FEATURES OF NUTRITIONAL STATUS IN PATIENTS WITH CHRONIC KIDNEY DISEASE: RELATION WITH INTERLEUKIN 6 AND FIBROBLAST GROWTH FACTOR 23
DOI:
https://doi.org/10.11603/1811-2471.2018.v0.i2.9210Keywords:
chronic kidney disease, nutritional status, protein-energy wasting, chronic inflammation, fibroblast growth factor 23, interleukin 6.Abstract
Malnutrition in patients with chronic kidney disease (CKD) is associated with an increased risk of morbidity and mortality. This study shows the association of markers of nutritional status, namely, the thickness of skinfold, with the marker of inflammation interleukin-6 and the phosphaturic hormone, fibroblast growth factor 23, which increases in CKD, which is associated with an increase in cardiovascular mortality.
The aim – to study the peculiarities of nutritional status of patients with CKD and to investigate the relations of FGF-23 and IL-6 with markers of nutritional status in CKD.
Material and Methods. The study involved 106 people, 47 women (44 %) and 59 men (56 %), age (49.6±13.9) years with CKD. We determined the level of albumin, IL-6, BMI, and the thickness of subscapular, triceps and abdominal skinfolds. The C-terminal fragment of FRF-23 was determined using a set of reagents for the immuno-enzyme analysis "Biomedica" and the STAT FAK 303 Plus machine.
Results and Discussion. The serum albumin level progressively decreased, reaching the minimum values at the terminal stage of renal failure (p<0.001). Among patients with CKD stage V malnutrition was observed in 31 % of patients, of whom 10 % had moderate malnutrition and 5 % had severe malnutrition. The skinfold thickness was reduced in parallel with the decline of GFR, gaining statistical significance at CKD stage III (p < 0.01) and reaching the lowest values ?at CKat CKD stage V. A saignificant negative relation between the skinfold thickness and FGF-23 concentration was found (r=-0.23; p<0.05). A saignificant negative relation was found between the skinfold thickness and the concentration of IL-6 (r=-0.23; p<0.05).
Conclusions. The skinfold thickness decreases with a decline in GFR and has an inverse relation with the level of IL-6, which indicates the nutritional properties of subcutaneous fat depots and the absence of proinflammatory effects of subcutaneous fat in patients with CKD.
References
Foley, R. N., Parfrey, P.S., & Harnett, J.D. (2006). Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J. Am. Soc. Nephrol, 7, 728-736.
Mehls, O., Ritz, E., & Hunziker, E.B. (1988). Improvement of growth and food utilization by human recombinant growth hormone in uremia. Kidney Int., 33, 45-52.
Hazel, S.J., Gillespie, C.M., & Moore, R.J. (1994). Enhanced body growth in uremic rats treated with IGF-I and growth hormone in combination. Kidney Int., 46, 58-68.
Guebre-Egziabher, F., Juillard, L., & Boirie, Y. (2009). Short-term administration of a combination of recombinant growth hormone and insulin-like growth factor-I induces anabolism in maintenance hemodialysis. J. Clin. Endocrinol. Metab., 94, 2299-2305.
Sherwin, R.S., Bastl, C., & Finkelstein, F.O. (1976). Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon. J. Clin. Invest., 57, 722-731.
Kopple, J.D, Cianciaruso, B., & Massry, S.G. (1980). Does parathyroid hormone cause protein wasting? Contrib. Nephrol., 20, 138-148.
Mak, R.H. (1996). Insulin resistance but IGF-I sensitivity in chronic renal failure. Am. J. Physiol., 271, F114-F119.
Korner, J., & Leibel, R.L. (2003). To eat or not to eat–how the gut talks to the brain. N. Engl. J. Med., 349, 926-928.
Mafra, D., Jolivot, A., & Chauveau, P. (2010). Are ghrelin and leptin involved in food intake and body mass index in maintenance hemodialysis? J. Ren. Nutr., 20, 151-157.
Mak, R.H., & Cheung, W. (2007). Adipokines and gut hormones in end-stage renal disease. Perit. Dial. Int., 27 (Suppl 2), S298-S302.
Stenvinkel, P., Heimburger, O., & Paultre, F. (1999). Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure. Kidney Int., 55, 1899-1911.
Zimmermann, J., Herrlinger, S., Pruy, A., Metzger, T., & Wanner, C. (1999). Inflammation enhances cardiovascular risk and mortality in hemodialysis patients. Kidney Int., 55, 648-658.
Honda, H., Qureshi, A.R., & Heimburger, O. (2006). Serum albumin, C-reactive protein, interleukin 6, and fetuin a as predictors of malnutrition, cardiovascular disease, and mortality in patients with ESRD. Am. J. Kidney Dis., 47, 139-148.
Tripepi, G., Mallamaci, F., & Zoccali, C. (2005). Inflammation markers, adhesion molecules, and allcause and cardiovascular mortality in patients with ESRD: searching for the best risk marker by multivariate modeling. J. Am. Soc. Nephrol., 16, S83-S88.
Martin, A., David, V., & Quarles, L.D. (2012). Regulation and function of the FGF23/klotho endocrine pathways. Physiol. Rev., 92, 131-155.
Gutierrez, O.M., Mannstadt, M., & Isakova, T. (2008). Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N. Engl. J. Med., 359, 584-592.
Kopple, J.D., Greene, T., & Chumlea, W.C. (2000). Relationship between nutritional status and the glomerular filtration rate: results from the MDRD study. Kidney Int., 57, 1688-1703.