Understanding and preventing contrast-induced acute kidney injury

Abstract

Contrast-induced acute kidney injury (CIAKI) occurs in up to 30% of patients who receive iodinated contrast media and is generally considered to be the third most common cause of hospital-acquired AKI. Accurate assessment of the incidence of CIAKI is obscured, however, by the use of various definitions for diagnosis, the different populations studied and the prophylactic measures put in place. A deeper understanding of the mechanisms that underlie CIAKI is required to enable reliable risk assessment for individual patients, as their medical histories will determine the specific pathways by which contrast media administration might lead to kidney damage. Here, we highlight common triggers that prompt the development of CIAKI and the subsequent mechanisms that ultimately cause kidney damage. We also discuss effective protective measures, such as rapidly acting oral hydration schemes and loop diuretics, in the context of CIAKI pathophysiology. Understanding of how CIAKI arises in different patient groups could enable a marked reduction in incidence and improved outcomes. The ultimate goal is to shape CIAKI prevention strategies for individual patients.

Quercetin protects against radiocontrast medium toxicity in human renal proximal tubular cells

“…Radiocontrast media induced‐Acute kidney injury (CI‐AKI) is still an important consequence of the use of RCM, occurring in up to 30% of patients who receive iodinated contrast media and it is considered to be the third most common cause of hospital acquired AKI (Fahling, Seeliger, Patzak, & Persson, ). It has been proposed that the toxic effects of RCM could be due to oxidative stress and subsequent generation of reactive oxygen species (ROS) (Andreucci, Solomon, & Tasanarong, ; Pisani et al, ) and changes in intracellular signaling pathways, including the upregulation of cell signaling molecules that have been implicated in cell death/inflammation, such as the JNKs (Andreucci, ; Andreucci et al, ; Andreucci, Faga, Russo et al, ; Lee, Sheu, Yen, Lai, & Chang, ).…”

The glucagon‐like peptide‐1 receptor agonist Exendin‐4, ameliorates contrast‐induced nephropathy through suppression of oxidative stress, vascular dysfunction and apoptosis independent of glycaemia

“…With regard to the role of diabetes, all markers for renal function, oxidative stress, vascular dysfunction, and apoptosis as well as the renal histology were more adversely affected in the diabetic CIN group compared to the respective non‐diabetic control. This outcome is not surprising, considering the vast evidence identifying the role of the diabetic hemodynamic changes, medullary hypoxia and oxidative stress in aggravating the pathophysiology of CIN …”

“…CM‐induced apoptosis was previously explained by the disturbance of mitochondrial enzyme activity and mitochondrial membrane potential in tubular epithelium, or by the activation of shock proteins and the synchronous inhibition of cytoprotective enzymes and prostaglandins . On the tissue level, exposure to CM caused vacuolar degeneration in tubular epithelium, which can be a result of direct cell toxicity through cell membrane damage …”

Repeated mechanical thrombectomy for acute ischemic stroke in a dialysis patient: A case report and literature review

“…Contrast-induced nephropathy (CIN) is a main cause of acute renal failure, occurring within 72 hours after the use of iodinated radiographic contrast material (CM). 23 Risk factors for CIN include diabetes, cardiovascular disease, collagen vascular disease, dehydration, aminoglycoside antibiotics, the use of non-steroidal anti-inflammatory drugs, and old age, 24,25 and the most important predictor of CIN risk is chronic kidney disease (CKD), which increases the risk by more than 20 times. 22 The pathophysiology of CIN is not fully understood, but it may be caused by direct tubular toxicity and renal ischemic injury.…”