Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Michele Andreucci, Teresa Faga, Raffaele Serra, Giovambattista De Sarro, Ashour Michael, Michele Andreucci, Teresa Faga, Raffaele Serra, Giovambattista De Sarro, Ashour Michael

Abstract

An important side effect of diagnostic contrast drugs is contrast-induced acute kidney injury (CI-AKI; a sudden decrease in renal function) occurring 48-72 hours after injection of a contrast drug that cannot be attributed to other causes. Its existence has recently been challenged, because of some retrospective studies in which the incidence of AKI was not different between subjects who received a contrast drug and those who did not, even using propensity score matching to prevent selection bias. For some authors, only patients with estimated glomerular filtration rate <30 mL/min/1.73 m2 are at significant risk of CI-AKI. Most agree that when renal function is normal, there is no CI-AKI risk. Many experimental studies, however, are in favor of the existence of CI-AKI. Contrast drugs have been shown to cause the following changes: renal vasoconstriction, resulting in a rise in intrarenal resistance (decrease in renal blood flow and glomerular filtration rate and medullary hypoxia); epithelial vacuolization and dilatation and necrosis of proximal tubules; potentiation of angiotensin II effects, reducing nitric oxide (NO) and causing direct constriction of descending vasa recta, leading to formation of reactive oxygen species in isolated descending vasa recta of rats microperfused with a solution of iodixanol; increasing active sodium reabsorption in the thick ascending limbs of Henle's loop (increasing O2 demand and consequently medullary hypoxia); direct cytotoxic effects on endothelial and tubular epithelial cells (decrease in release of NO in vasa recta); and reducing cell survival, due to decreased activation of Akt and ERK1/2, kinases involved in cell survival/proliferation. Prevention is mainly based on extracellular volume expansion, statins, and N-acetylcysteine; conflicting results have been obtained with nebivolol, furosemide, calcium-channel blockers, theophylline, and hemodialysis.

Keywords: AKI; ARF; acute kidney injury; contrast media; intracellular signaling; renal failure.

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
After intravascular injection, contrast drugs cause immediate and short-term renal vasodilatation. Notes: Vasodilatation is very soon followed by renal vasoconstriction that causes 1) a decrease in renal blood flow (RBF) and glomerular filtration rate (GFR) and 2) vasa recta constriction (favored by increased effects of angiotensin II, adenosine, and endothelin), with consequent medullary hypoxia. Though contrast drugs are rapidly filtered by renal glomeruli and excreted with urine, their high osmolality will cause osmotic diuresis. This is responsible for an increase in sodium delivery to the medullary ascending limb of Henle’s loop and consequent increase in sodium reabsorption. However, in this medullary area there is already significant O2 demand due to the low blood supply. The increased O2 consumption due to increased sodium reabsorption will cause significant medullary hypoxia with epithelial tubular injury that further decreases the GFR; a contribution to this obstruction is made by proinflammatory cytokines and complement activation that lead to protein precipitation. The latter injury is also due to a direct cytotoxic effect of contrast drugs, because of their high concentration in the tubular lumen due to the reabsorption of tubular fluid in the proximal tubules. The endothelial cells directly damaged by contrast drugs will lead to formation of reactive oxygen species (ROS) that will decrease nitric oxide, thereby contributing to vasa recta constriction and medullary hypoxia. Renal medullary hypoxia itself leads to formation of ROS. The final result will be an important decrease in GFR. Adapted from Andreucci M, Faga T, Pisani A, et al. Pathogenesis of acute renal failure induced by iodinated radiographic contrast media. Austin J Nephrol Hypertens. 2014;1(1):1005. Abbreviations: All, angiotensin ll; NO, nitric oxide; PG, prostaglandin; ONOO–, peroxynitrite anion.

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