The Correlation Between Lipid Profile and Renal Function Tests in Patients with Cardiovascular Disease

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Hardi Rafat Baqi
Shkar Rzgar K. Rostam


Cardiovascular disease patients frequently suffer from the incidence of renal dysfunctions, the prevalence of the correlation, however, remains ambiguous. This study aims to see how CVD and renal function are related to the subjected group of patients suffer from symptoms of CVD. The method recruited for this objective was using of serum lipid profile test as a marker for evaluating the CVD and making correlations to the blood urea, serum uric acid, and serum creatinine levels as markers for assessing renal function on 159 individuals with CVD symptoms in Erbil city. Two statistical analysis methods (The linear regression and Pearson’s correlation) were employed for determining the existence from a lack of relationship between them. The results showed a statistically significant correlation p<0.05 by both methods between the renal function markers and TC. The UA was correlated to TG, LDL-C, and VLDL-C p<0.05 by regression analysis. The SCr was correlated to TG and LDL-C p<0.05 by both methods, and to VLDL by regression analysis. According to the outcome of the current study both lipid profile and renal function markers are correlated in mostly a statistically significant manner. Yet, the results are not conclusive, further studies are needed in this area for indemnify the irrefutable evidence concerning this relation.


Lipid profile, Renal function, CVD, Kidney disease


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[1] K. Borch-Johnsen and S. Kreiner, “Proteinuria: value as predictor of cardiovascular mortality in insulin dependent diabetes mellitus.,” Br. Med. J. (Clin. Res. Ed)., vol. 294, no. 6588, pp. 1651–1654, Jun. 1987, doi: 10.1136/bmj.294.6588.1651.
[2] J. Tuomilehto et al., “Incidence of cardiovascular disease in Type 1 (insulin-dependent) diabetic subjects with and without diabetic nephropathy in Finland.,” Diabetologia, vol. 41, no. 7, pp. 784–790, Jul. 1998, doi: 10.1007/s001250050988.
[3] A. B. Reiss, I. Voloshyna, J. De Leon, N. Miyawaki, and J. Mattana, “Cholesterol Metabolism in CKD,” Am. J. Kidney Dis., vol. 66, no. 6, pp. 1071–1082, Dec. 2015, doi: 10.1053/j.ajkd.2015.06.028.
[4] WHO, “Cardiovascular disease,” 2020.,cerebrovascular disease (stroke) (accessed Aug. 16, 2020).
[5] Y. Kokubo et al., “Relationship between blood pressure category and incidence of stroke and myocardial infarction in an urban Japanese population with and without chronic kidney disease: the Suita Study,” Stroke, vol. 40, no. 8, pp. 2674–2679, 2009.
[6] M. C. Thomas et al., “Serum lipids and the progression of nephropathy in type 1 diabetes.,” Diabetes Care, vol. 29, no. 2, pp. 317–322, Feb. 2006, doi: 10.2337/diacare.29.02.06.dc05-0809.
[7] C. G. Kenneth R Feingold, Introduction to Lipids and Lipoproteins. 2000.
[8] C. G. Magnussen, R. Thomson, V. J. Cleland, O. C. Ukoumunne, T. Dwyer, and A. Venn, “Factors Affecting the Stability of Blood Lipid and Lipoprotein Levels From Youth to Adulthood,” vol. 165, no. 1, pp. 68–76, 2011.
[9] R. W. J. F. de Freitas, M. F. M. de Araújo, A. C. S. Lima, D. C. R. Pereira, A. M. P. G. Alencar, and M. M. C. Damasceno, “Study of lipid profile in a population of university students,” Rev. Lat. Am. Enfermagem, vol. 21, no. 5, pp. 1151–1158, 2013, doi: 10.1590/S0104-11692013000500019.
[10] M. P. Brandão, F. L. Pimentel, and M. F. Cardoso, “Impact of academic exposure on health status of university students,” Rev. Saude Publica, vol. 45, no. 1, pp. 49–58, 2011, doi: 10.1590/S0034-89102011000100006.
[11] P. G. Scheffer et al., “Increased plasma apolipoprotein C-III concentration independently predicts cardiovascular mortality: the Hoorn Study.,” Clin. Chem., vol. 54, no. 8, pp. 1325–1330, Aug. 2008, doi: 10.1373/clinchem.2008.103234.
[12] A. Bobik, “Apolipoprotein CIII and atherosclerosis: beyond effects on lipid metabolism.,” Circulation, vol. 118, no. 7. United States, pp. 702–704, Aug. 2008, doi: 10.1161/CIRCULATIONAHA.108.794081.
