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OBJECTiVES: Oxidative stress plays a role in the pathogenesis of diabetic nephropathy. It has been reported in many studies that antioxidant therapy may decrease complications related to diabetes mellitus. We aimed to evaluate the protective effects of erdostein on diabetic renal injury in diabetic rats. maTERial and mETHOdS: Thirty rats were randomly divided into 5 experimental groups (Group 1: control, group 2: erdostein, group 3: alloxan, group 4: alloxan+erdostein, and group 5: alloxan+insulin, n=6 each). Rats were made diabetic using alloxan injection intraperiteonally. Erdostein (10 mg/kg/day) orally and insulin two times a day (3 g/kg) intraperitoneally were administered for four weeks. All rats were then sacrificed and kidney histopathological examinations were performed by light microscopy. RESulTS: The diabetic rats had diabetic nephropathic changes in the kidney on histological examination but the rats treated with erdostein showed significantly less histopathological changes, similar to the control group compared with the diabetic rats not treated with erdostein (p 0.05). COnCluSiOn: Based on the present data, we conclude that erdostein may show protective effects on renal injury due to diabetes mellitus. KEY WORdS: Diabetic nephropathy, Erdostein, Renal failure, Alloxan Yazisma Adresi: Faruk TuRGuT Fatih Universitesi Tip Fakultesi, Nefroloji Bilim Dali, Ankara, Turkiye Gsm : 0 505 642 17 12 E-posta : turgutfaruk@yahoo.com Gelis Tarihi : 07.06.2010 Kabul Tarihi : 25.08.2010 Faruk TuRGuT1 ayse CaRliOglu2 Rabia alKan3 derya aKdEnIz3 Hacer HalTas4 ozlem saHIn BalCiK5 Ebru uz1 omer Faruk KaRaTas6 1 Fatih Universitesi Tip Fakultesi, Nefroloji Bilim Dali, Ankara, Turkiye 2 Fatih Universitesi Tip Fakultesi, Endokrinoloji Bilim Dali, Ankara, Turkiye 3 Fatih Universitesi Tip Fakultesi, Ic Hastaliklari Anabilim Dali, Ankara, Turkiye 4 Fatih Universitesi Tip Fakultesi, Patoloji Anabilim Dali, Ankara, Turkiye 5 Fatih Universitesi Tip Fakultesi, Hematoloji Bilim Dali, Ankara, Turkiye 6 Fatih Universitesi Tip Fakultesi, Uroloji Anabilim Dali, Ankara, Turkiye Turgut F ve ark: Diyabetik Nefropatide Erdostein Etkisi Cilt/Vol: 19, No: 3, 2010, Sayfa/Page: 157-161 158 Turk nefroloji diyaliz ve Transplantasyon dergisi Turkish Nephrology, Dialysis and Transplantation Journal

Currently, the pathogenesis of nondipper hypertension remains largely unclear in patients without any renal or endocrine pathology. It is well known that overt hypothyroidism is strongly associated with diastolic hypertension. However, no study has addressed the pathogenic role of TSH, free T3 (FT3), and free T4 (FT4) in nondipper hypertension. The aim of the present investigation is to evaluate if higher TSH, low FT3 and FT4 would be associated with a nondipper hypertension profile, in patients with normal renal function and without any overt thyroid hormone disorder. 131 subjects were screened and those who met the following inclusion criteria were enrolled: (1) glomerular filtration rate (GFR) >60 ml/min; (2) no history of thyroid disorders; (3) no history of thyroid hormone medication. All subjects underwent 24-hour ambulatory blood pressure monitoring on a usual working day. Of the total population, 59 patients (45%) were classified as dippers and 72 (55%) were classified as nondippers. The only significant differences between dipper and nondipper patients appear to be related to FT3 levels and GFR. Nondipper patients had lower FT3 levels (4.5 ± 0.6 vs. 4.0 ± 0.9 pmol/l, p = 0.02) and low GFR (80.5 ± 12.2 vs. 86.9 ± 16.9 ml/min, p = 0.03), compared to dipper patients. The final regression model included serum TSH, FT3 levels, and GFR; the only independent predictor of nondipper hypertension was FT3 (p = 0.04). In conclusion, even if the mechanisms of our findings remain incompletely understood, we demonstrate a graded independent relation between lower level of FT3 and the risk of nondipping. Further studies are warranted to confirm this relationship and to elucidate the pathogenetic mechanisms of this relationship.

