Apolipoprotein c-iii (apo-c3) Metabolism in Patients with End Stage Renal Disease Treated with Long Term Hemodialysis.
AJTES Vol 2, No 2, July 2018
Full Text PDF


apolypoprotein-C3 (Apo-C3)
end stage renal disease

How to Cite

Zylbeari, L., Haxhirexha, K., Behxheti, N., Haxhirexha, F. D., Zylbeari, G., Bexheti, Z., Alimani, J., Ahmeti, S., Qalili, A., & Lika, H. (2018). Apolipoprotein c-iii (apo-c3) Metabolism in Patients with End Stage Renal Disease Treated with Long Term Hemodialysis. Albanian Journal of Trauma and Emergency Surgery, 2(2), 174-181. https://doi.org/10.32391/ajtes.v2i2.15


Background: End Stage Renal disease (ESRD) as it was historically termed is a term that encompasses all degrees of decreased renal function, from damaged–at risk through mild, moderate, and severe chronic kidney failure. ESRD is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost (see Epidemiology).
Material and Methods: The blood sample for routine analysis (lipidogram) and specific analysis was taken at 08o'clock in the morning with the room temperature that variated from 19 to 24°C, before the hemodialysis session, minimum 12 hours of fasting - with tendency to avoid the absorption effect of food by the intestine as well as avoid absorption of lipids and formation of chilomicrones. In all samples regardless of their group, the concentration of ApoC-II and lipids were analyzed in a period of 12 months in a period of 12 months (the measurements were made every three months, it means we totally made 3 measurements in 9 months).
Results: The results from patients and controlling group for Apo-C3 and lipid profile (ChT, TG, HDL-ch, LDL-ch) are given in table number 3. A significant statistical difference with p<0.0001 is found from the results of the lipidic profile and ApoC-III of patients with ESRD treated with HD compared with the results of the controlling group for the same parameters.
Conclusion: In this study patients with ESRD treated with HD have high parameters of ApoC-III, TG, LDL-ch but low concentrations of HDL-ch due to impaired catabolism of apolipoproteins in this specific group of patients. In all patients symptoms of CDV (myocardial infarction, angina pectoris, ischemia), acute coronary syndrome were noticed.

Full Text PDF


O'Hare AM, Choi AI, Bertenthal D,et al. Age affects outcomes in chronic kidney disease. J Am Soc Nephrol. 2007 Oct. 18(10):2758-65

Waknine Y. Kidney Disease Classification to Include Albuminuria. Medscape Medical News; July 24, 2016.

Guideline] Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int Suppl. 2013. 3:1-150.

Schnaper HW. Remnant nephron physiology and the progression of chronic kidney disease. Pediatr Nephrol. 2014 Feb. 29 (2):193-202.

United States Renal Data System. Chapter 1: CKD in the General Population. USRDS annual data report: Epidemiology of Kidney Disease in theUnited States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2015.

Kaysen G. A. Hyperlipidemia in chronic kidney disease. Int. J. Artif. Organs. 20007,30: 987–994.

Samuelsson O., Attman P. O., et al. Lipoprotein abnormalities without hyperlipidaemia in moderate renal insufficiency. Nephrol. Dial. Transplant.1994, 9: 1580–1590.

Chan MK,Varghese Z, Moorhead JF. Lipid abnor- malities in uremia, dialysis and transplantation.Kidney Int. 1981;(19): 119- 625.

Wanner C, Zimmermann J, Quaschning T, GalleL. Inflammation, dyslipidemia and vascular risk factors in hemodialysis patients. Kidney Int Suppl. 1997; 62:S53-5.

Ponticelli C.et al. Lipid abnormalities in maintenance dialysis patients and renal transplant recipients. Kidney Int Suppl. 1978; 8: S 72.

Haas LB,Wahl PW, Sherrard DJ. A longitudinal study of lipid abnormalities in renal failure.

Nephron 1983; 33:145.

Ooi E. M., Barrett P. H., Chan D. C., Watts G. F. 2008. Apolipoprotein C-III: understanding an emerging cardiovascular risk factor. Clin. Sci. (Lond.). 114: 611–624.