[13] A. S. Go, G. M. Chertow, D. Fan, C. E. McCulloch, and C. Hsu, “Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization.,” N. Engl. J. Med., vol. 351, no. 13, pp. 1296–1305, Sep. 2004, doi: 10.1056/NEJMoa041031.
[14] E. L. Schiffrin, M. L. Lipman, and J. F. E. Mann, “Chronic kidney disease: effects on the cardiovascular system.,” Circulation, vol. 116, no. 1, pp. 85–97, Jul. 2007, doi: 10.1161/CIRCULATIONAHA.106.678342.
[15] R. T. Gansevoort et al., “Chronic kidney disease and cardiovascular risk: epidemiology, mechanisms, and prevention.,” Lancet (London, England), vol. 382, no. 9889, pp. 339–352, Jul. 2013, doi: 10.1016/S0140-6736(13)60595-4.
[16] S. Gowda, P. B. Desai, S. S. Kulkarni, V. V Hull, A. A. K. Math, and S. N. Vernekar, “Markers of renal function tests,” N. Am. J. Med. Sci., vol. 2, no. 4, pp. 170–173, Apr. 2010, [Online]. Available:
[17] Y. Zuo, C. Wang, J. Zhou, A. Sachdeva, and V. C. Ruelos, “Simultaneous determination of creatinine and uric acid in human urine by high-performance liquid chromatography,” Anal. Sci., vol. 24, no. 12, pp. 1589–1592, 2008.
[18] J. V. Corbett, Laboratory tests and diagnostic procedures. Englewood Cliffs, NJ: Prentice Hall Health, 2000.
[19] D. Rudan, O. Polasek, I. Kolcić, and I. Rudan, “Uric acid: the past decade,” Croat. Med. J., vol. 51, no. 1, pp. 1–6, Feb. 2010, doi: 10.3325/cmj.2010.51.1.
[20] L. M. Ruilope et al., “Renal function and intensive lowering of blood pressure in hypertensive participants of the hypertension optimal treatment (HOT) study.,” J. Am. Soc. Nephrol., vol. 12, no. 2, pp. 218–225, Feb. 2001.
[21] M. J. Brown et al., “Morbidity and mortality in patients randomised to double-blind treatment with a long-acting calcium-channel blocker or diuretic in the International Nifedipine GITS study: Intervention as a Goal in Hypertension Treatment (INSIGHT).,” Lancet (London, England), vol. 356, no. 9227, pp. 366–372, Jul. 2000, doi: 10.1016/S0140-6736(00)02527-7.
[22] J. F. Mann, H. C. Gerstein, J. Pogue, J. Bosch, and S. Yusuf, “Renal insufficiency as a predictor of cardiovascular outcomes and the impact of ramipril: the HOPE randomized trial.,” Ann. Intern. Med., vol. 134, no. 8, pp. 629–636, Apr. 2001, doi: 10.7326/0003-4819-134-8-200104170-00007.
[23] L. M. Ruilope, D. J. Van Veldhuisen, E. Ritz, and T. F. Luscher, “Renal function: The cinderella of cardiovascular risk profile,” Journal of the American College of Cardiology, vol. 38, no. 7. pp. 1782–1787, 2001, doi: 10.1016/S0735-1097(01)01627-8.
[24] L. Zhang et al., “Prevalence of chronic kidney disease in China: a cross-sectional survey.,” Lancet (London, England), vol. 379, no. 9818, pp. 815–822, Mar. 2012, doi: 10.1016/S0140-6736(12)60033-6.
[25] J. Coresh et al., “Prevalence of chronic kidney disease in the United States.,” JAMA, vol. 298, no. 17, pp. 2038–2047, Nov. 2007, doi: 10.1001/jama.298.17.2038.
[26] S. I. Hallan et al., “International comparison of the relationship of chronic kidney disease prevalence and ESRD risk.,” J. Am. Soc. Nephrol., vol. 17, no. 8, pp. 2275–2284, Aug. 2006, doi: 10.1681/ASN.2005121273.
[27] A. A. House et al., “Heart failure in chronic kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference,” Kidney Int., vol. 95, no. 6, pp. 1304–1317, Jun. 2019, doi: 10.1016/j.kint.2019.02.022.
[28] P. O. Attman and O. Samuelsson, “Dyslipidemia of kidney disease.,” Curr. Opin. Lipidol., vol. 20, no. 4, pp. 293–299, Aug. 2009, doi: 10.1097/MOL.0b013e32832dd832.
[29] N. D. Vaziri, “Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences.,” Am. J. Physiol. Renal Physiol., vol. 290, no. 2, pp. F262-72, Feb. 2006, doi: 10.1152/ajprenal.00099.2005.
