Otozomal dominant polikistik böbrek hastalarında hastalık evresi ile serum endotrophin düzeyleri arasındaki ilişki
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Tarih
2024
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Hitit Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Otozomal dominant polikistik böbrek hastalığı (ODPBH) en sık görülen kalıtsal böbrek hastalığıdır. Renal kistlerin parankimal basısı sonucu, endotel disfonksiyonu, inflamasyon ve renal hasar gelişmektedir. Endotrophin, kollagen tip VI'nın ?3 zincirinin C-terminalinden çıkan bir parça olup, renal fibrozis ve kronik böbrek hasarı gelişimi için bir risk faktörü olduğu gösterilmiştir. Çalışmamızda ODPBH'de serum endotrophin düzeyleri ile total böbrek volümü (TBV), endotel disfonksiyonu, inflamasyon ve kardiyak morfoloji arasındaki ilişkiyi değerlendirmeyi amaçladık. Gereç ve Yöntem: Çalışmaya 38'i kadın 70 kişilik ODPBH hastası (yaş ortalaması 45,27±11,4 yıl) ve 31'i kadın 55 kişilik sağlıklı kontrol (yaş ortalaması 43,1±7,1 yıl) grubu alındı. ODPBH grubu renal fonksiyonu korunmuş (Grup1) ve renal fonksiyonu bozulmuş (Grup 2) olarak iki gruba ayrıldı. Çalışma grubunun karotis arter intimamedia kalınlığı (KİMK), flow-mediated vasodilatation (FMD) ölçümü ve ekokardiyografi değerlendirilmesi yapıldı. TBV, MRG'de manuel izleme yöntemi ile hesaplandı. Endotrophin düzeyi ELİSA yöntemi ile ölçüldü. Endotrophin, TBV, FMD'nin renal fonksiyonlar, ekokardiyografik parametreler ve inflamatuar markerler ile ilişkisi korelasyon analizi ile değerlendirildi. Bulgular: Endotrophin düzeyi, hasta grubunda (16,4 (14,3-21,2) ng/ml) kontrol grubuna (18,2 (13,0-48,9) ng/ml) göre istatistiksel olarak farklı saptanmadı (P= 0,524). Hasta grubunda FMD [%6,3 (3,1-10,1)] kontrol grubuna [%9.4 (6,1-17,9)] göre düşüktü (P= 0,001). KİMK düzeyi hasta grubunda (0,65±0,11 mm) kontrol grubuna göre (0,53±0,06 mm) istatistiksel olarak anlamlı düzeyde yüksek saptandı (P< 0,001). Sol ventrikül kitle (LVM) ve sol ventrikül kitle indeksi (LVMI) hasta grubunda kontrol grubuna göre istatistiksel olarak anlamlı düzeyde yüksek saptandı (sırasıyla, P< 0,001, P= 0,013).V Grup 1 ile Grup 2 hastalar arasında serum endotrophin düzeyleri açısından istatistiksel olarak anlamlı düzeyde farklılık saptanmadı [sırasıyla, 17,3 (14,9-22,5) ng/ml, 16,0 (14,1-19,9) ng/ml, P= 0,472]. KİMK, Grup 2 hastalarda (0,71±0,12 mm), Grup 1 hastalara (0,64±0,10 mm) göre istatistiksel olarak anlamlı düzeyde yüksek, (P= 0,043) FMD ise farklı değildi (P= 0,736). TBV'nin Grup 2 hastalarda [1299,0 (1124,0- 2986,0) mm3], Grup 1 hastalara [933,0 (526,5-1653,0)mm3] göre istatistiksel olarak anlamlı düzeyde yüksek olduğu saptandı (P= 0,044). İki grup arasında LVM ve LVMI değerleri açısından istatistiksel olarak anlamlı düzeyde farklılık saptanmadı. Serum endotrophin düzeyleri ile CRP düzeyleri arasında pozitif anlamlı korelasyon olduğu saptandı (P= 0,038). TBV ile yaş ve proteinüri arasında pozitif (sırasıyla P= 0,017, P= 0,013), eGFH arasında negatif (P= 0,002) korelasyon saptandı. Sonuçlar: ODPBH'de serum endotrophin düzeyi erken evre hastalıktan itibaren yükselmektedir. Serum endotrophin düzeyi ile inflmasyon arasında pozitif anlamlı korelasyon varken; TBV, kardiyak morfoloji ve endotel disfonksiyonu ile subklinik aterosklerozis arasında anlamlı korelasyon saptanmadı. Anahtar Kelimeler: Endotrophin, Endotel disfonksiyonu, Total Böbrek Volümü, Otozomal Dominant Polikistik Böbrek Hastalığı
Aim: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease. Due to the pressure of renal cysts, endothelial dysfunction, inflammation, and renal damage develop. Endotrophin, a fragment derived from the C-terminal of the ?3 chain of collagen type VI, has been shown to be a risk factor for renal fibrosis and the development of chronic kidney damage. In our study, we aimed to evaluate the relationship between serum endotrophin levels in ADPKD patients and total kidney volume (TKV), endothelial dysfunction, inflammation, and cardiac morphology. Material and Method: A total of 70 ADPKD patients (38 female, mean age 45,27±11,4 years) and 55 healthy controls (31 female, mean age 43,1±7,1 years) were included in the study. The ADPKD group was divided into two groups: preserved renal functions (Group 1) and impaired renal functions (Group 2). Carotid artery intimamedia thickness (CIMT), flow-mediated vasodilation (FMD) measurements, and echocardiographic evaluation were performed. TKV of patients were calculated using the manual tracing method on MR images. Endotrophin levels were measured by ELISA. The correlation analysis between endotrophin, TKV, FMD, renal function, echocardiographic parameters, and inflammatory markers was evaluated. Results: Endotrophin levels did not differ statistically significantly between the patients [16,4(14,3-21,2) ng/mL] and the controls [18,2(13,0-48,9) ng/mL] (P= 0,524). FMD was lower in the patient group [6,3% (3,1-10,1)] compared to the control group [9,4% (6,1-17,9)] (P= 0,001). CIMT was statistically significantly higher in the patients (0,65±0,11 mm) compared to the controls (0,53±0,06 mm) (P< 0,001). Left ventricular mass (LVM) and left ventricular mass