Huff M. W., Fidge N. H., Nestel P. J., Billington T., Watson B. 1981. Metabolism of C- apolipoproteins: kinetics of C-II, C-III1 and C-III2,and VLDL-apolipoprotein B in normal and hyperlipoproteinemic subjects. J. Lipid Res. 22:1235–1246.

Sundaram M., Zhong S., Khalil M. B., Links P. H., Zhao Y., Iqbal J., Hussain M. M., Parks R. J., Wang Y., Yao Z. 2010. Expression of apolipoprotein C-III in McA-RH7777 cells enhances VLDL assembly and secretion under lipid-rich conditions. J. Lipid Res. 51: 150–161.

Cohn J. S., Tremblay M., Batal R., Jacques H., Rodriguez C., Steiner G., Mamer O., Davignon J.2004.Increased apoC-III production is acharacteristic feature of patients with hypertriglyceridemia. Atherosclerosis. 177: 137–145.

Chan D. T., Irish A. B., Dogra G. K., Watts G. F. 2008. Dyslipidaemia and cardiorenal disease:mechanisms, therapeutic opportunities and clinical trials. Atherosclerosis. 196: 823–834.

Chan D. T., Dogra G. K., Irish A. B., Ooi E. M., Barrett P. H., Chan D. C., Watts G. F. 2009. Chronic kidney disease delays VLDL-apoB-100 particle catabolism: potential role of apolipoprotein C-III. J. Lipid Res. 50: 2524–2531.

Zölner N. Kirchs KZ. Fotometriska- oboenametoda. Ges Exp Med. 1962; 135: 545.

Bucola G, David H. Quantitative determinationof serum triglycerides by use of enzymes. Clin Chem.1973; 19: 476-82.

Allain CC, Poon LS, Chan CS, Richmond W. Enzymatic determination of total serum cholesterol.Clin Chem.1974;20:470-5.

Friedewald WT, Levy RJ, Fredrickson DS. Estimation of concentration of low density lipoprotein cholesterol without the use of the preparative ultracentrifuge. Clin Chem.1972;18:499- 502.

Wamick G, Benderson J, Allbers J. Quantitationof high density lipoprotein subclasses after separation by dextran sulfate and Mg+ precipitation. Clin Chem. 1982; 28: 1574-81.

Tilly P, et al. Biological and genetic determinants of serum apo C-III concentration: reference limits from the STANISLAS cohort study. J Lipid Res.2003;44:430-436.

Kimak E., Solski J. 2002. ApoA- and apoB- containing lipoproteins and Lp(a) concentration in non-dialyzed patients with chronic renal failure. Ren. Fail. 24: 485–492.

Saland J. M., Ginsberg H. N. 2007. Lipoprotein metabolism in chronic renal insufficiency. Pediatr. Nephrol. 22: 1095–1112.

Clavey V., Lestavel-Delattre S., Copin C., Bard J. M., Fruchart J. C. 1995. Modulation of lipoprotein B binding to the LDL receptor by exogenous lipids and apolipoproteins CI, CII, CIII, and E. Arterioscler. Thromb. Vasc. Biol. 15: 963–971.

Sehayek E., Eisenberg S. 1991. Mechanisms of inhibition by apolipoprotein C of apolipoprotein E- dependent cellular metabolism of human triglyceride-rich lipoproteins through the low density lipoprotein receptor pathway. J. Biol. Chem. 266: 18259–18267.

Holdsworth G., Stocks J., Dodson P., Galton D. J. 1982. An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III. J. Clin. Invest. 69: 932–939.

Kraus L. M., Kraus A. P., Jr 2001. Carbamoylation of amino acids and proteins in uremia. Kidney Int. Suppl. 78: S102–S107.

Zheng C., Khoo C., Furtado J., Sacks F. M. 2010. Apolipoprotein C-III and the metabolic basis for hypertriglyceridemia and the dense low-density lipoprotein phenotype. Circulation. 121: 1722–1734.

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.