The potential use of biomarkers in predicting contrast-induced acute kidney injury

Abstract

Contrast-induced acute kidney injury (CI-AKI) is a problem associated with the use of iodinated contrast media, causing kidney dysfunction in patients with preexisting renal failure. It accounts for 12% of all hospital-acquired kidney failure and increases the length of hospitalization, a situation that is worsening with increasing numbers of patients with comorbidities, including those requiring cardiovascular interventional procedures. So far, its diagnosis has relied upon the rise in creatinine levels, which is a late marker of kidney damage and is believed to be inadequate. Therefore, there is an urgent need for biomarkers that can detect CI-AKI sooner and more reliably. In recent years, many new biomarkers have been characterized for AKI, and these are discussed particularly with their use in known CI-AKI models and studies and include neutrophil gelatinase-associated lipocalin, cystatin C (Cys-C), kidney injury molecule-1, interleukin-18, N-acetyl-β-d-glucosaminidase, and L-type fatty acid-binding protein (L-FABP). The potential of miRNA and metabolomic technology is also mentioned. Early detection of CI-AKI may lead to early intervention and therefore improve patient outcome, and in future any one or a combination of several of these markers together with development in technology for their analysis may prove effective in this respect.

Time evolution of methotrexate‐induced kidney injury: A comparative study between different biomarkers of renal damage in rats

“…Under normal conditions, filtered NGAL is almost completely reabsorbed by the proximal tubules resulting in minimal uNGAL levels, but it is highly expressed in damaged renal tubules and can be quickly detected in urine . There are several clinical studies and reviews remarking the potential role of the increased urinary excretion of NGAL as a reliable diagnostic and prognostic biomarker of acute renal injury of different aetiologies . Surprisingly, the present results showed that not only uNGAL does not increase but also it decreases at all the time points evaluated after MTX administration.…”

Comparison of nephrotoxicity between two gadolinium-contrasts, gadodiamide and gadopentetate in patients with mildly diminished renal failure

“…In addition, gadodiamide slightly but significantly reduced CCr (P = 0.039) and eGFR (P = 0.039) in patients with stage 2 CKD. It is well known that cystatin-C rises more rapidly than serum-creatinine when GFR decreases (Andreucci et al, 2016). Taken together, these findings suggest that gadodiamide has slight, but clinically unimportant, nephrotoxicity in subgroups of patients with CKD.…”

“…Second, administration of the nonionic contrast medium gadodiamide slightly, but significantly, increased serum cystatin-C (P = 0.028), whereas administration of the ionic contrast medium gadopentetate had no effect on renal function. Cystatin-C is a cysteine protease inhibitor produced by nucleated cells at a constant rate and found to be a potential biomarker of early stages of iodinated CIN, which could indicate acute kidney injury (AKI) earlier than Serum-creatinine (Ling et al, 2008;Andreucci et al, 2016). Third, CKD subgroup analysis showed that gadodiamide significantly increased cystatin-C in patients with stage 1 (P = 0.047), but not stages 2 and 3, CKD.…”

Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise

“…Both KIM-1 and NGAL are thought to be "kidney troponin" and reflect AKI before creatinine level increases. There are studies showing that uNGAL is increased 1 h [19] and uKIM-1 2 h after kidney damage [19][20][21][22]. One of the aims of this study was to investigate if these markers are sensitive enough to discover very mild and short lasting kidney dysfunction.…”