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    ACUTE RENAL FAILURE ASSOCIATED WITH RHABDOMYOLYSIS DUE TO FIBRATE USE
    (Istanbul Univ, Faculty Medicine, Publishing Office, 2011) Yilmaz, Gulay; Cavus, Turker; Cakir, Hasan; Narli, Erkan
    Sixty two years old female patient presented to our emergency service with diffuse, muscle pain, nausea and vomiting. Her laboratory investigations showed that urea, creatinine, AST, ALT, creatine kinase and phosphorus were increased. The patient was admilted with the diagnosis of acute renal failure. The patient whose history included diabetes mellitus (DM) type 2 and hypertension has received fenofibrate 200 mg daily for hypertrigliceridemia for two months. Last ten days she has had too much muscle pain. On the basis of the clinical and laboratory examinations, a diagnosis of acute renal failure secondary to fenofibrate-induced rhabdomyolysis was made. Fenofibrate was stopped. Intravenous fluid replacement and bicarbonate therapy were started. Hemodialysis was not needed. She was discharged after the clinical and laboratory findings returned to normal.
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    Carotid intima media thickness is independently associated with urinary sodium excretion in patients with chronic kidney disease
    (Taylor & Francis Ltd, 2015) Ustundag, Sedat; Yilmaz, Gulay; Sevinc, Can; Akpinar, Seval; Temizoz, Osman; Sut, Necdet; Ustundag, Ayten
    Atherosclerosis-induced premature vascular diseases are the leading cause of mortality among patients with chronic kidney disease (CKD). The pathogenetic mechanism of atherosclerosis in patients with CKD has not been fully explained. Experimental studies have demonstrated that high dietary sodium intake not only increases circulatory volume and blood pressure, but also facilitates development of atherosclerosis by reducing production-bioavailability of nitric oxide due to oxidative stress and accordingly by enhancing endothelial and arterial stiffness. In this study, we investigated the relationship between sodium consumption and carotid artery intima-media thickness, which is the indicator of atherosclerosis, by determining daily urinary sodium excretion, which is a reliable indicator of sodium consumption, in our patient group. Our patient group included 193 patients with stage 2-4 non-diabetic CKD and without a history of atherosclerotic disease. We determined that 77% of our patients have been consuming more than 2 g of sodium per day, which is the upper limit of sodium consumption recommended for patients with CKD. We determined a positive linear correlation between carotid artery intima-media thickness and patient age (p < 0.001), C-reactive protein (p < 0.001), urinary sodium excretion (p < 0.001), body mass index (p = 0.002), systolic blood pressure (p = 0.002), hemoglobin (p = 0.030), triglycerides (p = 0.043), and diastolic blood pressure (p = 0.049). We also found a negative linear correlation between carotid artery intima-media thickness and glomerular filtration rate (p = 0.008). We found that urinary sodium excretion is the determinant of intima-media thickness even if all factors associated with intima-media thickness are adjusted, and that intima-media thickness increases by 0.031 (0.004-0.059) mm per 2 g increase in daily sodium excretion, independent from overall factors (p = 0.025). Our results reveal a relation between urinary sodium excretion and carotid artery intima-media thickness and suggest that excessive sodium consumption predisposes development of atherosclerosis in patients with CKD.
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    Fibroblast Growth Factor-23 and Carotid Artery Intima Media Thickness in Chronic Kidney Disease
    (Clin Lab Publ, 2015) Yilmaz, Gulay; Ustundag, Sedat; Temizoz, Osman; Sut, Necdet; Demir, Muzaffer; Ermis, Veli; Sevinc, Can
    Background: The cause of early-accelerated atherosclerosis development observed in Chronic Kidney Disease (CKD) is not fully understood. The determination of the relationship between the levels of fibroblast growth factor 23 (FGF-23) and the development of endothelial dysfunction, left ventricular hypertrophy, and myocardial infarction lends support to the possibility that FGF-23 plays a role in the development of atherosclerosis in CKD. Only a few studies, however, have been conducted that analyze the relationship between FGF-23 levels in the progression of CKD and the development of atherosclerosis, and these studies have generally been limited to those patients receiving dialysis therapy due to end stage renal disease (ESRD). Methods: In the present study, carotid artery intima-media thicknesses (IMT) were measured ultrasonically as a marker of atherosclerosis in 91 patients with CKD stage 3 - 4 (61 female and 30 male, age between 19 - 65 years, glomerular filtration rate [GFR] 15 - 60 mL/min 1.73 m(2), CKD was not related to diabetes mellitus, and without cardiovascular-cerebral disease) in contrast to 36 healthy volunteers (26 female and 10 male, age between 19 - 65 years, GFR > 90 mL/min 1.73 m(2), and without any diagnoses of acute or chronic disease), and a possible role of FGF-23 on atherosclerosis was analyzed. Results: Patients were similar to controls with respect to age, gender, smoking status, body mass index, and plasma glucose and lipid profile. On the other hand, IMT measurements (p < 0.00001) and FGF-23 levels (p = 0.00012) were significantly higher in patients than controls. IMT was measured above the subclinical atherosclerosis limit of 0.750 mm in 54% of the patients. Multivariate regression analysis showed that patients' age, high sensitive c-reactive protein (hsCRP), and FGF-23 levels were independent predictors of IMT (p < 0.00001, r = 0.559). Independent of other variables, every 1 mu mol/L increase in FGF-23 levels resulted in 0.444 mm increase of IMT measurements in patients with CKD. Conclusions: Our findings suggest that monitoring serum FGF-23 may be useful as a non-invasive indicator of subclinical atherosclerosis in patients with chronic kidney disease.
