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Abstract

Aim:

Comparative assessment of some blood and urine laboratory parameters in patients with type 2 diabetes depending on the development of contrast-induced acute kidney injury (CI-AKI).

Materials and Methods:

A retrospective analysis was conducted in two groups of diabetic patients who underwent EVCRP. The first group included patients who developed CI-AKI (n = 29), while the second group consisted of patients without complications (n = 27). The average age of patients was 58.79 ± 1.27 years. CI-AKI was defined as an increase in serum creatinine concentration by ≥25% from baseline within 48 h post-procedure. The control group consisted of 20 healthy volunteers with a mean age of 57.9 ± 2.27 years. The diagnosis of CI-AKI was established based on clinical and laboratory research methods and consultations with specialists.

Results:

During the entire post-procedural observation period in the CI-AKI− group, the blood creatinine concentration remained significantly lower compared with the CI-AKI+ group (statistically significant intergroup differences were observed on the 2nd and 4th postprocedural days [P < 0.001] and on the 6th to 10th postprocedural days [P < 0.05]). According to anamnestic data, the duration of diabetes was comparable. However, glycemia (according to the concentration of glycated hemoglobin) in the CI-AKI+ group was significantly higher than in the CI-AKI− group (P < 0.001). Blood lipid concentrations were significantly higher in patients with diabetes compared to the control group. A highly significant difference was observed in cholesterol levels between the diabetes and control groups (P < 0.001). Additionally, triglyceride levels were significantly elevated in the CI-AKI+ group compared to the control group (P < 0.05), and a similar significant difference was noted between the CI-AKI− group and the control group (P < 0.05). In this case, the concentration of blood cholesterol was comparable in both groups of diabetes.

Conclusions:

The study identified several risk factors associated with developing CI-AKI in patients with diabetes mellitus following EVCRP. These findings highlight the importance of glycemic control and metabolic regulation in reducing CI-AKI risk in diabetic patients. Future research should focus on preventive strategies to optimize glucose levels and lipid profiles to mitigate renal complications in this patient population.

Introduction

Contrast-induced acute kidney injury (CI-AKI) is the third most common hospital-acquired kidney injury after AKI induced by renal hypoperfusion and nephrotoxic drugs. The incidence of CI-AKI is significantly increased in patients with diabetes mellitus. Diabetic nephropathy is an independent risk factor for chronic kidney disease (CKD) and CI-AKI.¹ CI-AKI has a significant adverse effect on the prognosis of patients and is associated with increased hospitalization time and treatment costs.² Research is being conducted worldwide on the pathogenesis and effective preventive therapy of CI-AKI. Recent studies have shown that pathogenetic mechanisms of kidney injury during endovascular procedures may include factors such as the role of hyperglycemia, immunological changes, and common signaling pathways.³ Hyperglycemia activates lipid peroxidation, associated with vasoconstriction and insufficient kidney oxygen supply. Inflammatory and toxic damage can develop both in the acute period and the post-infectious phase against the background of the rehabilitation period. Presently, the etiology of CI-AKI is not completely clear, and studies on the relationship between CI-AKI and DN are limited. Therefore, the analysis of the pathogenetic mechanisms of contrast nephropathy development against the background of type 2 diabetes mellitus and the development of effective preventive therapy methods is an urgent problem of modern medicine.⁴ Therefore, the analysis of pathogenetic mechanisms of the development of contrast nephropathy against the background of type 2 diabetes mellitus and the development of methods of effective preventive therapy is a pressing problem of modern medicine.

Our country is currently conducting large-scale work to improve the health care system, diagnostic methods, treatment, and prevention of complications of diseases. According to world statistics, CKD develops in approximately 15% of people in the general population and in every second patient with hypertension and diabetes. In Uzbekistan, the prevalence of CKD has been steadily rising. In 2018, 107,659 patients with CKD were officially registered nationwide, with an incidence rate of 3272.3 cases per 1 million people. Among them, 23,261 individuals developed CKD as a result of diabetes mellitus.

