Impact of diabetic and pre-diabetic state on development of contrast-induced nephropathy in patients with chronic kidney disease

Toprak, Ömer; Ci̇ri̇t, Mustafa; Yeşìl, Murat; Bayata, Serdar; Tanrısev, Mehmet; Varol, Umut; Ersoy, Rifki; Esi, Ertap

doi:10.1093/ndt/gfl636

Cited by 95 publications

(78 citation statements)

References 29 publications

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“…Therefore, the hyperglycemia itself makes the kidney more susceptible to CIAKI. 22 Several in vitro studies also 11,12 demonstrated that high-glucose condition enhanced the susceptibility of renal cells to the cytotoxic effects (apoptosis) of both the HOCM and LOCM. In other words, the combination of high-glucose and contrast media has a synergistic effect on accentuating renal tubular apoptosis and therefore increasing the risk of CIAKI.…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…7 Many studies have found Diabetes Mellitus (DM) as an independent risk factor for CIN. 5,15,30 Toprak et al showed that in patients with preexisting renal insufficiency, Diabetes Mellitus independently increased the risk of development of CIN and need for dialysis as opposed to pre-DM and Normal Fasting states, 31 while Berns showed that the incidence of CIN in diabetics was increased if serum creatinine is more than 4.0 mg% compared to 2 to 4 mg%. Clearly, there is a synergistic effect of diabetes and pre existing renal insufficiency.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for contrast induced nephropathy: A study among Italian patients

Evola

Lunetta

Macaione

et al. 2012

Indian Heart Journal

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Atherosclerosis Percutaneous coronary intervention Coronary angiography a b s t r a c tThis study aimed to make a profile of patients at highest risk of developing contrast induced nephropathy (CIN) in order to take appropriate prevention measures. 591 patients undergoing coronary procedures were divided into two groups: patients with (CIN-group) and without (no-CIN) an increase in creatinine level equal or more than 25% from baseline values within 24e48 h after the coronary procedure. All patients underwent an accurate anamnesis, objective exam, hematochemical measurements, and diagnostic exams. The results of this study while confirming that, average age ( p ¼ 0.01), diabetes mellitus IntroductionContrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure, accounting for 10% of all cases of hospital-acquired renal failure. 1 It is commonly defined as an acute deterioration of the renal function characterized by a significant increase in serum creatinine levels, usually more than 0.5 mg/dl (44 mmol/L) or 25% of baseline levels, within 24e48 h after exposure to a contrast agent compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded. 2 The CIN is associated with increased mortality and morbidity and costs, 3e5 in fact, although usually transient, its resolution needs 1e3 weeks on average, the impairment of renal function may be permanent in some cases with the risk of progression towards chronic renal failure and the necessity of a temporary or permanent dialysis. 6 Prevention is the key to reduce the incidence of CIN and it begins with identification of the high risk patient coupled with appropriate peri-procedural management. Many studies have been conducted to identify the main risk factors for CIN, in fact many score systems have been proposed 7e12 and increasing number of guidelines have been suggested in literature 13,14 to help lessen the complication of CIN. Available online at www.sciencedirect.com journal homepage: w ww.el sevier.com/locate /ihj i n d i a n h e a r t j o u r n a l 6 4 ( 2 0 1 2 ) 4 8 4 e4 9 1

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“…In study by Berns et al [1], CIN occurred in 27% of diabetics with baseline serum creatinine 2.0 to 4.0 mg/dL and in 81% of those with serum creatinine >4.0 mg/dL. In a study by Toprak et al [28], a total of 421 patients with CockcroftGauldt estimated creatinine clearance between 15 and 60 mL/min were divided into three groups: diabetes mellitus (n ¼ 137; glucose 126 mg/dL), pre-diabetes (n ¼ 140; glucose between 100 and 125 mg/dL), and normal fasting glucose (n ¼ 144; glucose < 100 mg/ dL). CIN, defined as an increase of 25% in creatinine over baseline within 48 hr of angiography, occurred in 20% of diabetics, 11.4% of pre-diabetics, and 5.5% of patients with normal fasting glucose level.…”

Section: Diabetes Mellitusmentioning

confidence: 94%

Contrast‐induced nephropathy

Pučelíková

Dangas

Mehran

2007

Cathet Cardio Intervent

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Contrast induced nephropathy (CIN) is an iatrogenic disorder, resulting from exposure to contrast media. Contrast-induced hemodynamic and direct cytotoxic effects on renal structures are highly evident in its pathogenesis, whereas other mechanisms are still poorly understood. CIN is typically defined as an increase in serum creatinine by either 0.5 mg/dl or by 25% from baseline within the first 2-3 days after contrast administration. Although rare in the general population, CIN has a high incidence in patients with an underlying renal disorder, in diabetics, and the elderly. The risk factors are synergistic in their ability to produce CIN. The best way to prevent CIN is to identify the patients at risk and to provide adequate peri-procedural hydration. The role of various drugs in prevention of CIN is still controversial and warrants future studies. Despite remaining uncertainty regarding the degree of nephrotoxicity produced by various contrast agents, in current practice non-ionic low-osmolar contrast media are preferred over the high-osmolar contrast media in patients with renal impairment.

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Impact of diabetic and pre-diabetic state on development of contrast-induced nephropathy in patients with chronic kidney disease

Abstract: Our data support that patients with DM are at a higher risk of developing CIN, but patients with pre-DM are not at as high a risk for developing CIN as diabetes patients.

Cited by 95 publications

References 29 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 for contrast induced nephropathy: A study among Italian patients

Contrast‐induced nephropathy

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