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    THE RELATIONSHIP BETWEEN CALCIFICATION INHIBITOR LEVELS IN CHRONIC KIDNEY DISEASE AND THE DEVELOPMENT OF ATHEROSCLEROSIS
    (Oxford Univ Press, 2020) Sevinc, Can; Yilmaz, Gulay; Ustundag, Sedat
    [Abstract Not Available]
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    The relationship between calcification inhibitor levels in chronic kidney disease and the development of atherosclerosis
    (Taylor & Francis Ltd, 2021) Sevinc, Can; Yilmaz, Gulay; Ustundag, Sedat
    Aim We aimed to investigate the factors affecting the development of atherosclerosis and the role of calcification inhibitors fetuin-A, matrix-Gla protein (MGP), osteoprotegerin (OPG) in atherosclerosis progress. Material and methods The study was planned to investigate the relationship of serum OPG, MGP and fetuin-A levels with the development of atherosclerosis in the stage 2-3-4-5 chronic kidney disease (CKD) patients who did not require dialysis treatment. Results 32 (17 female, 15 male) healthy individuals and 92 (49 females, 43 males) CKD patients were included. The mean carotid intima-media thickness (CIMT), C-reactive protein (CRP), fetuin-A, OPG and MGP of the two groups were compared statistically. In CKD patients, age, body mass index (BMI), CRP, triglyceride, urea, systolic blood pressure (SBP), fasting blood sugar have a positive linear relationship, fetuin-A, OPG, GFR have a negative linear relationship with CIMT. The mean CIMT, right CIMT, left CIMT, blood urea, CRP, urinary albumin excretion creatinine and age show a negative linear relationship with fetuin-A. Conclusion Fetuin-A levels begin to decline from the early stages of CKD and are significantly lower in patients with atherosclerosis as expressed with CIMT. This suggests that fetuin-A may be used as an early marker in CKD for increased cardiovascular risk. Early recognition of these risk factors is important and large-scale studies on vascular calcification inhibitors are needed.
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    The relationship between mean platelet volume and neutrophil/lymphocyte ratio with inflammation and proteinuria in chronic kidney disease
    (Medknow Publications & Media Pvt Ltd, 2017) Yilmaz, Gulay; Sevinc, Can; Ustundag, Sedat; Yavuz, Yasemin Coskun; Hacibekiroglu, Tuba; Hatipoglu, Esra; Baysal, Mehmet
    Atherosclerosis, which develops as a result of inflammation, is the most important cause of morbidity and mortality in chronic kidney disease (CKD). In this study, we investigated the relationship of mean platelet volume (MPV) and neutrophil/lymphocyte ratio (NLR) with inflammation and proteinuria in patients with CKD Stage 3-4. Healthy individuals who applied to nephrology clinic for checkup purposes acted as controls. Fifty-three patients and 30 healthy controls were included in the study. Patients with diabetes mellitus, active infection, malignancy, and coronary artery disease were excluded from the study. Biochemistry values and hemograms were recorded for all patients and for control group. NLR was calculated. The relationship between MPV/NLR and protein, fibrinogen, and proteinuria was evaluated. Our study showed a statistically significant difference between CKD group and healthy control (HC) group in uric acid, fibrinogen, C-reactive protein, and NLR values (P < 0.01, P < 0.01, P = 0.01, P < 0.01, respectively). No statistically significant difference was found between CKD and HC groups for MPV (P = 0.307). Correlation analysis revealed a statistically significant relationship between NLR and creatinine (P < 0.00, r = 0.571), uric acid (P < 0.00, r = 0.436), glomerular filtration rate (P < 0.00, r = 0.418), 24 h urine protein (P = 0.004, r = 0.311), and 24 h urine microalbumin (P = 0.001, r = 0.354). A statistically significant relationship was detected between MPV and platelet count (P < 0.001, r = 0.422), age (P = 0.004, r = 0.312), uric acid (P = 0.04, r = 0.226), and fibrinogen (P = 0.023, r = 0.249). Whereas, a statistically significant relationship was detected between NLR and microalbuminuria/proteinuria, there was no statistically significant relationship between MPV and microalbuminuria/proteinuria. Our study showed that the NLR is high in CKD group and is correlated with uric acid and proteinuria, which are known to be associated with atherosclerosis, in patients with CKD. NLR may be a determinant of inflammation and atherosclerosis in patients with CKD.