Does Aspirin Affect The Kidneys

Does Aspirin Affect The Kidneys – Keywords Abstract1. Chronic kidney disease is a risk factor for acute coronary artery disease2. Acute kidney injury 3. Impact of chronic kidney disease in ACS4 patients. CKD and ACS diagnosis5. Prognostic impact of CKD in ACS6 patients. CKD and treatment options in ACS7. Conclusions Author Participation Approval and ethical consent to participate Funding Acknowledgments Conflicts of interest References

Cardiology Unit, Department of Clinical and Molecular Medicine, Faculty of Medicine and Psychology, Sapienza University of Rome, Sant’Andrea Hospital, 00189 Rome, Italy

Does Aspirin Affect The Kidneys

Posted: September 30, 2021 | Updated: December 20, 2021 | Received: December 21, 2021 | Published: February 8, 2022

Aspirin Side Effects, Uses, Dosage, Interactions, Alternatives

Background: Coronary artery disease (CAD) and chronic kidney disease (CKD) can interact. Patients with CAD and CKD are at increased risk of ischemic and bleeding events. Methods: In this review, we summarized the existing literature focusing on the relationship between renal failure and acute coronary syndrome (ACS) in terms of risk factors, complications and prognosis. We also discuss the best evidence-based strategies to prevent renal decline in patients with CAD. Results: CKD patients received less invasive treatment (percutaneous or surgical revascularization) and effective antithrombotic drugs. However, recent evidence suggests that it may benefit from selective invasive treatment, particularly in cases of ACS. Conclusion: CKD and CAD patients represent a challenging population, randomized controlled trials and meta-analyses are needed to determine the best treatment strategies during episodes of ACS.

The prevalence of chronic kidney disease (CKD) in the general population is 13% and increases to 20-25% in patients with acute coronary syndrome (ACS) [1]. CKD is an independent risk factor for cardiovascular events, often presenting with pauci-symptomatic clinical signs and atypical ECG changes, making the diagnosis of ACS more challenging.

It has been found that as kidney function declines, cardiovascular risk increases. Indeed, patients with renal impairment are most likely to experience an acute myocardial infarction (AMI) [2] and dialysis patients have a higher incidence of ACS. Indeed, chronic inflammation, hyperhomocysteinemia and oxidative stress leading to endothelial dysfunction, coronary calcification, and the use of immunosuppressants are all associated with atherosclerosis and accelerated coronary events [3]. Regular exposure of blood to the dialysis membrane can also cause platelet reactivity (PR), which increases the risk of ischemia and resistance to antithrombotic therapy in dialysis patients [ 4 , 5 ].

According to the Acute Kidney Injury (AKI) Network, AKI is defined as an absolute increase in serum creatinine (sCr) of 0.3 mg/dL or more or a 1.5-fold or more increase from baseline. This definition was accepted in the general guidelines developed by the KDIGO (Kidney Disease – Improving Global outcome) organization and is now most commonly used for the causes of acute kidney injury [5].

Aspirin: Uses, Side Effects, Dosage & Reviews

An additional definition related to contrast agents used during percutaneous coronary intervention (PCI) has been proposed for AKI. This is based on an absolute increase in sCr levels of at least 0.5 mg/dL (44 microMol/L) within 48–72 hours after contrast exposure or a relative increase in sCr

Several factors, such as parenchymal ischemia, direct and indirect tubular or endothelial injury, contribute to the development of contrast-induced AKI [7]. Contrast agent (CM) increases viscosity in the renal tubules, leading to renal hypoperfusion through vasoconstriction [ 8 ]. In particular, hypoxic damage caused by CM affects the core and cortical regions, resulting in a decrease in estimated glomerular filtration rate (eGFR) and concomitant tubular damage. An increase in reactive oxygen species and a decrease in nitric oxide lead to renal vasoconstriction, which ultimately causes further tubular and endothelial damage. This effect varies with CM osmolarity and viscosity, with high osmolarity iodine-based contrast media (HOCM) causing maximal damage. In addition, HOCM affects the shape of erythrocytes, causing difficulties in the passage of the vasa recta and hypoxia as a result of the medullary region [8, 9, 10, 11].

The main risk factor associated with contrast-induced AKI is pre-existing renal impairment [5]. The risk of induction-AKI contrast becomes clinically apparent with initial sCr concentrations

[12]. Other risk factors for the development of contrast-induced AKI are diabetes mellitus (DM), high blood pressure, heart failure, old age, volume deficit, hemodynamic instability, myeloma, concomitant use of nephrotoxic drugs, and high volume or high osmolality of CM [13, 14]. Based on this evidence, several predictive models have been identified to reduce the risk of developing contrast-induced AKI after PCI with prophylactic targeted therapy, guide the decision-making process, and avoid additional renal injury [ 5 ]. In particular, pre- and post-contrast exposure models and biomarkers for predicting competition-induced AKI were proposed [ 14 , 15 , 16 , 17 , 18 ].

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The basic strategies for preventing and treating contrast-induced AKI are aimed at restoring blood flow. The high osmolarity and increased viscosity of CM can be reduced by adequate hydration to reduce the concentration of CM. To date, several hydration strategies have been developed. In the POSEIDON trial, fluid-guided left ventricular end-diastolic pressure reduced contrast-induced AKI compared with standard care [15]. Another strategy is based on the use of the RenalGuard® System, in which the loss caused by the infusion of furosemide (0.25 mg/kg) is compensated by an intravenous infusion of the same saline solution. In the REMEDIAL II trial, use of the RenalGuard® System resulted in a reduction in the incidence of contrast-enhanced AKI [16].

European guidelines recommend the use of a pre-procedural infusion of isotonic solutions, starting 12 hours before angiography and continuing for at least 24 hours afterwards, to reduce the risk of contrast-induced AKI, especially if eGFR is present.

. Pretreatment with high doses of statins is also recommended for patients who have not received statins [19, 20, 21]. Based on the correlation between high osmolarity and contrast-induced AKI, iso-osmolar CM may have a beneficial effect on renal injury, but there are conflicting data in the literature [22, 23].

Although the use of adequate hydration remains a cornerstone in preventing the development of contrast-induced AKI, much attention has been paid to reducing CM volume. Several strategies have been developed in this regard, including the use of automated systems for contrast injection, such as: ACIST CVi® (ACIST Medical Systems, Eden Prairie, MN, USA), MEDRAD® Avanta System (MEDRAD Inc. ., Warrendale, PA, USA) and the AVERT™ system, then the second-generation DyeVert™ system (Osprey Medical, Minnetonka, MN, USA). In the AVERT trial, the AVERT™ system, while demonstrating a reduction in CM volume compared with conventional methods, failed to reduce the incidence of contrast-induced nephropathy (CIN), suggesting that it reduces volume. Acquired CM is not sufficient to reduce the incidence of AKI [24]. The DyeVert™ system was recently evaluated in a retrospective analysis [25] of 112 patients with ACS undergoing primary PCI: use of the DyeVert resulted in a significantly lower volume of contrast agent used (130 [120–188] mL vs. 99 [69–136] mL; p

Chronic Kidney Disease: The Canary In The Coal Mine

0.001) and lower incidence of contrast-induced AKI (odds ratio [OR] = 0.37; 95% confidence interval [CI] 0.14–0.95; p = 0.047) compared with propensity score-matched controls. An ongoing trial (ClinicalTrials.gov Identifier: NCT04714736) is evaluating the DyeVert™ system in the ACS setting.

Some studies have focused on non-angiography-guided PCI [26]. One of them, the MOZART study, showed how effective ultrasound-guided PCI reduced the need for CM. In another study, a total of 31 patients with advanced CKD (eGFR

) who underwent elective PCI without contrast medium were analyzed. A minimum contrast coronary angiogram was performed initially, followed by intravascular ultrasound (IVUS)-guided zero-contrast PCI (no earlier than 7 days after angiography). There were no significant cardiovascular events or CIN [27]. However, further trials are needed to demonstrate the effective ability of this imaging-guided PCI strategy to reduce the incidence of CIN [28, 29].

About 25–30% of all patients with ACS have at least low renal function [30, 31]. Noninvasive assessment of renal function is mandatory for every patient with confirmed or suspected ACS admitted to the hospital [32]. Impaired renal function and CKD affect every step of the diagnostic and therapeutic pathway of ACS and have important prognostic value.

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High-sensitivity cardiac troponin (hs-cTn) is the best biomarker for early diagnosis of ACS, but it is chronically elevated in chronically ill patients, limiting its clinical utility [ 31 , 33 ]. In a retrospective study, 3,295 chest pain patients were classified into subgroups based on age, sex, and renal function. AMI was diagnosed in 84% of patients and hs-cTn levels were comparable between AMI and non-AMI patients in all subgroups. Optimal cut-off value of high-sensitivity cardiac troponin I (hscTnI) to diagnose AMI in CKD (eGFR)

) was higher in men than in women, and 100% specificity was achieved in all groups, except in men over 60 years of age with severe eGFR decline (

CKD may improve the short- and long-term prognosis of patients with ACS (Figure 1). Patients with moderate and severe CKD have significantly increased hospitalizations, mortality and

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