Chronic Renal Failure and Cardiovascular Disease: History
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Subjects: Cardiac & Cardiovascular Systems
Contributor:
Keren Skalsky

Coronary artery disease (CAD) is highly prevalent in patients with chronic kidney disease (CKD), with a linear increase in the risk of cardiovascular mortality with decreasing eGFR. The concomitant renal disease often poses a major challenge in decision making as symptoms, cardiac biomarkers and noninvasive studies for evaluation of myocardial ischemia have different sensitivity and specificity thresholds in this specific population.

  • chronic kidney disease
  • coronary artery disease
  • coronary angiography
  • kidney transplant
  • renal failure
  • myocardial infarction

1. Introduction: The Scope of the Clinical Problem

Coronary artery disease (CAD) is highly prevalent in patients with chronic kidney disease (CKD) [1], with a linear increase in the risk of cardiovascular mortality with decreasing eGFR [2][3]. The latter is reported to be twice as high in patients’ estimated glomerular filtration rate (eGFR) of 30–59 mL/min/1.73 m2, compared to individuals with normal kidney function, and three times higher at eGFR of 15–29 mL/min/1.73 m2 [4]. Concomitant renal disease poses a major challenge in decision making as symptoms, cardiac biomarkers and noninvasive studies for evaluation of myocardial ischemia have different sensitivity and specificity thresholds in this specific population. Iodinated contrast agents should be used with extreme caution to prevent further deterioration of renal function secondary to contrast induced nephropathy (CIN). Moreover, the effectiveness of coronary intervention in those patients is of great doubt as most clinical studies exclude patients with advance CKD. The resulting consequence might be the under treatment of cardiovascular risk factors and inappropriate, low rates of coronary angiography in patients with CKD, also known as “renalism” [5].

2. A Brief Review of the Pathophysiology

The pathophysiology of combined cardiovascular and kidney disease extends across several interfaces. First, conventional risk factors for atherosclerosis can affect both organs with coronary artery disease, renal artery stenosis, endothelial dysfunction and small vessel disease [6]. Second are the hemodynamic interactions, including resistant hypertension, fluid overload and major alterations in blood pressure with abnormal regulatory response [7]. Next is the activation of the renin–angiotensin–aldosterone system, which is recognized in both CKD and heart failure, and plays an important role in the maintenance of cardiovascular homeostasis [8][9]. Anemia and chronic inflammation can contribute to the overlap of morbidities, along with uremic toxins [10]. Lastly, the mineral-bone disorder complicating CKD causes hyperphosphatemia and positive calcium balance, which stimulate vascular calcifications, accelerated atherosclerosis and structural changes in the heart [11]. The phrase “cardiorenal syndrome” represents the mutual influence of the acute or chronic dysfunction of the heart or kidney on the other organ [12].

3. Basic Definitions

CKD is defined as the abnormality of kidney structure or function, present for more than 3 months, with implications for health. It is classified based on the eGFR category and albuminuria category. On the basis of eGFR and urine albumin measurements, chronic kidney disease is classified into six stages of eGFR (G1, 2, 3A, 3B, 4, and 5) and three proteinuria stages (A1, 2, and 3) [13] (Table 1).
Table 1. GFR categories in CKD.

GFR Category

GFR (mL/min/1.73 m2)

Terms

G1

≥90

Normal or high

G2

60–89

Mildly decreased

G3a

45–59

Mildly to moderately decreased

G3b

30–44

Moderately to severely decreased

G4

15–30

Severely decreased

G5 *

<15

Kidney failure

* 5D and 5T indicate end-stage renal disease patients who undergo chronic dialysis (5D) treatment or have undergone kidney transplantation (5T).

4. Chronic Coronary Syndrome and Renal Failure

4.1. Noninvasive Diagnostic Tests

Among patients with CKD, there are limited options for non-invasive diagnostic tests. The recently published European Society of Cardiology (ESC) guidelines regarding chronic coronary syndrome suggest using either coronary CTA or functional stress imaging as the preferred methods for risk stratification [14]. In patients with CKD, the risk of contrast-induced kidney damage is increased [3], and thus the use of coronary CTA is less acceptable. Moreover, patients with CKD, and especially those under dialysis, tend to have a high calcium score, which can reduce the coronary CTA specificity [15].
The next optional non-invasive testing would be the myocardial perfusion single-photon emission computed tomography (SPECT) test and stress echocardiography. Since patients with CKD, and especially advanced CKD and dialysis, have limited exercise capacity due to muscle fatigue, peripheral vascular disease, peripheral neuropathy, anemia, volume overload and other comorbidities, the Bruce protocol is not always possible. The alternative would be a dobutamine stress echocardiography (DSE) or SPECT scan with dipyridamole/adenosine infusion.
DSE is considered a good prognostic tool for the predictive evaluation of patients with CKD [16], but among renal transplant candidates, its sensitivity and specificity for the diagnosis of CAD was found be as low as 52% and 74%, respectively [17]. A single center experience of CAD screening using DSE in 40 hemodialysis patients found 0 sensitivity of the test. Authors concluded that, in CKD patients, the decision regarding coronary angiography should be based on other noninvasive tests and cardiovascular risk factors [18]. Moreover, adverse effects during DSE testing are relatively frequent, precluding the achievement of a target heart rate in about 5 to 10% of tests [19].