[30] P. O. Attman, O. Samuelsson, and P. Alaupovic, “Lipoprotein metabolism and renal failure.,” Am. J. kidney Dis. Off. J. Natl. Kidney Found., vol. 21, no. 6, pp. 573–592, Jun. 1993, doi: 10.1016/s0272-6386(12)80030-8.
[31] L. A. Stevens and A. S. Levey, “Measured GFR as a confirmatory test for estimated GFR.,” J. Am. Soc. Nephrol., vol. 20, no. 11, pp. 2305–2313, Nov. 2009, doi: 10.1681/ASN.2009020171.
[32] M. T. Jalali, A. M. Honomaror, A. Rekabi, and M. Latifi, “Reference ranges for serum total cholesterol, HDL-cholesterol, LDL-cholesterol, and VLDL-cholesterol and triglycerides in healthy iranian ahvaz population,” Indian J. Clin. Biochem., vol. 28, no. 3, pp. 277–282, 2013, doi: 10.1007/s12291-012-0268-x.
[33] L. Berglund et al., “Evaluation and treatment of hypertriglyceridemia: An endocrine society clinical practice guideline,” J. Clin. Endocrinol. Metab., vol. 97, no. 9, pp. 2969–2989, 2012, doi: 10.1210/jc.2011-3213.
[34] T. Malati and M. R. U. Mahesh, “Reference intervals for serum total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, Lp (a), apolipoprotein A-I, A-II, B, C-II, C-III, and E in healthy South Indians from Andhra Pradesh,” Indian J. Clin. Biochem., vol. 24, no. 4, pp. 343–355, 2009, doi: 10.1007/s12291-009-0063-5.
[35] W. Hao and A. Friedman, “The LDL-HDL profile determines the risk of atherosclerosis: A mathematical model,” PLoS One, vol. 9, no. 3, 2014, doi: 10.1371/journal.pone.0090497.
[36] C. Higgins, “Urea and the clinical value of measuring blood urea concentration,” Acutecaretesting.Org, no. August, pp. 1–6, 2016, doi: 10.1039/b204949j.
[37] A. O. Hosten, “BUN and Creatinine.,” H. K. Walker, W. D. Hall, and J. W. Hurst, Eds. Boston, 1990.
[38] W. Mullens et al., “Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.,” J. Am. Coll. Cardiol., vol. 53, no. 7, pp. 589–596, Feb. 2009, doi: 10.1016/j.jacc.2008.05.068.
[39] C. A. Lawson et al., “Chronic kidney disease, worsening renal function and outcomes in a heart failure community setting: A UK national study.,” Int. J. Cardiol., vol. 267, pp. 120–127, Sep. 2018, doi: 10.1016/j.ijcard.2018.04.090.
[40] I. Löfman, K. Szummer, I. Hagerman, U. Dahlström, L. H. Lund, and T. Jernberg, “Prevalence and prognostic impact of kidney disease on heart failure patients.,” Open Hear., vol. 3, no. 1, p. e000324, 2016, doi: 10.1136/openhrt-2015-000324.
[41] M. Rahman et al., “Relation of serum lipids and lipoproteins with progression of CKD: The CRIC study.,” Clin. J. Am. Soc. Nephrol., vol. 9, no. 7, pp. 1190–1198, Jul. 2014, doi: 10.2215/CJN.09320913.
[42] H. Zhang et al., “Association Between the Lipid Profile and Renal Dysfunction in the Heart Failure Patients.,” Kidney Blood Press. Res., vol. 44, no. 1, pp. 52–61, 2019, doi: 10.1159/000498834.
[43] L. Visconti et al., “Lipid disorders in patients with renal failure: Role in cardiovascular events and progression of chronic kidney disease.,” J. Clin. Transl. Endocrinol., vol. 6, pp. 8–14, Dec. 2016, doi: 10.1016/j.jcte.2016.08.002.
[44] H. Moradi, M. V Pahl, R. Elahimehr, and N. D. Vaziri, “Impaired antioxidant activity of high-density lipoprotein in chronic kidney disease.,” Transl. Res., vol. 153, no. 2, pp. 77–85, Feb. 2009, doi: 10.1016/j.trsl.2008.11.007.
[45] E. S. Schaeffner et al., “Cholesterol and the Risk of Renal Dysfunction in Apparently Healthy Men,” J. Am. Soc. Nephrol., vol. 14, no. 8, pp. 2084 LP – 2091, Aug. 2003, [Online]. Available:
[46] W. F. Keane, “Lipids and the kidney,” Kidney Int., vol. 46, no. 3, pp. 910–920, 1994.
[47] N. D. Vaziri, “Molecular mechanisms of lipid disorders in nephrotic syndrome,” Kidney Int., vol. 63, no. 5, pp. 1964–1976, 2003.