should be considered to use established risk scores for prognosis estimation.
IIa C
For initial diagnostic purposes, it is not recommended to routinely measure
additional biomarkers such as h-FABP or copeptin, in addition to hs-cTn. III B

©ESC
Table 5 Major and minor criteria for high bleeding risk according
to the Academic Research Consortium – High Bleeding Risk at the
time of percutaneous coronary intervention (bleeding risk is high
if at least one major or two minor criteria are met)(2)
MAJOR MINOR
Moderate or severe baseline
thrombocytopeniab (platelet count
<100 × 109/L)
Chronic use of oral non-steroidal anti-
inflammatory drugs or steroids
Chronic bleeding diathesis Any ischaemic stroke at any time not
meeting the major criterion
Liver cirrhosis with portal hypertension
Active malignancyc (excluding non-melanoma
skin cancer) within the past 12 months
bBaseline thrombocytopenia is defined as thrombocytopenia before PCI.
cActive malignancy is defined as diagnosis within 12 months and/or ongoing requirement for treatment (including surgery, chemotherapy, or radiotherapy).

©ESC
Table 5 Major and minor criteria for high bleeding risk according
to the Academic Research Consortium – High Bleeding Risk at the
time of percutaneous coronary intervention (bleeding risk is high
if at least one major or two minor criteria are met)(3)
MAJOR MINOR
Previous spontaneous intracranial haemorrhage (at any time)
Previous traumatic intracranial haemorrhage within the past
12 months.
Presence of a brain arteriovenous malformation.
Moderate or severe ischaemic stroked within the past 6 months.
Recent major surgery or major trauma within 30 days prior
to PCI.
Non-deferrable major surgery on DAPT.
dNational Institutes of Health Stroke Scale score >5

©ESC
Figure 13
Central illustration.
Management strategy for
non-ST-segment elevation
acute coronary syndrome
patients.

©ESC
Figure 13 (1) Central illustration. Management strategy
for non-ST-segment elevation acute coronary syndrome
patients.

©ESC
patients.

Management of
CKD with Heart Failure

Pathophysiology of heart failure (HF) in chronic kidney disease (CKD) progressing to end-stage kidney

RECOMMENDATION
 When RAAS inhibitors,ARNI or SGLT2 INHIBITORS are started,initial decrease
in the glomerular filtration pressure decrease GFR and increase serum
creatinine.
 However,these changes are generally transient and occur despite
improvement in outcomes and slower worsening renal function in the long
term.
 So,transient decrease in renal function should not prompt their
interruption.
 An increase in serum creatinine of <50% above baseline,as long as it is
<3mg/dl,or a decrease of <10% from baseline,as long as eGFR
>25ml/min/1.73m2, can be considered as acceptable.
 With respect to diuretic therapy,small and transient rises in serum
creatinine during treatment of acute HF are not associated with poorer
outcomes when the patient is free of cogestion.

 Beta blockers reduce mortality even in HFrEF patients with
moderately severe (eGFR 30-44ml/min/1.73m2) renal
dysfunction,whereas limited evidence available regarding patients
with severe renal impairement (eGFR<30ml/min/1.73m2)
 Sacubitrill/valsartan,compaired with enalapril,leads to a slower
decline in renal function,despite slight increase in ACR.
 Patients with HF and concomitant CKD are higher risk of events but
the beneficial effects of MT are similar,if not greater,than in people
with normal renal function.

 While CKD and worsening renal fuction both
appear common in HFpEF as compared to in
HFmEF and HFrEF, they appear to be less
associated with worse outcomes in HFpEF than in
HFmEF and HFrEF.

KDIGO GUIDELINE:
CKD AND CVD
 1. It is recommended that all people with CKD be
considered at increased risk for cardiovascular
disease.(1A)
 2. It is recommended that the level of care for
ischemic heart disease offered to people with CKD
should not be prejudiced by their CKD.(1A)

 3. It is suggested that adults with CKD at risk for atherosclerotic
events be offered treatment with antiplatelet agents unless
there is an increased bleeding risk that needs to be balanced
against the possible cardiovascular benefits.(2B)
 4. It is suggested that the level of care for heart failure offered
to people with CKD should be same as is offered to those without
CKD.(2A)
 5.In people with CKD and heart failure, any escalation in therapy
and /or clinical deterioration should prompt monitoring of eGFR
and serum potassium concentration.(Not Graded)

CAVEATS WHEN INTERPRETING TESTS
FOR CVD IN PEOPLE WITH CKD
 BNP/N-terminal-proBNP(NT-proBNP)
1.In people with GFR <60ml/min/1.73m2(GFR categories G3a-
G5),we recommend that serum concentrations of BNP/NT-proBNP
be interpreted with caution and in relation to GFR with respect to
diagonosis of heart failure and assesement of volume status.(1B)
 Troponins
2.In people with GFR<60ml/min/1.73m2(GFR categories G3a-
G5),we recommend that serum concentrations of troponin be
interpreted with caution with respect to diagonosis of acute
coronary syndrome.(1B)

 Non-invasive testing
3.We recommend that people with CKD presenting chest
pain should be investigated for underlying cardiac disease
and other disorders according to same local practice for
people without CKD(and subsequent treatment should be
initiated similarly).(1B)
4.We suggest that clinicians are familiar with the
limitations of non-invasive cardiac tests(e.g,exercise
ECG,neuclear imaging,echocardiography etc.) in adults
with CKD and interpret the results accordingly.(2B)

Patients with CKD have high cardiovascular risk, with cardiovascular
death being the leading cause of death. Several
novel therapies to decrease the risk of cardiovascular
diseases in CKD are in clinical development or have been
already established, raising the hope that cardiovascular
risk in patients with CKD may be modifiable in the future.
Still, the lack of data from large cardiovascular outcome
trials in the high-risk group of patients with CKD
should be a call for action to ensure that novel therapeutic
options are assessed in dedicated trials in the CKD population, in particular in
those with advanced CKD,
thus paving the way toward a more evidence-based approach
to reduce cardiovascular risk in CKD
Conclusion

TAKE HOME MESSAGES
 Diagonosis of NSTE-ACS is challenging.
 Same diagonostic and therapeutic strategies should be
applied.
 Dose adjustment should be made whenever necessary.
 Low or iso-osmolar contrast media are recommened in
invasive strategies

 The level of care for ischemic heart disease offered to
people with CKD should not be prejudiced by their CKD.
 The level of care for heart failure offered to people with
CKD should be the same as is to those without CKD.
 Transient decrease in renal function should not prompt
interruption of therapy in heart failure.
 Beneficial effects of MT are similar to patients with normal
renal function.

 At the initiation of dialysis, all patients—
regardless of symptoms—require assessment for
cardiovascular disease (CAD, cardiomyopathy,
valvular heart disease, CBVD, and PVD), as well as
screening for both traditional and nontraditional
cardiovascular risk factors

Management of CKD in Ischemic Heart Disease

Management of CKD in Ischemic Heart Disease

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