The clinical and renal consequences of contrast-induced nephropathy

Finn, William F.

doi:10.1093/ndt/gfl213

Cited by 159 publications

(160 citation statements)

References 33 publications

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“…1 And, it is closely related to prolonged hospitalization and higher rates of in-hospital, 1-and 5-year mortality. [2][3][4] Patients with diabetes are at particularly high risk of developing CIAKI. A recent metaanalysis found 43 possible risk factors for CIAKI, but diabetes was the only independent predictor of CIAKI.…”

Section: Introductionmentioning

confidence: 99%

Role of ERK1/2 and JNK phosphorylation in iodine contrast agent-induced apoptosis in diabetic rat kidneys

Jiao

Liu

et al. 2015

Renal Failure

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Background: The risk of contrast-induced acute kidney injury (CIAKI) is significantly increased in patients with diabetes mellitus. This study aimed to investigate molecular mechanisms of contrast media-induced apoptosis in diabetic rat kidneys, especially the involvement of ERK1/2 and JNK signal pathways. Methods: Diabetic Sprague-Dawley rats were induced by intraperitoneal injection of streptozotocin. Ten weeks later the normal and diabetic rats were administered high-osmolar contrast media (HOCM; meglumine diatrizoate) or normal saline (10 mL/kg) injection for 2 consecutive days. At 24 h after the operation, the rats were sacrificed, the blood samples were collected for examining serum creatinine and the kidneys were collected for determining the expression of caspase-3 by immunohistochemistry and the expression of Bcl-2, Bax, upstream signal molecule p-JNK, and p-ERK1/2 by western blotting. Results: The serum creatinine was significantly increased in diabetes + contrast media group (DC group) after operation compared with in the diabetic group (D group; 103.89 ± 9.01 mmol/L vs. 71.52 ± 7.03 mmol/L, p50.05). While creatinine clearance rate (Ccr) was significantly decreased in DC group after operation (1.49 ± 0.33 mL/min vs. 2.60 ± 0.54 mL/min, p50.05). Especially, in the diabetic kidney, the expression of caspase-3 was also significantly increased after intravenous injection of HOCM compared with normal saline. The expression level of upstream signal molecule p-JNK protein was apparently increased, but p-ERK1/2 protein was significantly decreased (both p50.05). Conclusions: The ionic HOCM-induced renal cells apoptosis in diabetic rats through activating the caspase-3 apoptotic pathway, which might be mediated by upstream MAPK (inhibiting p-ERK1/2 expression and promoting p-JNK expression) signal pathways.

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Section: Introductionmentioning

confidence: 99%

Role of ERK1/2 and JNK phosphorylation in iodine contrast agent-induced apoptosis in diabetic rat kidneys

Jiao

Liu

et al. 2015

Renal Failure

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“…[1][2][3][4] The rates of CIN vary, depending on the study definitions employed and underlying risk factors, and range from 0.6% to 30% or higher among risk groups. [5][6][7][8] CIN is also associated with increased duration of hospitalisation and early and late mortality. In-hospital mortality due to CIN ranges from 7% to 22%.…”

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confidence: 99%

Risk factors and outcomes of contrast-induced nephropathy in hospitalised South Africans

