Contrast-induced acute kidney injury and diabetic nephropathy

Calvin, Andrew D.; Misra, Sanjay; Pflueger, Axel

doi:10.1038/nrneph.2010.116

Cited by 94 publications

(85 citation statements)

References 132 publications

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“…This is especially true for procedures such as percutaneous cardiac interventions that often require large amounts of CM and entail intra-arterial CM administration [1][2][3][4]. Besides conditions such as pre-existing renal impairment and diabetes mellitus, volume depletion (dehydration) is a major risk factor for contrast media induced nephropathy (CIN) [1,2,4,5].…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

2015

J Urol Nephrol

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Dehydration is a major risk for contrast media (CM) induced acute kidney injury, yet prospective studies in human patients without ample hydration are not feasible. The freely drinking rat can serve as a model for hydropenic humans.We compared the effects of two CM, iso-osmolar iodixanol and lowosmolar iopamidol, on urine flow, urine viscosity and glomerular filtration rate (GFR) in non-hydrated rats, and studied the impact of hydration by saline. In four groups of rats, either iodixanol 320 mg iodine/mL or iopamidol 370 mg iodine/mL was injected as 1.5 mL bolus into the thoracic aorta. Two groups had access to drinking water only and two groups received additional saline infusion (4 mL/hour per kg) starting 60 min before CM injection. Urine was collected (10 min sampling periods), urine viscosity measured, and GFR determined by creatinine clearance. In nonprehydrated rats, iodixanol led to a massive increase in urine viscosity and a transient 50% drop in GFR. Iopamidol had a much stronger diuretic effect than iodixanol, urine viscosity increased much less and GFR was unaffected. Saline infusion blunted the viscosity rise and transient decline in GFR caused by iodixanol. It is concluded that the choice of CM and ample hydration are important elements in the prevention of CM induced kidney injury. Low-osmolar iopamidol has a better renal safety profile than iso-osmolar iodixanol, at least in non-hydrated subjects. Hydration by saline counteracts the renal tubular concentration of CM thereby alleviating the increase in urine viscosity and the decline in GFR.

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Section: Introductionmentioning

confidence: 99%

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

2015

J Urol Nephrol

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“…The degree of medullary vasoconstriction may markedly differ from the cortex, as may the factors involved [15,18,19]. Cortical vasoconstriction, or more precisely, preglomerular vasoconstriction is one cause of CM-induced reduction in the glomerular filtration rate (GFR) [15]. Preglomerular constriction can also reduce medullary flow, as descending vasa recta emerge from efferent arterioles; however, GFR reduction tends to reduce oxygen demand due to decreased workload of tubular reabsorbtion.…”

Section: Pathophysiology Of Cinmentioning

confidence: 99%

“…The influence of contrast media on renal haemodynamics may play a major role in the pathogenesis of CIN [14,15]. The outer medulla is especially vulnerable to hypoxia: oxygen requirements are high due to salt reabsorption in Henle's thick ascending limbs, but oxygen delivery is sparse.…”

Section: Pathophysiology Of Cinmentioning

confidence: 99%

“…Because medullary perfusion comprises <10% of total renal blood flow, the vasoconstrictive response of total renal blood flow to CM observed in several studies reflects cortical rather than medullary effects. The degree of medullary vasoconstriction may markedly differ from the cortex, as may the factors involved [15,18,19]. Cortical vasoconstriction, or more precisely, preglomerular vasoconstriction is one cause of CM-induced reduction in the glomerular filtration rate (GFR) [15].…”

Section: Pathophysiology Of Cinmentioning

confidence: 99%

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Effects of Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Contrast-Induced Nephropathy

Zhou

Duan

2013

Kidney Blood Press Res

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Contrast-induced nephropathy (CIN) is considered the third leading cause of iatrogenic acute kidney injury in high-risk patients undergoing radiographic procedures. The main mechanism leading to CIN is medullary hypoxia due to decreased renal blood flow, secondary to renal artery vasoconstriction and direct tubular toxicity by contrast medium. Furthermore, experimental data suggests that an activated renin-angiotensin-aldosterone system (RAAS) plays a role in the pathophysiology of CIN. However, the role of RAAS blockers, including angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in CIN is controversial. They have been reported to be effective in the prevention of CIN in previous studies, but some studies have concluded that they were associated with an increased risk of CIN, especially in patients with pre-existing renal impairment. In summary, there is no solid data to link ACE inhibitors and ARB to CIN, and larger randomised controlled trials are necessary to further investigate their role in the development of CIN. In this review, we discuss the pathophysiology of CIN, the role of RAAS on the development of CIN, and the effect of RAAS blockers on CIN.

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“…Contrast-induced acute kidney injury (CIAKI) is the revised name for what was formerly called radiocontrast-induced acute kidney injury [1,2,3]. CIAKI is a common and potentially serious complication of the administration of contrast media used for diagnostic imaging in many clinical situations including coronary angiography [4,5,6].…”

Section: Introductionmentioning

confidence: 99%

Relative and Absolute Changes in Urinary Neutrophil Gelatinase-Associated Lipocalin and Correlation with Small Increases in Serum Creatinine Levels after Coronary Angiography: An Observational Study

Souza

Reis²,

Botelho³

et al. 2015

Nephron

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Introduction/Aims: The Acute Kidney Injury Network classification is based on small increases in serum creatinine (sCr) for stage 1. This study investigated whether changes in the urinary concentration of neutrophil gelatinase-associated lipocalin (uNGAL) could predict small increases in sCr in patients undergoing coronary angiography. Methods: The uNGAL was measured before contrast infusion and 2 and 4 h afterwards. Patients were divided into 2 subgroups: G₁ (n = 103), where sCr increased by <0.3 mg/dl, and G₂ (n = 22), where sCr increased by ≥0.3 mg/dl 48 h after the angiography. To determine the sensitivity and specificity for the absolute and relative variations of uNGAL, a receiver operating characteristic curve analysis was performed. Results: In G₂, the uNGAL concentration increased over baseline values (15.9 vs. 9.2 ng/dl; p < 0.05), and it was also 2-fold higher in G₂ versus G₁ (15.9 vs. 8.0 ng/dl; p < 0.001). The uNGAL remains an independent predictor of the small increases in sCr, and, for an increase of 50% over baseline levels, it showed 60% sensitivity and 81% specificity. Conclusion: Changes in uNGAL concentration 2 h after the infusion of contrast media showed marginal sensitivity to predict small increases in sCr.

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Contrast-induced acute kidney injury and diabetic nephropathy

Cited by 94 publications

References 132 publications

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

Effects of Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Contrast-Induced Nephropathy

Relative and Absolute Changes in Urinary Neutrophil Gelatinase-Associated Lipocalin and Correlation with Small Increases in Serum Creatinine Levels after Coronary Angiography: An Observational Study

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