Using different equations for estimating glomerular filtration rate in patients with type 1 diabetes


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

Aim. To compare different methods of estimating GFR calculated by creatinine and cystatin С in patients with type 1 diabetes with normal and moderately decreased renal filtration function. Material and methods. The study involved 57 patients with type 1 diabetes, 37 men and 20 women, aged from 21 to 57 years (median ЗО years), with disease duration after diagnosis from 33 to 2 years (median 8 years). The control group comprised 15 non-diabetic people aged 19 to 42 years (median - 28 years), with normal levels of abuminuria and blood creatinine. The majority of patients with type 1 diabetes were found to have decompensated diabetes mellitus. The mean value of glycated hemoglobin in patients was 8%. The renal glomerular function was estimated by level of GFR and triple testing of urine albumin excretion. Renal tubular function in type 1 diabetes was tested by examining serum cystatin С. Results. GFR estimating equations, which did not include serum of cystatin С produced higher GFR. As a result, the majority of patients had normal or elevated GFR showing hyperfiltration. Using cystatin-C-based equations resulted in a several-fold reduction in the number of patients with hyperfiltration and increased number of cases with GFR below 90 ml/min/m2. The assessment of the relationship between SDMA and GFR showed negative correlation with both cystatin-C-based and creatinine-based equations. Conclusion. These findings revealed that GFR estimating equations based on both creatinine and cystatin С produce more accurate results compared with the reference estimating equations.

