Obez çocuk ve adolesanlarda böbrek fonksiyonlarının denetimi ve metabolik sendrom bileşenleri ile ilişkisi
Abstract
Evaluation of the renal functions of obese children and adolescents and the relationship with the metabolic syndrome components Objective: In parallel with the increasing rate of obesity insulin resistance and the frequency of the metabolic syndrome is also increasing at childhood. Kidney damage has begun to attract more attention increasingly among the problems caused by obesity. Chronic kidney disease is regarded as an important complication of obesity in adulthood. However, there isn't enough literature about the effects of childhood obesity over the renal functions. Different methods can be used in the control of renal functions but there is not also an ideal method for evaluation of renal functions in obese children. Creatinine clearance calculation is often a useful method for evaluation of the renal functions. GFR measurement methods using body surface area may give false results particularly in obese individuals because of the increased body surface area. Cystatin-C is a glomerular filtration marker which is less effected from the muscle mass and the diet. Its' higher rates are stimulatory of renal failure. In this study; renal function status and its relation with metabolic syndrome at obese children and adolescents were tried to be detected by analyzing the creatinine clearance, creatinine clearance calculated with fat free mass, GFR calculated with body cell mass, cystatin-C and proteinuria levels. Material and Method: 108 participants, who were diagnosed with overweight or obesity at general examination control and referred to AUTF Pediatric Endocrinology policlinic between 1 January 2014 and 1 January 2015 were enrolled to study. Control group is composed of 46 healthy child and adolescent at the ages between 6 and 18 that was admitted to general policlinic with the aim of routine control. Anthropometric measurements of participants were performed and they were evaluated according to normograms. Body fat composition of patients was determined by bioimpedans measurement device (TANİTA®). Along with routine obesity studies (fasting plasma glucose, fasting insulin, lipid profile, liver enzymes); creatinine, Cystatin-C, 24 hours urine creatinine and protein studies were performed. Metabolic syndrome components were investigated at participants. GFRs' were calculated according to varied GFR measurement methods. Relations between Cystatin-C results and metabolic syndrome components were researched. Results: Hyperinsulinism was shown at 35% of obese participants and 4.3% of control group, 14.8% of obese participants' were diagnosed with metabolic syndrome. Elevated triglyceride levels were shown at 22% of obese participants and 6.5% of control group, low HDL levels were shown at 37% of obese participants and 15% of control group, hypertension diagnosed at 9.2% of obese participants and 4.3% of control group, elevated levels of fasting plasma glucose were shown at 1.8% of obese participants. There was no statistical difference in terms of gender between obese participants with or without metabolic syndrome and control groups. Although obese and control groups were similar in terms of age and gender, we determined that obese participants were in later stages of puberty. At comparison of Cystatin-C levels, there wasn't any statistically significance between obese group and control group. However, Cystatin-C was significantly higher than those without metabolic syndrome in obese patients with metabolic syndrome. Creatinine levels were not significantly different between obese and control groups. Low GFR values were detected at obese participants with metabolic syndrome comparing to obese patients without metabolic syndrome and control group when we calculate GFR with Cystatin-C derived Filler formula and Cystatin-C and blood creatinine derived Bouvet formula. GFR values of obese group were higher than control group when they were calculated with all creatinine derived, BCM derived and only one Cystatin-C and creatinine derived formula (Donadio et al. 1998). GFRs' were determined under 60ml/min/1.73m² (Stage III CKD) at one patient of metabolic syndrome group with creatinine clearance analysis and six participants of control groups with Cystatin-C and creatinine derived formula offered by Donadio et al (1998). Results of BCM derived GFR calculation formulas were similar with results of creatinine derived formulas. We didn't detect statistically significant correlation between serum creatinine and total cholesterol, LDL, HDL, triglyceride, fasting plasma glucose and fasting insulin results. We detected positive directional significant correlation between Cystatin-C results and total cholesterol, LDL, triglyceride and fasting insulin; negative directional significant correlation between Cystatin-C and HDL. We didn't detect statistically significant difference between obese group with metabolic syndrome, obese group without metabolic syndrome and control group participants in terms of proteinuria levels. We didn't detect nephrotic levels of proteinuria and grade IV or upper grades of CKD at any of the participants. Conclusion: GFR elevation without proteinuria at obese children and adolescents is an indicator of renal damage grade is in the limits of functional grades. But as the obesity period increases GFR begins to decline and this suggests the possible start of renal damage process. Cystatin-C levels may help predicting kidney damage, especially in obese children with metabolic syndrome. The increased GFR, with or without metabolic syndrome, is a useful indicator revealing the negative effects of obesity on the kidney.