Contrast-induced kidney injury: mechanisms, risk factors, and prevention

Abstract

In general, iodinated contrast media (CM) are tolerated well, and CM use is steadily increasing. Acute kidney injury is the leading life-threatening side effect of CM. Here, we highlight endpoints used to assess CM-induced acute kidney injury (CIAKI), CM types, risk factors, and CIAKI prevention. Moreover, we put forward a unifying theory as to how CIAKI comes about; the kidney medulla's unique hyperosmolar environment concentrates CM in the tubules and vasculature. Highly concentrated CM in the tubules and vessels increases fluid viscosity. Thus, flow through medullary tubules and vessels decreases. Reducing the flow rate will increase the contact time of cytotoxic CM with the tubular epithelial cells and vascular endothelium, and thereby damage cells and generate oxygen radicals. As a result, medullary vasoconstriction takes place, causing hypoxia. Moreover, the glomerular filtration rate declines due to congestion of highly viscous tubular fluid. Effective prevention aims at reducing the medullary concentration of CM, thereby diminishing fluid viscosity. This is achieved by generous hydration using isotonic electrolyte solutions. Even forced diuresis may prove efficient if accompanied by adequate volume supplementation. Limiting the CM dose is the most effective measure to diminish fluid viscosity and to reduce cytotoxic effects.

The Role of Serum Cystatin C in the Early Detection of Contrast-Induced Nephropathy after Coronary Intervention

“…The results of the present study are in agreement with the most results obtained by others reports Kato et al and Mehran et al [19][20][21][22][23][24][25][26][27]. In present study was found a highly significant increment in serum creatinine and cystatin C while decrease in eGFR 24 hours after angiography (p<0.001, 0.01) when compared between two groups (CIN+, CIN-).…”

“…In present study was found a highly significant increment in serum creatinine and cystatin C while decrease in eGFR 24 hours after angiography (p<0.001, 0.01) when compared between two groups (CIN+, CIN-). This result is consistent with Wang et al, Liu et al and Nozue et al founded serum level of cystatin C is a reliable marker for CIN at 24 hours p<0.001 and serum creatinine increased significantly at 48 hours, also study carried by Wacker-Gussmann et al [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31] found that cystatin C level and the cystatin C/creatinine ratio independently predict the risk of CIN in patients undergoing coronary angiography, but another study by Ribichini et al [32] found a significant increase in serum cystatin C concentrations 12 hours earlier than serum creatinine, therefore a rise of serum cystatin C at 12 hours from baseline was the earliest predictor of CIN than serum creatinine [18].…”

“…This may be explained by a larger amount of contrast media we used in PCI group [22]. Therefore contrast volume >100 ml may be identified as a risk factor of occurrence CIN [23,24]. Although all patients involved in our study were given low-osmolar contrast agent Omnipaque (Iohexol) 350 mg/1 ml), osmality of 844.…”

“…Although several studies have revealed that serum cystatin C cut off level >1.2 or >1.18 or >1.3 mg/l, 94% sensitivity and 48% specificity is more accurate for diagnostic CIN than serum creatinine [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. While study obtained by Ribichini et al found that absolute changes in serum creatinine proved more accurate than serum cystatin C for predicting CIN at an early stage 12 hours after angiography [18].…”

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

“…In addition, hydration decreases urine viscosity, which, in turn, may speed up excretion of the contrast medium 27, 28. Hence, rather than the average‐rate long‐term fluid administration, more‐rapid hydration may help attenuate the increase in urine viscosity attributed to contrast administration, thereby aiding in contrast excretion and shortening the length of time tubular cells are exposed to the contrast medium.…”