Radiological examinations play an increasingly important role in diagnosing and treating many pathological conditions, making it necessary to use iodine-containing contrast agents more and more often.⁵ The concept of acute renal failure caused by using iodine-containing contrast agents has changed and expanded in recent years. Initially, this complication was referred to as contrast-induced nephropathy (CIN). The concepts of post-contrast acute kidney injury and CI-AKI appeared in cases where there is an unambiguous connection between the use of iodine-containing contrast and impaired renal function.⁶ The Committee on Contrast Media Safety of the European Society of Urogenital Radiology proposes the following criteria for CI-AKI: an increase in serum creatinine concentration of 0.5 mg/dL (44.2 μmol/L) or more, or more than 25% from baseline, within 3 days after intravascular injection of iodinated contrast, if other causes of acute kidney injury have been excluded.⁷ Then, the creatinine concentration continues to increase for another 3–5 days and decreases to the initial level by day 10–14.⁸ The KDIGO (The Kidney Disease: Improving Global Outcome 2023) criteria for CI-AKI include an increase in creatinine concentration by 0.3 mg/dL or 1.5–1.9 times from the initial level after the use of iodine-containing contrast for 48–72 h.⁹ DM, with its acute and chronic complications, is a common disease that is becoming a pandemic, a pathology associated with secondary lesions of various organs and systems. Although recent studies do not consider DM a direct risk factor for CI-AKI, it is a predisposing factor for the development of CIN.¹⁰ DN is a late chronic complication of DM and an independent risk factor for CKD and CI-AKI.¹¹ The incidence of CI-AKI increases in patients with kidney damage, especially in patients with DN.¹² The data show that the incidence of CI-AKI is approximately 13% in patients without diabetes and 5.7%–29.4% in diabetics.¹³ The pathophysiology of CI-AKI is mainly associated with two mechanisms: hypoxic damage to the renal parenchyma (hypoxia of the renal medulla) and the toxic effect of the contrast agent on the renal capillaries and tubules.¹⁴ Hyperglycemic status is associated with an increase in the production of free radicals, which subsequently aggravates the described mechanisms.¹⁵

Material and Methods

The study included patients with diabetes who had undergone EVCRP. Two groups of patients were retrospectively formed. The study included 56 patients with type 2 DM. Group 1 (CI-AKI+) included 29 patients who developed CI-AKI in the postprocedural period. Group 2 (CI-AKI−) included 27 patients with an uncomplicated postprocedural period, and the average age of patients was 58.79 ± 1.27 years. The control group consisted of 20 healthy volunteers with a mean age of 57.9 ± 2.27 years. The diagnosis of CI-AKI was established based on clinical and laboratory research methods and consultations with specialists, according to the World Health Organization’s Recommendations (2016). The stage of diabetic nephropathy was determined according to the KDIGO Clinical Practice Guidelines’ recommendations. The inclusion criteria for the study were patients aged 20–65 with type 2 diabetes, the estimated glomerular filtration rate (eGFR) level greater than 60 mL/min, and no contraindications to EVRCP. In the CI-AKI group, an increase in venous blood creatinine levels of more than 25% was observed within 48 h after the endovascular procedure. The determination of GFR by endogenous creatinine clearance is effective using the CKD-EPI formula. This study did not include patients with congenital kidney pathology, asymmetry, kidney cysts, wrinkled kidneys, or hydronephrosis who had undergone surgical interventions on the kidneys and ureters. Statistical data processing was done on a personal computer using Microsoft Excel 2016 and IBM SPSS Statistics 23. The study was conducted in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments. Ethical approval was obtained from the local institutional review board. Written informed consent was obtained from all participants.

Results

A retrospective analysis revealed that in diabetic patients from both groups, the baseline serum creatinine concentration before the endovascular procedure was significantly elevated, exceeding the upper limit of the normal reference range. Specifically, the levels were 90.41 ± 1.85 µmol/L in the CI-AKI+ group and 96.89 ± 1.40 µmol/L in the CI-AKI− group (P < 0.05), indicating preexisting renal function impairment. On the second day after EVCRP, in the CI-AKI+ group, there was a significant increase in blood creatinine concentration, which was a criterion for including patients in the group. In the CI-AKI− group, there was also an increase in creatinine concentration. Still, it did not reach clinical and statistical significance (62.69% vs. 3.17%, P < 0.001—the significance of the difference in relative dynamics between groups). Subsequently, the concentration of creatinine continued to increase, reaching a maximum on the fourth post-procedure day: the relative dynamics in the CI-AKI+ group were 65.06% versus 16.12% in the CI-AKI− group (P < 0.001 significance of the difference in relative dynamics between groups). The creatinine concentration in both groups decreased, reaching the initial values in the CI-AKI+ group by the 10th day after EVCRP. At the same time, in the CI-AKI− group, by the sixth day of observation and subsequently, the creatinine concentration decreased significantly below the initial values, which is probably associated with both the hydration carried out after EVCRP and the use of antiplatelet therapy and lifestyle modification. During the entire postprocedural observation period in the CI-AKI− group, the blood creatinine concentration remained significantly lower compared to the CI-AKI+ group (P < 0.001—statistical significance of intergroup differences on the 2nd and 4th postprocedural days; P < 0.05—statistical significance of intergroup differences on 6th to 10th postprocedural days) (Table 1).

