Serum Beta-Trace Protein versus Glomerulus Filtration Rate as a Predictor for Kidney Function among Hypertensive Patients

Ranisa Handayani, Yuyun Widaningsih, Fitriani Mangarengi, Uleng Bahrun

Abstract


Beta-Trace Protein (BTP) is a low-molecular-weight glycoprotein that can convert prostaglandin H2 into prostaglandin D2 and is associated with the vascular function's alteration. Serum beta-trace protein has been proposed as a promising marker in predicting kidney function in hypertensive patients. This study aimed to analyze the correlation between BTP and glomerulus filtration rate, particularly in hypertensive patients. A cross-sectional survey was conducted on 70 hypertensive participants admitted to Dr. Wahidin Sudirohusodo Hospital from July-August 2019. Beta-trace protein, serum urea, creatinine, blood pressure, and anthropometric were measured. The Glomerulus Filtration Rate (GFR) with Cockcroft Gault was graded using GFR stages. The hypertension was graded according to the category of the European Society of Cardiology (ESC) 2018. A descriptive test, Kruskal-Wallis test, Fisher exact test, Spearman correlation test, and logistic regression test were performed at a confidence level of 95%. Significant differences were found between the age, systole, diastole, blood urea, creatinine, and GFR (p=< 0.05). There was a significant difference between GFR and the degree of hypertension (p=< 0.001), but no differences were found in the mean value of BTP and the degree of hypertension (p=0.348). A significant negative correlation was found between GFR and BTP (p=0.028, r = -0.263). Logistic regression test s showed that the increased BTP led to 2.591 times greater possibility of end-stage renal disease with GFR < 15 mL/min/ 2 1.73 m (crude odds ratio 95% CI 1.168-5.475). Serum beta-trace protein possesses a prognostic ability of glomerulus filtration rate and can be used to predict the odd of end-stage renal disease in hypertensive patients.


Keywords


Serum beta-trace protein, glomerular filtration rate, hypertension

Full Text:

PDF

References


Kementerian Kesehatan Republik Indonesia.

H i p e rt e n s i [ I n t e r n e t] . A v a i l a b l e fr o m :

http://www.depkes.go.id. (accessed 2 June, 2019).

Whelton Paul K, Carey RM, Aronow WS, Casey Jr. DE,

Collins KJ, et al. Guideline for the prevention,

detection, evaluation, and management of high blood

pressure in adults. Journal of the American College of

Cardiology, 2017; 71(19): e127-248.

Brenner GM, Stevens CW. Antihypertensive drugs. In:

th

Brenner and Steven's pharmacology. 5 Ed.,

Philadelphia, Elsevier, 2018; 10: 103-115.

Lukito AA, Harmeiwaty E, Hustrini NM. Klasifikasi

tekanan darah klinik. Dalam: Konsensus

penatalaksanaan hipertensi 2019. 1 Ed., Jakarta,

Perhimpunan Dokter Hipertensi Indonesia, 2019; 7-8.

Reiss AB, Miyawaki N, Moon J, Kasselman LJ,

Voloshyna I, D'Avino A, De Leon J. CKD, arterial

calcification, atherosclerosis and bone health:

Inter-relationships and controversies. Atherosclerosis,

; 278: 49-59.

White CA, Ghaza-Shahi S, Adams MA. ß-trace protein:

A marker of GFR and other biological pathways.

American Journal of Kidney Diseases, 2015; 65(1):

-146.

Donadio C, Bozzoli L. Urinary beta-trace protein:

Unique biomarker to screen early glomerular filtration

rate impairment. Medicine, 2016; 95(49): e5553.

Song W, Ricciotti E, Liang X, Grosser T, Grant GR, et al.

Lipocalin-like prostaglandin D synthase but not

hemopoietic prostaglandin d synthase deletion

causes hypertension and accelerates thrombogenesis in mice. The Journal of Pharmacology and

Experimental Therapeutics, 2018; 367(3): 425-432.

Hirasawa N, Uehara Y, Yamakado M, Toya Y, Gomi T,

Ikeda T, Eguchi Y, et al. Lipocalin–type prostaglandin D

synthase in essential hypertension. Hypertension 39

(part 2), 2002; 449 – 454.

James MT, Hemmelgarn BR, Tonelli M. Early

recognition and prevention of chronic kidney disease.

Asian Pacific Society of Nephrology, 2010; 53-56.

Bhavsar NA. Appel LJ, Kusek JW, Contreras G, Bakris G,

et al. Comparison of measured GFR, serum creatinine,

cystatin C, and beta-trace protein to predict ESRD in

African Americans with hypertensive CKD. American

Journal of Kidney Disease, 2011; 58(6): 886-893.

Pandya Divya, Nagrajappa Anil Kumar, Ravi KS.

Assessment and correlation of urea and creatinine

levels in saliva and serum patients with chronic kidney

disease, diabetes, and hypertension-a research study.

Journal of Clinical and Diagnostic Research, 2016;

(10): 58-62.

Mohammed Kidher Mudher, Ewadh Mufeed Jalil,

Hamza Amer. Beta-trace protein level as a better

diagnostic marker of renal impairment in patients with

chronic kidney disease, diabetes mellitus, and renal

transplants. Journal of Pharmaceutical Sciences and

Research, 2018; 10(6): 1615- 1618.

Bacci MR, Cavallari MR, de Rozier-Alver RM, Alves BCA,

Fonseca FLA. The impact of lipocalin-type

prostaglandin-D-synthase as a predictor of kidney

disease in patients with type 2 diabetes. Drug Design,

Development, and Therapy, 2015; 22(9): 3179-3182.

Orenes-Pinero E, Manzano-Fernandez S, LopezCuenca A, Marin F, Valdes M, Januzzi JL. Beta-trace

protein: From GFR marker to cardiovascular risk

predictor. Clinical Journal of American Society of

Nephrology, 2013; 8: 873-881.

Spannaus KS, Kollerits B, Ritz E, Hersberger M,

Kronenberg F, von Eckardstein A. Serum creatinine,

cystatin C, and beta-trace protein in diagnostic staging

and predicting progression of primary nondiabetic

chronic kidney disease. American Association of

Clinical Chemistry, 2010; 56(5): 740-749




DOI: http://dx.doi.org/10.24293/ijcpml.v27i2.1618

Refbacks

  • There are currently no refbacks.


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