et al. 2016

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Despite preventive guidelines, iatrogenic contrast-induced nephropathy (CIN) ranks third as a cause of hospital-acquired AKI, impacts significantly on morbidity and mortality, and is associated with longer stays in hospitals, with higher medical costs. [1][2][3][4] The rates of CIN vary, depending on the study definitions employed and underlying risk factors, and range from 0.6% to 30% or higher among risk groups. [5][6][7][8] CIN is also associated with increased duration of hospitalisation and early and late mortality. In-hospital mortality due to CIN ranges from 7% to 22%. [9] McCullough et al. [9] reported early mortality of 1.1% in controls, 7.1% in CIN patients, and 35% in CIN patients that required dialysis. Owing to increased comorbidities, hospitalised patients have increased risk for developing CIN compared with ambulatory patients .[10]Inflammation and endothelial dysfunction, together with reactive oxygen species (ROS), are implicated in the pathogenesis of CIN. [8] Iodinated contrast media directly injures the renal tubular epithelium by producing ROS radicals that cause intra-renal vasoconstriction leading to ischaemia and death of tubular cells. [8,10,11] Serum albumin is an important antioxidant that reduces the formation of oxygen free radicals and is important in expanding intravascular volume. [12,13] However, the role of serum albumin in reducing the incidence of CIN remains unexplored.Sub-Saharan Africa has a dearth of data on rates of CIN. This study investigated the rates of CIN together with the influence of serum albumin, albuminuria, age, haemoglobin, and glomerular filtration rate (GFR) levels on CIN and patient outcomes. Methods Study design, setting and populationThis study was a prospective observational study conducted at Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa, from 1 July 2014 to 30 July 2015. Ethical approval was obtained from the human research ethics committee (HREC) of the University of the Witwatersrand and informed written consent was obtained from all patients. We consecutively recruited hospitalised patients undergoing computed tomography (CT) and angiography from the Divisions of Radiology and Cardiology, respectively. The following exclusion criteria were used: <18 years of age; evidence of pre-existing AKI (clinical or laboratory); end-stage renal disease (ESRD); renal replacement therapy (RRT); prior contrast media administration in the preceding 7 days; pregnancy; or incomplete data. Study proceduresThe study physician reviewed participants' medical records and examined the participants in order to determine pre-existing risk factors for CIN. The medical records were reviewed to determine patient duration of hospitalisation, dialysis requirements and mortality. Study phlebotomists collected blood samples prior to and post contrast media administration. Pre contrast, urine was collected and analysed for microalbuminuria using the Chemistrip Micral 30 immune assay test (Roche 11544039172). Serum creatinine was analysed using the Jaff...

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“…With the increasing use of contrast media in diagnostic and interventional procedures, CIN has become the third leading cause of hospital-acquired acute renal failure, accounting for 10 to 25% of all acute renal failure cases, [1][2][3][4] despite the introduction of newer and safer contrast media, the improvement of hydration protocols, and the introduction of additional preventive strategies (e.g., acetylcysteine). 5 Patients with CIN have been reported to have increased frequency of clinical adverse events, including permanent impairment of renal function, longer hospital stay, and increased 1-yr mortality rate 6,7 ; therefore, there is a great requirement for new, effective strategies for prevention of CIN.…”

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confidence: 99%

Asialoerythropoietin Prevents Contrast-Induced Nephropathy

Yokomaku¹,

Sugimoto²,

Kume³

et al. 2008

Journal of the American Society of Nephrology

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Strategies to prevent contrast-induced nephropathy (CIN) are suboptimal. Erythropoietin was recently found to be cytoprotective in a variety of nonhematopoietic cells, so it was hypothesized that the nonhematopoietic erythropoietin derivative asialoerythropoietin would prevent CIN. Nephropathy was induced in rats by injection of the radiocontrast medium Ioversol in addition to inhibition of prostaglandin and nitric oxide synthesis. Administration of a single dose of asialoerythropoietin before the induction of nephropathy significantly attenuated the resulting renal dysfunction and histologic renal tubular injury. Contrast-induced apoptosis of renal tubular cells was inhibited by asialoerythropoietin both in vivo and in vitro, and this effect was blocked by a Janus kinase 2 (JAK2) inhibitor in vitro. Furthermore, phospho-JAK2/signal transducer and activator of transcription 5 (STAT5) and heat-shock protein 70 increased after injection of asialoerythropoietin, suggesting that the effects of asialoerythropoietin may be mediated by the activation of the JAK2/STAT5 pathway. Overall, these findings suggest that asialoerythropoietin may have potential as a new therapeutic approach to prevent CIN given its ability to preserve renal function and directly protect renal tissue.

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The clinical and renal consequences of contrast-induced nephropathy

Cited by 159 publications

References 33 publications

Role of ERK1/2 and JNK phosphorylation in iodine contrast agent-induced apoptosis in diabetic rat kidneys

Role of ERK1/2 and JNK phosphorylation in iodine contrast agent-induced apoptosis in diabetic rat kidneys

Risk factors and outcomes of contrast-induced nephropathy in hospitalised South Africans

Asialoerythropoietin Prevents Contrast-Induced Nephropathy

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