Table 1.

Dynamics of Blood Creatinine Concentration in Patients with Diabetes Who Underwent EVCRP Depending on the Development of CI-AKI

Indicator	Days	CI-AKI+ (n = 29)	CI-AKI− (n = 27)	P value
Creatinine, µmol/L	1	90.41 ± 1.85	96.89 ± 1.40	P < 0.05
Creatinine, µmol/L	2	145.66 ± 3.30	99.52 ± 1.09	P < 0.001
Creatinine, µmol/L	3	147.31 ± 3.88	111.33 ± 3.38	P < 0.001
Creatinine, µmol/L	6	114.34 ± 5.09	99.56 ± 4.17	P < 0.05
Creatinine, µmol/L	8	109.97 ± 7.03	89.41 ± 2.33	P < 0.05
Creatinine, µmol/L	10	104.62 ± 6.96	88.81 ± 2.46	P < 0.05

CI-AKI, contrast-induced acute kidney injury.

It should be noted that inthree3 patients in the CI-AKI+ group (10.34%), creatinine concentration continued to increase until the eighth day of observation. In two patients, a reliable decrease in creatinine concentration was noted from 224 to 197 μmol/L and from 210 to 110 μmol/L, while in one patient, it continued to increase, and the procedure was performed on hemodialysis.

In this study, the CI-AKI+ and CI-AKI− groups were compared with representatives of the CG in terms of clinical and anamnestic indicators and kidney laboratory results (Table 2).

Table 2.

Biochemical Blood Test Parameters in Patients with Diabetes Depend on CI-AKI Development

Indicator	CG (n = 20)	CI-AKI+ (n = 29)	P value	CI-AKI− (n = 27)	P value
HbA1c, %	4.48 ± 0.09	10.17 ± 0.21	P < 0.001	7.48 ± 0.17	P < 0.001
Alanine aminotransferase (ALT), u/L	33.40 ± 1.24	51.21 ± 1.63	P < 0.001	46.33 ± 2.16	P < 0.001
Bilirubin, mmol/l	16.50 ± 0.62	17.81 ± 0.65	n/s	19.04 ± 0.93	P < 0.05
Albumin, g/l	40.10 ± 0.54	35.14 ± 0.72	P < 0.001	38.96 ± 1.02	n/s
Uric acid, mmol/L	4.08 ± 0.17	6.83 ± 0.16	P < 0.001	6.86 ± 0.15	P < 0.001
Cholesterol, mmol/L	4.87 ± 0.08	5.86 ± 0.14	P < 0.001	6.00 ± 0.14	P < 0.001
Triglycerides, mmol/L	2.06 ± 0.07	4.12 ± 0.15	P < 0.001	2.51 ± 0.16	P < 0.05
Glucose, mmol/L	4.83 ± 007	10.37 ± 0.29	P < 0.001	7.51 ± 0.1^	P < 0.001
eGFR, mL/min	110.45 ± 2.64	83.66 ± 2.52	P < 0.001	86.11 ± 1.60	P < 0.001

eGFR, estimated glomerular filtration rate.

According to anamnestic data, the duration of diabetes was comparable in both groups of patients: 14.93 ± 1.05 years and 13.37 ± 1.55 years, respectively (n/s), although glycemia (according to the concentration of glucose and glycated hemoglobin) in the CI-AKI+ group was significantly higher than in the CI-AKI– group (P < 0.001). It should be noted that in both comparison groups, the concentration of glucose and glycated hemoglobin significantly exceeded the CG indicator (P < 0.001 for all four comparisons) due to the condition of inclusion of patients in the study. The eGFR, a key indicator of renal function, showed significant differences among the study groups. In patients who developed CI-AKI, the mean eGFR was 83.66 ± 2.52 mL/min, which was significantly lower compared with both the CI-AKI– group (86.11 ± 1.60 mL/min) and the control group (110.45 ± 2.64 mL/min). These findings indicate impaired renal function in diabetic patients with CI-AKI, underscoring the importance of eGFR assessment in identifying and monitoring the risk of kidney complications associated with contrast agent exposure.