index (LVMI) were statistically significantly higher in the patients compared to the controls (P< 0,001, P= 0,013 respectively). There was no statistically significant difference in terms of serum endotrophin levels between Group 1 and Group 2 [respectively, 17,3(14,9-22,5) ng/ml, 16,0 (14,1-19,9) ng/ml, P= 0,472]. CIMT was statistically significantly higher inVII Group 2 (0,71±0,12 mm) compared to Group 1 (0,64±0,10 mm) (P= 0,043). There were no differences between two groups according to FMD levels (P= 0,736). TKV was statistically significantly higher in Group 2 [1299,0 (1124,0-2986,0) mm3] compared to Group 1 [933,0 (526,5-1653,0)mm3] (P= 0,044). There were no statistically significantly differences in LVM and LVMI values between the two groups. There was a positive statistically significant correlation between serum endotrophin and CRP (P= 0,038). There was a positive statistically significant correlation between TKV and age and proteinuria (P= 0,017, P= 0,013 respectively), and a negative correlation with glomerular filtration rate (P= 0,002). Conclusion: Serum endotrophin levels increase from the early stages of ADPKD. While there is a positive significant correlation between serum endotrophin levels and inflammation, there is no significant correlation between TKV, cardiac morphology, endothelial dysfunction, and subclinical atherosclerosis. Keywords: Endotrophin, Endothelial Dysfunction, Total Kidney Volume, Autosomal Dominant Polycystic Kidney Disease
Aim: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease. Due to the pressure of renal cysts, endothelial dysfunction, inflammation, and renal damage develop. Endotrophin, a fragment derived from the C-terminal of the ?3 chain of collagen type VI, has been shown to be a risk factor for renal fibrosis and the development of chronic kidney damage. In our study, we aimed to evaluate the relationship between serum endotrophin levels in ADPKD patients and total kidney volume (TKV), endothelial dysfunction, inflammation, and cardiac morphology. Material and Method: A total of 70 ADPKD patients (38 female, mean age 45,27±11,4 years) and 55 healthy controls (31 female, mean age 43,1±7,1 years) were included in the study. The ADPKD group was divided into two groups: preserved renal functions (Group 1) and impaired renal functions (Group 2). Carotid artery intimamedia thickness (CIMT), flow-mediated vasodilation (FMD) measurements, and echocardiographic evaluation were performed. TKV of patients were calculated using the manual tracing method on MR images. Endotrophin levels were measured by ELISA. The correlation analysis between endotrophin, TKV, FMD, renal function, echocardiographic parameters, and inflammatory markers was evaluated. Results: Endotrophin levels did not differ statistically significantly between the patients [16,4(14,3-21,2) ng/mL] and the controls [18,2(13,0-48,9) ng/mL] (P= 0,524). FMD was lower in the patient group [6,3% (3,1-10,1)] compared to the control group [9,4% (6,1-17,9)] (P= 0,001). CIMT was statistically significantly higher in the patients (0,65±0,11 mm) compared to the controls (0,53±0,06 mm) (P< 0,001). Left ventricular mass (LVM) and left ventricular mass index (LVMI) were statistically significantly higher in the patients compared to the controls (P< 0,001, P= 0,013 respectively). There was no statistically significant difference in terms of serum endotrophin levels between Group 1 and Group 2 [respectively, 17,3(14,9-22,5) ng/ml, 16,0 (14,1-19,9) ng/ml, P= 0,472]. CIMT was statistically significantly higher inVII Group 2 (0,71±0,12 mm) compared to Group 1 (0,64±0,10 mm) (P= 0,043). There were no differences between two groups according to FMD levels (P= 0,736). TKV was statistically significantly higher in Group 2 [1299,0 (1124,0-2986,0) mm3] compared to Group 1 [933,0 (526,5-1653,0)mm3] (P= 0,044). There were no statistically significantly differences in LVM and LVMI values between the two groups. There was a positive statistically significant correlation between serum endotrophin and CRP (P= 0,038). There was a positive statistically significant correlation between TKV and age and proteinuria (P= 0,017, P= 0,013 respectively), and a negative correlation with glomerular filtration rate (P= 0,002). Conclusion: Serum endotrophin levels increase from the early stages of ADPKD. While there is a positive significant correlation between serum endotrophin levels and inflammation, there is no significant correlation between TKV, cardiac morphology, endothelial dysfunction, and subclinical atherosclerosis. Keywords: Endotrophin, Endothelial Dysfunction, Total Kidney Volume, Autosomal Dominant Polycystic Kidney Disease
Açıklama
Hitit Üniversitesi, Tıp Fakültesi
Anahtar Kelimeler
Endotrophin, Endotel disfonksiyonu, Total Böbrek Volümü, Otozomal Dominant Polikistik Böbrek Hastalığı, Endotrophin, Endothelial Dysfunction, Total Kidney Volume, Autosomal Dominant Polycystic Kidney Disease, Endotrophin, Endotel disfonksiyonu, Total Böbrek Volümü, Otozomal Dominant Polikistik Böbrek Hastalığı, Endotrophin, Endothelial Dysfunction, Total Kidney Volume, Autosomal Dominant Polycystic Kidney Disease
