Tehran University Medical Journal

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Background: Autosomal-dominant polycystic kidney disease (ADPKD), a common hereditary disease, is characterized by the progressive development and enlargement of multiple cysts in both kidneys, and typically resulting in end stage renal disease (ESRD) by the fifth decade of life. Post-transplant diabetes mellitus (PTDM), a common complication after transplantation with an incidence rate of 2.5-20%, is associated with poor graft and patient survival. In few studies, PTDM has been more frequent in ADPKD transplanted patients. In the present study, we investigated whether there is any association between PTDM and ADPKD in our patients.
Methods: In this prospective study, 140 non-diabetic and nonsmoker successfully transplanted patients (27 ADPKD and 113 non ADPKD patients) were enrolled during three years. Both groups were matched for age, sex, body mass index (BMI), duration of renal replacement therapy before transplantation and also immunosuppressive protocols after transplant. Post-transplant diabetes mellitus was defined as Clinical Practice Guidelines advocated by Canadian Diabetes Association. All patients were followed for 12 months.
Results: PTDM occurred in 11.1% of ADPKD patients and in 13.1% of control group which was statistically insignificant (P > 0.05). The development of PTDM in ADPKD group was not related to sex, age, and hypertension, duration of renal replacement therapy before transplantation, BMI and serum creatinine levels (P > 0.05).
Conclusion: Post-transplant diabetes mellitus appears not to be associated with autosomal-dominant polycystic kidney disease as an etiology of end stage renal disease.

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Background: Ureteral obstruction, leading to urinary stasis and elevated pressure in the proximal part of urinary tract, causes progressive renal dysfunction. This study was designed to evaluate the status of oxidative stress and metabolic defect in acute unilateral ureteral obstruction (UUO).

Methods: Experiments were performed on three groups of male Sprague-Dawley rats (n=10 in each group). In the UUO group, rats were lightly anesthetized by ether and the left ureter was occluded by means of a sterile surgical procedure. Twenty-four hours after UUO-induction, both kidneys were removed and stored at -70 °C. In the sham group, anesthesia and surgery were performed without ureteral occlusion, and the control group received no surgical procedure. The kidney samples were assessed to measure the levels of ATP and ADP by the luciferin-luciferase method for determining metabolic status. In addition, the levels of malondialdehyde (MDA) and ferric reducing/antioxidant power (FRAP) of the kidneys were measured to evaluate the redox state. Data are expressed as means ±SEM per gram of kidney weight (gKW). The comparisons were performed using paired t-test for intra-group analysis, and ANOVA followed by Duncan's post-hoc test and then LSD test for inter-group analysis. Significance was taken at p<0.05.

Results: The comparisons between the UUO and sham groups indicated that 24 hours of UUO increased levels of MDA (51.42±1.86 vs. 38.64±1.02 nmol/gKW, respectively p<0.001) and ADP (0.67±0.04 vs. 0.47±0.045 µmol/gKW, respectively p<0.01), but decreased levels of FRAP (2.44±0.18 vs. 4.28±0.27 µmol/gKW, respectively), ATP (1.09±0.10 vs. 2.26±0.19 µmol/gKW, respectively) and ATP/ADP ratio (1.64±0.14 vs. 5.11±0.56, respectively) in the obstructed kidneys, all p<0.001. In the non-obstructed kidneys, the levels of ATP and ADP were higher (p<0.01 and p<0.001, respectively), while the levels of MDA and ATP/ADP ratio were equal to those of the sham group.

Conclusion: Twenty-four hours of acute UUO induces oxidative stress and reduces the aerobic metabolism in obstructed kidneys, whereas non-obstructed kidneys with a normal redox state show the higher levels of metabolism.

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Background: Red Blood Cell's (RBC)’s folate may be related to decreased risk of colorectal adenoma. Methylenetetrahydrofolate reductase (MTHFR) is a key regulatory enzyme in folate metabolism. The MTHFR C677T polymorphism is located in the Exon 4 region and is associated with the change of folate level. This study evaluated the associations between RBC’s Folate levels and colorectal adenoma risk, taking into account whether this associations is modified by MTHFR Polymorphism. Methods: In a case-control study conducted from January to October 2007 in Endoscopy-Colonoscopy ward of Shahid Faghihi Hospital, Shiraz. Participants were 177 case of colorectal adenoma who had pathologic-confirmed adenomatous polyps in full colonoscopy examination and 366 controls without polyps in full colonoscopy. Fasting venous blood were drawn from patients in order to determine RBC’s folate and to identify the MTHFR polymorphism by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: Gender Distribution in the patient group were 57.6% male and 42.3% female and control group consisted of 55.1% male and 43.9% female. 50.2% of cases and 49.2% of controls were in the age group “45 years and above”. The T allele frequency was 56.6% in control group and 34.4% in colorectal adenoma patients. There was a significant association between T allele in -677 position of MTHFR gene and colorectal adenoma susceptibility (OR: 1.85, 95% CI: 0.76-4.24, P<0.001). Mean concentration of RBC’s folate was not statistically significant among three groups with TT genotype (mutation homozygote), CT genotype (heterozygote), and CC genotype (wild-type homozygote) (P>0.05) but mean concentration of RBC’s folate was the lowest in TT genotype compare with two other genotype. Odd's Ratio for low (<140ng/ml) versus high level of RBC’s folate in participants with TT genotype was (OR: 2.08, 95% CI: 0.10-2.19, P<0.05) as compare with the CC ones. Conclusion: The result of this study suggested an inverse association between RBC's folate concentration and colorectal adenomas risk, which may be more relevant for those with the MTHFR TT genotype.