The functional state of the liver in both groups of patients with diabetes was characterized by an increase in alanine aminotransferase activity in peripheral blood (P < 0.001 in both groups of patients compared with CG, n/s—comparison between groups CI-AKI+ and CI-AKI−) with normal concentration of total bilirubin. This is probably due to metabolic damage to hepatocytes due to the development of nonalcoholic fatty liver disease. Albumin concentration in the CI-AKI− group was comparable with that in the CG, while in the CI-AKI+ group, it was reduced. This circumstance is probably associated with more marked proteinuria due to diabetic nephropathy. However, the frequency of diagnosed proteinuria in the groups CI-AKI+ and CI-AKI− was comparable (21 people, 72.41% vs. 16, 59.26%). The concentration of uric acid in both groups of patients with diabetes included in the study was higher than in representatives of the control group (P < 0.001 for both comparisons). It did not depend on the development of CI-AKI. Hyperuricemia probably has two mechanisms of pathogenesis: metabolic (metabolic disorders of protein metabolism associated with disorders of carbohydrate metabolism) and renal (decreased tubular excretion of medium molecules). Blood lipid concentration was also increased in patients with diabetes compared with the control group (P < 0.001—significance of the difference in cholesterol concentration between both groups of diabetes and control group and in triglyceride concentration between the CI-AKI+ group and the control group; P < 0.05—significance of the difference in triglyceride concentration between CI-AKI− and CG). In this case, the concentration of blood cholesterol was comparable in both groups of diabetes. The concentration of triglycerides in the CI-AKI+ group was significantly higher than in the group with an uncomplicated postprocedural period (P < 0.001 significance of the intergroup difference), which is associated with an increase in the concentration of triglycerides on the background of hypoproteinemia. Analysis of the results of hematological examination revealed the following patterns: the concentration of leukocytes in the peripheral blood of patients with diabetes did not differ from that of healthy individuals and did not depend on the subsequent development of CI-AKI. The concentration of hemoglobin and the number of red blood cells in the peripheral venous blood in patients with diabetes in both comparison groups was comparable and significantly lower compared with the CG (P < 0.001—significance of the difference in hemoglobin concentration between the CG and both groups of patients with diabetes, the number of erythrocytes between the CG and CI-AKI−; P < 0.01—the number of erythrocytes between the CG and CI-AKI+). Hemoglobin levels in both diabetic groups were significantly lower compared with the control group (P < 0.001), indicating the presence of anemia commonly associated with CKD or diabetic complications. However, no statistically significant difference was observed between the CI-AKI+ and CI-AKI− groups, suggesting that the development of CI-AKI did not have an additional impact on hemoglobin levels within the early postprocedural period (Table 3).

Table 3.

Hematological Characteristics of Patients Depending on the Development of CI-AKI

Indicators	CG (n = 20)	CI-AKI+ (n = 29)	P value	CI-AKI− (n = 27)	P value
Hemoglobin, g/L	140.20 ± 2.10	116.69 ± 4.09	P < 0.001	122.26 ± 2.69	P < 0.001
Red blood cells, *1012/л	4.18 ± 0.10	3.72 ± 0.08	P < 0.01	3.69 ± 0.09	P < 0.001
Leukocytes, *109/л	5.73 ± 0.21	5.82 ± 0.25	N/S	6.16 ± 0.26	n/s
Platelets, *109/л	235.70 ± 13.40	276.79 ± 9.29	P < 0.05	258.26 ± 11.45	n/s
ESR, mm/h	9.40 ± 0.65	23.14 ± 0.91	P < 0.001	24.19 ± 1.08	P < 0.001

The number of platelets in the peripheral blood of patients with diabetes mellitus in both groups was affected by the development of CI-AKI. The value was higher than in the control group; however, statistical significance was reached only in the CI-AKI+ group compared with the control group (P < 0.05). This circumstance can be assessed as physiological hyperplasia of the megakaryocyte lineage in response to a decrease in the number of erythrocytes. The ESR value in the examined patients with diabetes mellitus exceeded the values of the control group (P < 0.001, significance of the difference between the control group and both groups of patients with diabetes mellitus). It did not depend on the future development of contrast-induced kidney damage. The increase in ESR is probably associated with dysproteinemia, which may be characteristic of patients with diabetic nephropathy.

In the urine of the examined patients, a reliable increase in the number of leukocytes, erythrocytes, and cylinders was found in comparison with the CG. An increase in the number of cellular elements in the urine in the absence of signs of infection is a characteristic sign of diabetic nephropathy. Moreover, the severity of the disorders was significantly higher in the group of patients who subsequently developed CI-AKI (P < 0.001 reliability of the intergroup difference for all three indicators) (Table 4), which indicates an initially more pronounced impairment of the functional state of the kidneys in this group of patients, which predisposes to the development of AKI after the administration of iodine-containing contrast agent.