Full Text

Restricted Access

References

  1. Дедов И.И., Викулова О.К., Сухарева О.Ю. Скрининг диабетической нефропатии в Российской Федерации. В: Шестакова М.В., Дедов И.И. (ред.). Сахарный диабет и хроническая болезнь почек. М., 2009. С. 39-59.
  2. Fioretto P., Caramori M.L., Mauer M. The kidneys in diabetes: dynamic pathways of injury and repair. The Camillo Golgi Lecture 2007. Diabetologia. 2008;51:1051-1057.
  3. Бондарь И.А., Климонтов В.В. Функциональная морфология почек при сахарном диабете. В кн.: Шестакова М.В., Дедов И.И., ред. Сахарный диабет и хроническая болезнь почек. М., 2009. С. 149-176.
  4. Дедов И.И., Шестакова М.В. Сахарный диабет и артериальная гипертензия. М., 2006.
  5. Fioretto P., Sutherland D.E., Najafîan B. et al. Remodeling of renal interstitial and tubular lesions in pancreas transplant recipients. Kidney Int. 2006;69:907-912.
  6. Viberti G.C., Wiseman M.J. The kidney in diabetes: significance of the early abnormalities. Clin. Endocrinol. Metab. 1986;15:753-782.
  7. Microalbuminuria Collaborative Study Group. Predictors of the development of microalbuminuria in patients with Type 1 diabetes mellitus: a seven-year prospective study. Diabet. Med. 1999;16:918-925.
  8. Stone M.L., Craig M.E., Chan A.K., Lee J.W., Verge C.F., Donaghue K.C. Natural history and risk factors for microalbuminuria in adolescents with type 1 diabetes: a longitudinal study. Diabetes Care 2006;29: 2072-2077.
  9. Jerums G., Panagiotopoulos S., Maclsaac R.J. Diabetic nephropathy: epidemiology and clinical description. In: Boner G., Cooper M.E., ed. Management of Diabetic Nephropathy. L., N.-Y. 2003. Р. 37-60.
  10. Valmadrid C.T., Klein R., Moss S.E., Klein B.E. The risk of cardiovascular disease mortality associated with microalbuminuria and gross proteinuria in persons with older-onset diabetes mellitus. Arch. Intern. Med. 2000;160:1093- 1100.
  11. Casiglia E.,Zanette G., Mazza A., Donadon V., Donada C., Pizziol A., Tikhonoff V., Palatini P., Pessina A.C. Cardiovascular mortality in non- insulin-dependent diabetes mellitus. A controlled study among 683 diabetics and 683 age- and sex-matched normal subjects. Eur. J. Epidemiol. 2000;16:677- 684.
  12. Torffvit O., Lovestam-Adrian M., Agardh E., Agardh C.D. Nephropathy, but not retinopathy, is associated with the development of heart disease in Type 1 diabetes: a 12-year observation study of 462 patients. Diabet. Med. 2005;22(6):723-729.
  13. Groop P.H., Thomas M.C., Moran J.L., Wadèn J., Thorn L.M., Mäkinen V.P., Rosengàrd-Bdrlund M., Saraheimo M., Hietala K., Heikkilä O., Forsblom C.; FinnDiane Study Group. The presence and severity of chronic kidney disease predicts all-cause mortality in type 1 diabetes. Diabetes. 2009;58:1651-1658.
  14. Мухин Н.А., Фомин В.В., Моисеев С.В. Микроальбуминурия - универсальный маркер неблагоприятного прогноза. Клиническая медицина. 2008;11:4-9.
  15. Konyukh E.A., Paramonova N.S. Clinical features of acute and chronic glomerulonephritis in children with endothelial dysfunction. Zhurnal GrGMU. 2010;2:149 (in Russ.).
  16. Knight E.L., Verhave J. C., Spiegelman D., Hillege H.L., deZeeuw D., Curhan G. C., de Jong P.E. Factors in fluencing serum cystatin C levels other than renal function and the impact on renal function measurement. Kidney Int. 2004;65:1416-1421.
  17. Lemieux C., Maliba R., Favier J., Théorêt J.F., Merhi Y., Sirois M.G. Angiopoietins can directly activate endothelial cells and neutrophils to promote proinflammatory responses. Blood. 2005;105(4):1523-1530.
  18. Stevens L.A., Schmid C.H., Greene T., Li L., Beck G.J., Joffe M.M., Froissart M., Kusek J.W., Zhang Y.L., Coresh J., Levey A.S. Factors other than glo-merularfiltration rate affect serum cystatin C levels. Kidney Int. 2009;75:652-660.
  19. Magee G.M., Bilous R.W., Cardwell C.R., Hunter S.J., Kee F., Fogarty D.G. Is hyperfiltration associated with the future risk of developing diabetic nephropathy? A metaanalysis. Diabetologia. 2009;52:691-697.
  20. Köttgen A., Selvin E., Stevens L.A., Levey A.S., Van Lente F., Coresh J. Serum cystatin C in the United States: the Third National Health and Nutrition Examination Survey (NHANESIII). Am. J. Kidney Dis. 2008;51:385-394.
  21. Stam F., van Guldener C., Dekker J.M., Heine R.J., Bouter L.M., Stehouwer C.D. Endothelial dysfunction contributes to renal function-associated cardiovascular mortality in a population with mild renal insufficiency: the Hoorn study. J. Am. Soc. Nephrol. 2006;2:537-545.
  22. Berezinets O.L., Rossolovskiy A.N., Blyumberg B.I. Modern aspects of future developments and the progression of coronary artery disease in patients with chronic kidney disease. Byulleten' meditsinskikh Internet-konferentsiy. 2014;4(1):72-74(in Russ.).
  23. Landray M.J., Wheeler D.S., Newman D.J., Blann A.D., McGlynn F.J., Ball S., Townend J.N., Baigent C. Inflammation, Endothelial dysfunction and platelet activation in patients with chronic kidney disease: the chronic renal impairment in Birmingham (CRIB) Study. Am. J. Kidney Dis. 2004;43:244-253.
  24. Martens C.R., Edwards D.G. Peripheral Vascular Dysfunction in Chronic Kidney Disease. Cardiol. Res. Pract. 2011;1:2-6.
  25. Böger R.H., Lentz S.R., Bode-Böger S.M., Knapp H.R., Haynes W.G. Elevation of asymmetrical dimethylarginine may mediate endothelial dysfunction during experimental hyperhomocyst(e)inaemia in humans. Clin. Sci (Colch). 2001;100(2):161-167.

Supplementary files

Supplementary Files
Action
1. JATS XML

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies