Introduction
CKD, chronic kidney disease, impaired renal autoregulation, hyperuricemia, tubulopathy, AKI, metabolic syndrome, CI-AKI, hospitalized, acute kidney injury
CONTRAST-INDUCED ACUTE KIDNEY INJURY, DIABETES MELLITUS, HEMODYNAMIC INSTABILITY, HYPERURICEMIA, METABOLIC SYNDROME, OXIDATIVE STRESS, HYPERTENSION, CORONARY ARTERY DISEASE, TUMOR LYSIS SYNDROME
Contrast-induced acute kidney injury (CI-AKI) is considered the third commonest cause of acute kidney injury among hospitalized patients. The incidence of CI-AKI has gradually increased especially with percutaneous coronary intervention (PCI). It is more noticed among patients experiencing primary PCI due to hemodynamic instability and inadequate prophylaxis [Uric acid is a biological factor which has been shown to be a neurostimulator, proinflammatory and activator of the innate immune response as well as have a pro- and antioxidant effect. These effects might provide a possible explanation for the association of uric acid with the development of chronic hypertension, diabetes mellitus, metabolic syndrome, coronary artery disease as well as chronic kidney disease. Regarding chronic kidney disease (CKD), several clinical studies have concluded that hyperuricemia is an important risk predictor for the onset and progression of CKD [Recently, uric acid has been proposed to be a potential mediator of acute kidney injury (AKI) via both systemic effects of hyperuricemia and local effects via crystal-dependent mechanisms and crystal-independent mechanisms. In crystal-dependent mechanisms, hyperuricemia, especially in tumor lysis syndrome, leads to crystal-induced tubulopathy, with elevated tubular pressure and increased renal vascular resistance leading to a decline in GFR and eventually AKI. In the crystal-independent mechanisms, it has been experimentally shown that without crystal deposition, even mild hyperuricemia may increase the risk for AKI, via pro-inflammatory and anti-angiogenic mechanisms. Uric acid induces renin-angiotensin-aldosterone system (RAAS) activation, increased inflammatory mediators (MCP-1, ICAM), increased reactive oxygen radicals, decreased nitric oxide bioavailability, impaired renal autoregulation, and subsequent decline in GFR. All these postulated effects can potentially increase the susceptibility for AKI [Febuxostat, a non-purine selective xanthine oxidase inhibitor, has a strong hypouricemic effect with no serious negative outcomes, even for patients with CKD stages 1–3. Febuxostat can also have reno-protective effects in addition to the urate-lowering therapy due to its inhibitory effect on oxidative stress and inflammatory biomarkers [Some clinical studies were conducted to compare the reno-protective and uric acid-lowering therapy effects between febuxostat and allopurinol among CKD patients [