Table 4.

The Specific Gravity of Urine in the CG and Patients Depends on CI-AKI Development

Indicator	CG (n = 20)	CI-AKI+ (n = 29)	P value	CI-AKI− (n = 27)	P value
Relative density of urine, g/L	1026.00 ± 0.50	1026.97 ± 0.59		1027.19 ± 0.58
Leukocytes, 103/л	1.85 ± 0.20	5.83 ± 0.25	P < 0.001	4.30 ± 0.27	P < 0.001
Red blood cells, 103/л	0.95 ± 0.21	9.03 ± 0.62	P < 0.001	4.37 ± 0.29	P < 0.001
Cylinder, 103/л	0.10 ± 0.03	2.15 ± 0.19	P < 0.001	1.17 ± 0.13	P < 0.001

Discussion

The results of this study demonstrated that one of the key risk factors for the development of contrast-induced acute renal failure in patients with diabetes mellitus after EVCRP is severe hyperglycemia. This discussion is consistent with literature data indicating a significant role of chronic hyperglycemia in damage to the renal endothelium and impaired renal blood flow, which increases the susceptibility of the kidneys to the nephrotoxic effects of contrast agents.¹⁶ The level of uric acid was significantly higher in patients with CI-AKI. Studies have shown that hyperuricemia is an independent risk factor for the development of CI-AKI in patients with type 2 diabetes mellitus. This is because uric acid can induce inflammation, oxidative stress, and narrowing of the renal blood vessels, making the kidneys more vulnerable to contrast exposure.²¹ Hypertriglyceridemia, detected in patients with CI-AKI, may also play a pathogenetic role, contributing to endothelial dysfunction and the development of oxidative stress, which leads to a decrease in renal clearance and increases the risk of renal damage.¹⁶ The literature highlights that hyperlipidemia in patients with diabetes may be associated with the progression of CKD.¹⁷ Reduced blood albumin concentration (hypoalbuminemia) in patients with CI-AKI supports the hypothesis of the role of nutritional status and systemic inflammation in the pathogenesis of acute kidney injury.¹⁸ Hypoalbuminemia is associated with increased vascular permeability and renal microcirculation deterioration, making the kidneys more vulnerable to the effects of contrast agents.¹⁹ Patients with CI-AKI also exhibited elevated platelet levels, especially those with diabetes mellitus. This reflects increased inflammatory activity and a tendency toward microthrombosis, which may impair renal blood flow after contrast administration. The platelet-to-lymphocyte ratio has also proven to be a useful marker of CI-AKI risk and poorer outcomes in diabetic patients.²² The revealed relationship between CI-AKI and the degree of vascular damage confirms the data that patients with severe atherosclerosis and impaired organ perfusion have an increased risk of developing acute kidney injury when exposed to nephrotoxic agents.²⁰ In this study, patients with CI-AKI had a significantly higher number of affected vascular beds, indicating the importance of assessing macro- and microangiopathy in patients with diabetes before performing EVСRP.²⁰ Additionally, the significant increase in hematuria, proteinuria, and cylindruria in the CI-AKI group reflects the severity of renal injury. It is consistent with other studies demonstrating the importance of monitoring biomarkers of renal injury in patients at high risk for CI-AKI.

Conclusions

Based on the obtained data, it can be suggested that patients with diabetes who are at high risk of CI-AKI should thoroughly prepare before administering contrast agents. Key preventive measures may include correcting hyperglycemia, lipid profile, and hypoalbuminemia; assessing vascular status; and monitoring renal injury biomarkers. Further studies are needed to determine the optimal strategies for preventing CI-AKI in this category of patients.

Footnotes

Authors’ Contributions

Data curation: B.B.N. Formal analysis: B.B.N. Investigation: L.T.D. Methodology: S.U.M. Project administration: S.U.M. Software: B.B.N. Resources: B.B.N. Supervision: L.T.D. Validation: D.S.A. Visualization: D.S.A. Writing—original draft: S.U.M. Writing—review and editing: L.T.D.

Author Disclosure Statement

The authors declare no conflicts of interest.

Funding Information

The authors received no financial support for the research, authorship, and/or publication of this article.

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Laboratory Changes in Contrast-Induced Nephropathy in Patients with Type 2 Diabetes Mellitus