4.2. The Cardiac Catheterization, Coronary Revascularization Strategies and Pharmacotherapy

A retrospective study of patients on renal replacement therapy, aiming to determine the sensitivity and specificity of various noninvasive ischemic tests, found the thallium dipyridamole scintigraphy to have 80% sensitivity and only 37% specificity. The authors concluded that “angiography seems to be the only method to clearly document CAD in patients on renal replacement therapy” [20]. Nevertheless, the evidence regarding the efficacy of cardiac catheterization in the non-acute setting in patients with CKD is conflicting, as most cardiovascular trials excluded patients with advanced kidney disease. Moreover, there is paucity of data to confirm the prognostic benefit of angiography or even coronary revascularization among stable coronary patients with CKD.
The use of an iodinated contrast agent should be addressed aiming at minimizing exposure, and every effort should be made to minimized the potential damage to the kidneys, as detailed in chapter B.2 [3][4][21].
Overall decisions regarding the diagnostic and treatment modalities in CKD patients with suspected chronic coronary syndrome, should be tailor-made with careful consideration of the patient’s complaints, medical history, laboratory tests, images, renal function and prognosis. As a part of the integrated and multifactorial approach, the “heart team” forum should consult with nephrologists, diabetologists and primary care physicians on how to optimize the medical care for the heart, the kidneys and the cardiovascular risk factors altogether. This approach has been recently proven to improve cardiovascular outcomes in diabetic patients with CKD in a multicenter randomized control trial, with a long durability of protection [22].

4.3. Advanced CKD: Pre-Dialysis, Dialysis and Renal Transplant Candidates—Different Populations

The definition of advanced CKD has been generalized. Patients can be categorized into three subgroups: pre-dialysis patients, those on renal replacement therapy and renal transplant candidates. Each subgroup has unique features to be considered when choosing the diagnostic studies and treatment options in CAD.
Pre-dialytic patients should be carefully examined to prevent further deterioration of renal function, including avoiding certain drugs (as discussed in the next chapter) and minimizing iodine contrast exposure. The clinical presentation in this group may be conflicting as it is difficult to distinguish between effort dyspnea resulting from volume overload and that secondary to significant CAD stenosis. The consideration of nephrotoxic drugs and iodine contrast exposure are less crucial in patients already on renal replacement therapy, although there is even more limited data on the prognostic efficacy of drug therapy and PCI in this subgroup of patients, as the proportion of dialytic patients in clinical trials in mostly very small.

5. Acute Coronary Syndrome and Renal Failure

5.1. Cardiac Biomarkers in the Presence of Renal Failure

Increased levels of high-sensitivity cardiac troponin (hs-cTn) are necessary for the diagnosis of non-ST elevation myocardial infarction (NSTEMI) in the general population, and are broadly used in clinical practice to distinguish unstable angina from NSTEMI [21]. Impaired renal function is one of the major confounders of cardiac troponin concentration [23]. Increased levels of the cardiac biomarker troponin in patients with CKD are common. The raised values typically reflect the continuous myocardial damage caused by long-term exposure to uremic toxins, left ventricular hypertrophy, CAD and heart failure [24][25]. This might explain the fact that patients with troponin concentrations above 99th percentile have a two-fold greater risk of subsequent myocardial infarction or cardiac death at 1 year, regardless of the diagnosis [26][27]. Another suggested mechanism is reduced renal clearance causing increasing levels of troponin over time, as renal function deteriorates [25][28]. Recently published clinical trial in patients presented to the hospital with suspected ACS found that elevated hs-cTn levels increased as kidney function declined, from 10% in patients with normal kidney function to 66% at an eGFR of less than 30 mL/min/1.73 m2. The proportion of patients with type 1 myocardial infarction decreased from 74% to 35% [29].
These data make the interpretation of the laboratory results and the diagnosis of NSTEMI more challenging. In CKD patients, the 0/1 h hs-cTn algorithm of the ESC was found to have comparable sensitivity of rule out (i.e., a threshold of <5 ng/L can be used to rule out myocardial injury). Nevertheless, the specificity of rule in and overall efficacy was decreased [30]. Furthermore, those patients might have ECG abnormalities associated with electrolyte abnormalities and left ventricular hypertrophy, which make clinical evaluation even more challenging. Therefore, ECG changes should be differentiated from old abnormalities and absolute changes in cardiac troponin should be assessed when considering the diagnosis of acute MI [21].

