CI-AKI occurs in approximately 10–20 % of patients with CKD undergoing cardiac catheterization [25]. It is directly associated with the volume of contrast media used in the procedure [26]. CI-AKI is associated with longer hospital stays, higher costs, and worse cardiovascular outcomes [27]. Some pre-procedure properties, such as anemia and proteinuria [28], may help identify patients most at-risk for developing CI-AKI. Other known risk factors for CI-AKI include congestive heart failure, hypotension, age greater than 75 years, peripheral vascular disease and diabetes. Heart failure alone seems more predictive than GFR [29]. Peri-procedural bleeding has also been shown to be associated with CI-AKI, with more severe bleeding resulting in increased incidence of CI-AKI [30]. Prevention is currently focused primarily on ensuring adequate hydration pre- and post-procedure [25]. Other strategies include limiting the quantity of contrast medium used in the procedure (for example, by using biplane angiography or adjunctive intravascular ultrasound). Complex procedures may be staged to minimize exposure to large volumes of contrast.

Patients with CKD have baseline platelet dysfunction that may increase the likelihood of perioperative bleeding during coronary angiography and percutaneous intervention. Patients with CKD who present with ST-segment elevation myocardial infarction have significantly higher rates of major bleeding than patients without CKD (19.3 vs 6.7 % in one large trial [31]).

Screening for anemia is often part of the routine pre-procedural evaluation for patients undergoing coronary angiography. Due to erythropoietin deficiency, patients with advanced CKD are often anemic prior to the procedure. Correction of significant anemia may be required prior to cardiac catheterization.

The femoral approach was for many years the standard approach for arterial access in the cardiac catheterization laboratory. More recently, the popularity of radial arterial access has grown as its advantages have been proven. However, the radial approach also carries the risk of radial artery thrombosis or occlusion. In patients with advanced CKD in whom dialysis may be required in the future, maintaining the integrity of upper extremity vasculature is important for future creation of an arteriovenous fistula. At this time, data are limited regarding the impact of radial arterial access on arteriovenous fistula formation in patients with CKD [32]. CKD and potential future dialysis requirements remain one factor for consideration by the interventionalist when selecting an access site in the cardiac catheterization laboratory.

In patients undergoing coronary angiography who require percutaneous intervention, multiple studies have shown that placement of a drug-eluting stent, when no contraindication exists, is preferable to bare metal stent placement. Drug-eluting stent placement results in lower rates of major adverse cardiac events at 1 year [33]. The randomized, multicenter RENAL-DES study demonstrated reduced rates of clinical restenosis for drug-eluting stents compared to bare metal stents in patients with CKD [34].

Patients with CKD have higher rates of vascular complication at the access site, particularly for femoral access sites. These complications are more likely to require blood transfusion [35]. Peri-procedural myocardial injury, as reflected by troponin levels, is also more likely to occur in patients with CKD who are undergoing elective percutaneous intervention [36]. Despite these potential complications, cardiac catheterization should be pursued when indicated. Additional risks for patients with CKD should be taken into consideration on an individual basis, but appropriate therapy should generally not be withheld in this population. The 23,262 subject SWEDEHEART trial concluded that: Early invasive therapy is associated with greater 1-year survival in patients with non-ST-elevation myocardial infarction and mild-to-moderate renal insufficiency, but the benefit declines with lower renal function, and is less certain in those with end-stage renal failure or on dialysis [37].

The benefit of aspirin in medical treatment of coronary artery disease is clear, and extends to patients with CKD. Its use at low dose in patients with CKD does not lead to increased major bleeding, or contribute to worsening CKD [44]. Current guidelines recommend that aspirin be prescribed for secondary prevention of coronary artery disease in patients with CKD. It may also be used for primary prevention, even in patients who require dialysis. Monitoring for gastrointestinal bleeding is reasonable.

Clopidogrel is a thienopyridine that inhibits the adenoside diphosphate receptor, and therefore helps to block platelet aggregation. Use and safety of clopidogrel in patients with CKD has been studied. Clopidogrel is recommended for up to 1 year after an acute coronary syndrome, and for a variety of other indications. Several studies have shown that clopidogrel can be used safely in CKD patients with acute coronary syndrome, with reduced mortality and without increased risk of bleeding [45]. However, a sub-analysis of the Clopidogrel for the Reduction of Events during Observation (CREDO) trial suggested that patients with mild or moderate CKD may receive less benefit from clopidogrel [46]. In addition, patients with CKD may have lower response to clopidogrel as measured by adenosine diphosphate-induced platelet aggregation, which may lead to poorer outcomes [47].