Background and Aims: In patients with renal disease, an association between abnormal circadian blood pressure profile and abnormalities in bone and mineral metabolism, including vascular calcifications, is well known. However, such a link has not yet been reported in hypertensive patients with normal renal function. We aimed to evaluate if higher serum phosphate, calcium, parathyroid hormone (PTH) level and the calcium×phosphate (Ca×P) product would be associated with a nondipper hypertension, in patients with normal renal function and without any PTH disorder. Methods: 190 hypertensive subjects with the following inclusion criteria were enrolled: (1) normal phosphate and PTH levels; (2) glomerular filtration rate (GFR) >60 ml/min, and (3) no history of calcium, phosphate, vitamin D medication and hyperparathyroidism. Results: Of the total population, 76 patients (40%) were classified as dippers and 114 (60%) as nondippers. Nondipper patients had higher levels of phosphate (3.70 ± 0.61 vs. 3.35 ± 0.44 mg/dl, p = 0.001), Ca×P product (35.4 ± 6.5 vs. 31.5 ± 5.0, p = 0.001) and PTH (75.7 ± 28.8 vs. 46.6 ± 17.1 pg/ml, p = 0.000) compared to dipper patients. Independent predictors (multiple regression) for nondipper hypertension were PTH (β = 0.43, p = 0.001) and phosphate (β = 0.9, p = 0.03). Conclusion: We demonstrate a graded independent relation between higher levels of phosphate, PTH, Ca×P product and the risk of nondipping in hypertensive patients with an estimated GFR of >60 ml/min and normal mineral metabolism.

Chronic kidney disease presenting acutely is not uncommon, often avoidable and associated with adverse outcomes. In the early stages of chronic kidney disease, there may be no symptoms. However, when kidney function is less than one-tenth of normal, the symptoms may arise. The patients in end-stage renal disease may also present with nonspecific symptoms. A 46 year old man admitted to our hospital with knee pain. He had no other complaints. His blood urea and creatinin levels were 232 mg/dl and 19.5 mg/dl respectively. He was anemic and venous blood gas revealed pH: 7.10, HCO3-: 10 mEq/L. But his physical examination was normal. The glomerular filtration rate was greatly reduced, altough his blood pressure was within normal limits. Hemodialysis had been initiated immediately and within 24 hours blood urea nitrogen had decreased to 145 mg/dl. The clinicians must be aware of non-spesific symptoms such as arthralgia, which should masquerade the underlying chronic kidney disease. The identification, follow-up and appropriate referral of patients with raised serum creatinine is likely to reduce its incidence., Kronik böbrek hastalığının akut olarak ortaya çıkması nadir değildir. Bu durumdan sıklıkla kaçınılabilir, fakat gelişmesi halinde olumsuz sonuçlar doğurabilir. Kronik böbrek hastalığı erken dönemlerde asemptomatik seyredebilir. Böbrek fonksiyonları normal düzeyinin onda birinin altına düştüğünde semptomlar ortaya çıkabilir. Fakat, son dönem böbrek yetmezliği hastaları non-spesifik semptomlarla da başvurabilirler. Hastanemize başvuran 46 yaşındaki erkek hastanın diz ağrısı dışında şikayeti yoktu. Üre ve kreatinin değerleri sırasıyla 232 mg/dl ve 19.5 mg/dl idi. Anemisi mevcuttu. Venöz kan gazı değerlendirmesinde pH: 7.10, HCO3-: 10 mEq/L idi. Fakat hastanın fizik muayenesi normaldi. Hesaplanan glomerüler filtrasyon hızı oldukça düşük olarak bulunmasına karşın kan basıncı normal sınırlar içerisindeydi. Acil olarak hemodiyalize alınan hastanın kan üre nitrojeni 24 saat içerisinde 145 mg/dl\'ye geriledi. Klinisyenler kronik böbrek hastalığını maskeleyebilecek artralji gibi non-spesifik semptomlara karşı uyanık olmalılardır. Bu durumun insidansının azaltılabilmesi, yüksek serum kreatinini olan hastaların tanınması, takibi ve uygun olarak sevk edilmeleri ile sağlanabilir. Klin Deney Ar Derg 2010; 1(3): 216-8.