5.2. The Cardiac Catheterization, Coronary Revascularization Strategies and Pharmacotherapy

Although individuals with CKD have a worse prognosis in the setting of MI than individuals with normal renal function, they are less likely to receive an early invasive strategy and potent P2Y12 inhibitors as recommended by the guidelines [31][32][33][34]. Data from the SWEDEHEART registry published in 2009 found that an early invasive strategy in patients with NSTEMI and CKD stage G2 to G4 is associated with better outcomes and greater 1-year survival. The benefit declined with lower renal function, and is less certain in those with stage G5 CKD or on dialysis [35]. A more recent study on both STEMI and NSTEMI patients found invasive management to be associated with significantly lower in-hospital mortality in comparison to a conservative approach in all CKD stages, including patients on hemodialysis [36].
When choosing an invasive strategy, measures should be taken to prevent acute chronic kidney injury and CIN, as those may increase the risk of major adverse cardiovascular events and mortality. The definition of acute kidney injury is based on an elevation of ≥0.3 mg/dL in creatinine levels 48 h post PCI [37], although recent publications suggest using serum and urine biomarkers for the early diagnosis of the complication, before the expected serum creatinine increases. Suggested biomarkers vary and include Cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), β2-microglobulin and inflammatory cytokines IL18 and TNFα [38][39][40]. Current ESC guidelines recommend the use of low volume iso or hypo-osmolar contrast materials during the cardiac catheterization of individuals with CKD. Adequate hydration prior and post intervention is the mainstay of acute kidney injury prevention, with the administration of 1 mL/kg/h isotonic saline 12 h before contrast exposure, and continued for 24 h after the procedure. To prevent over-congestion, the recommended volume of fluids is lowered to 0.5 mL/ kg/h if left ventricle ejection fraction is lower than 35% or New York Heart Association (NYHA) functional classification is above 2 [3][21][41]. High-dose statins were also described as beneficial [42].
The principles leading to the decision about the revascularization method are similar to those detailed in chapter A.2. CABG should be considered over PCI in suitable patients with multivessel CAD, whose surgical risk profile is acceptable and life expectancy is above 1 year [43][44].
The choice of antiplatelet agents should be considered carefully according to each individual bleeding and ischemic risk as CKD is one of the risk factors for both bleeding and ischemic events. Nevertheless, in the clinical scenario of ACS, the dual antiplatelet therapy was found to have significant net benefits in preventing cardiovascular events among patients with renal insufficiency [21]. Specifically, the treatment with ticagrelor in patients with CKD and ACS compared with clopidogrel was found to reduce ischemic events and mortality with no significant increase in major bleedings. Data from the PLATO (Platelet Inhibition and Patient Outcomes) trial suggested that the absolute reduction of ischemic events in CKD patients treated with ticagrelor was even more pronounced compared to those with normal renal function (4.7%/year vs. 1%/year) irrespective to the therapeutic strategy (conservative vs. invasive; percutaneous vs. surgical). The trial excluded patients receiving dialysis [45]. The efficacy and safety of prasugrel compared to ticagrelor were tested in the ISAR-REACT 5 trial (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment).
Key massages for the diagnosis and treatment in patients with acute coronary syndrome and CKD are summarized in Table 2.
Table 2. Key messages in acute coronary syndrome and kidney disease.

Diagnosis

  • Increased levels of the cardiac biomarker troponin are common, thus absolute changes in cardiac troponin should be assessed when considering the diagnosis of acute MI.

Treatment

  • Early invasive strategy in ACS and CKD stage G2 to G4 is preferred.

  • CABG should be considered over PCI in suitable patients with multivessel CAD, whose surgical risk profile is acceptable and life expectancy is above 1 year.

  • The treatment with new P2Y12 inhibitors, ticagrelor and prasugrel, in patients with CKD and ACS, is preferred over clopidogrel.

This entry is adapted from the peer-reviewed paper 10.3390/jcm11051335

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