Prasugrel is a third-generation thienopyridine P2Y12 receptor antagonist. It has potent P2Y12 inhibition and offers a faster time to peak effect than clopidogrel. The TRITON-TIMI 38 trial demonstrates its superiority over clopidogrel in patients with CKD and in patients without CKD but this benefit was observed at the cost of a smaller but significant increase in bleeding complications [48]. Pharmacokinetics and pharmacodynamics of prasugrel do not appear to differ between healthy subjects and patients with moderate CKD [49]. Dose adjustment in renal impairment is not necessary. There is limited published data regarding its use in patients with severe CKD.

Ticagrelor is a reversible P2Y12 receptor antagonist. Ticagrelor, like prasugrel, offers more effective platelet inhibition than clopidogrel. In the PLATO trial, ticagrelor significantly reduced the primary endpoint (a composite of cardiovascular death, myocardial infarction and stroke) at 12 months when compared with clopidogrel in patients with acute coronary syndrome [50]. Patients receiving ticagrelor in this study did not have significantly increased major bleeding but did have numerically more non-procedure related bleeding. Side effects of ticagrelor include ventricular pauses and shortness of breath. Ticagrelor is cleared hepatically and does not require dose adjustment in patients with chronic kidney disease, although there is limited published data regarding use in patients with severe CKD and end-stage renal disease.

Heparin is frequently used in the cardiac catheterization laboratory, and is a standard of care treatment in patients with acute coronary syndrome. Unfractionated heparin is only available parenterally and requires monitoring and dose adjustment in patients with CKD [51]. Low molecular weight heparin (LMWH) has similar efficacy and more convenient dosing. However, LMWH is renally cleared and its use in patients with CKD may result in supratherapeutic levels and increased risk of bleeding. It is frequently avoided in patients with advanced CKD, and if used, does require dose adjustment based on renal function and measurement of Anti-Xa levels.

Glycoprotein (GP) IIb/IIIa inhibitors may improve outcomes in some subsets of patients with acute coronary syndrome. Currently available agents include abciximab, tirofiban and eptifibatide. Abciximab does not require dose adjustment for renal dysfunction; tirofiban and eptifibatide do require dose adjustment. Each of these agents has been studied in patients with CKD, but further study is needed. National Kidney Foundation clinical practice guidelines recommend abciximab or tirofiban for CKD patients who require dialysis [52].

Bilvalrudin is a direct thrombin inhibitor. In a substudy of the ACUITY trial, Bivalirudin therapy was compared with heparin plus a glycoprotein IIb/IIIa inhibitor in patients with CKD undergoing percutaneous intervention for acute coronary syndrome. There were no significant differences in ischemic outcome, but patients with CKD who received bivalirudin monotherapy had fewer bleeding events at 30 days [53]. Adjustments for renal dysfunction must be made, and patients with GFR less than 30 mL/min/1.73 m² were excluded from the study.

Beta-blockers are a cornerstone of management and secondary prevention in patients with coronary heart disease. Their benefit in reducing the risk of future cardiovascular events extends to patients with chronic kidney disease [54], although their use in this population is more limited than in the general population. In one large trial, even after myocardial infarction the utilization of beta-blocker therapy declined as renal function worsened [55]. In patients with CKD and systolic heart failure, beta-blockers result in a 28 % relative reduction in all-cause mortality, and a 34 % relative reduction in cardiovascular mortality [56]. Side effects of beta-blockers include bradycardia and hypotension. Most beta-blockers do not require dose adjustment for renal impairment.

Statin therapy is recommended for both primary and secondary prevention of coronary artery disease in a wide variety of clinical scenarios. Studies of statin therapy specifically in patients with CKD are less common. A meta-analysis of statin use in patients with varying stages of CKD demonstrated a significant reduction in fatal and non-fatal cardiovascular events in patients using statin therapy, but no overall mortality benefit [57]. One recent study of CKD patients following percutaneous coronary intervention demonstrated reduced all-cause mortality in patients prescribed statin therapy [58]. Most statins have some degree of renal excretion [59], but in general do not require dose adjustment. It should be noted that the American College of Cardiology and American Heart Association 2013 Guidelines for lipid management provide no recommendations for lipid lowering in dialysis patients due to insufficient information [60].

Use of ACE inhibitors or angiotensin-2 receptor blockers is recommended for most patients with CKD, as it has been shown to slow the progression of kidney disease and may reduce cardiovascular risk [61]. Doses should be titrated carefully, and patients should be monitored for the development of hyperkalemia or hypotension.

Nitrate therapy may be used to treat angina pectoris. Extended release isosorbide dinitrate does not accumulate in patients with CKD and no dose adjustment is needed.

Co-existence of other conditions such as diabetes mellitus and hypertension is very common in patients with CKD. Aggressive management of risk factors is important for all patients with coronary artery disease.