Biochemical and Hematological Alterations in Chronic Kidney Disease in Iraqi Patients
DOI:
https://doi.org/10.36320/ajb/v17.i2.19639Keywords:
chronic kidney disease (CKD), parathyroid hormone (PTH), chronic kidney disease-mineral bone disorder (CKD-MBD), secondary hyperparathyroidism (SHPT), Renal failure (RF), Cardiovascular diseases (CVD), fibroblast growth factor 23 (FGF23), hemodialysis (HD), Enzyme-linked immunosorbent assay (ELISA).Abstract
In patients with stages five of chronic kidney disease, the clinical syndrome known as chronic kidney disease–mineral bone disorder dysfunction includes the development of secondary hyperparathyroidism hormone, as well as abnormalities in vitamin D as well as mineral metabolism is characterized by biochemical and hormonal It is the alterations to hyperphosphatemia and hypocalcemia that cause it with that cause it elevated risk for mortality, cardiovascular disease, bone fractures, and the advancement of chronic kidney diseases.
Methods: For this research, 120 blood samples were collected from patients with chronic kidney disease and 60 volunteers. A sandwich Enzyme-linked immunosorbent assay was used to estimate the serum levels of human parathyroid hormone, and use competitive Enzyme-linked immunosorbent assay was used to estimate Vitamin D, and Urea, creatinine, albumin, Calcium, phosphorus, glucose, and bilirubin were measured using a spectrophotometer. Glomerular filtration rate was estimated indirectly, and a hematocytometer measured Hematological Parameters, and the results were statistically processed in SPSS.
Results: The study showed no significant difference (p>0.407) in the mean age among patient groups was 44.51±12.33 years, while the control group was 41.13±10.22 years. the study also examined body weight distribution, finding no significant difference(p->0.32) between patients 24.54±3.44 and the control group 25.11±3.21. and finding no significant difference in Total serum bilirubin (P>0.067). The resulting data showed a significant difference (P<0.001) in the increase in the mean levels of urea, creatinine, phosphorus, glucose, and parathyroid hormone in chronic kidney disease patients compared to the healthy control group. The results showed a decrease in the mean ± SD of hemoglobin, packed cell volume, white blood cells, platelets, albumin level, glomerular filtration rate, calcium, and vitamin D in kidney failure patients compared to the healthy control group.
Conclusions: The disease known as chronic kidney disease-mineral bone disorder is complex; knowing the actual cut-off for risk-related factors such as vitamin D deficiency, calcium, high Parathyroid hormone, and phosphate disorders, as well as their implications for future cardiovascular disease, bone health, and mortality risk, deserves further study.
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References
[1] Brito, R. B. D. O., Rebello, J. F., Grabulosa, C. C., Pinto, W., Morales Jr, A., Elias, R. M., ... & Dalboni, M. A. (2020). 25-vitamin D reduces inflammation in uremic environment. Scientific Reports, 10(1), 128.
[2] Silva, E. C. D., Taminato, M., Fonseca, C. D. D., Moraes, G. M. D., Longo, M. C. B., Grothe, C. E., ... & Barbosa, D. A. (2018). Uso da vitamina D e infecção em pacientes com doença renal crônica. Revista Brasileira de Enfermagem, 71, 2792-2799.
[3] Vaish, A., Vaishya, R., & Iyengar, K. P. (2024). Metabolic Syndrome and Its Impact on Bone and Joint Health: A Comprehensive Review. Apollo Medicine, 09760016241307374.
[4] Obi, Y., Hamano, T., & Isaka, Y. (2015). Prevalence and prognostic implications of vitamin D deficiency in chronic kidney disease. Disease markers, 2015(1), 868961.
[5] Liu, W. C., Wu, C. C., Hung, Y. M., Liao, M. T., Shyu, J. F., Lin, Y. F., ... & Yeh, K. C. (2016). Pleiotropic effects of vitamin D in chronic kidney disease. Clinica chimica acta, 453, 1-12.
[6] Mahmood, H., & Abass, E. A. A. (2022). Association between periostin and bone minerals in osteoporosis and osteopenia Iraqi patients. Int. J. Health Sci, 9633-9644.
[7] Ciosek, Ż., Kot, K., Kosik-Bogacka, D., Łanocha-Arendarczyk, N., & Rotter, I. (2021). The effects of calcium, magnesium, phosphorus, fluoride, and lead on bone tissue. Biomolecules, 11(4), 506.
[8] Brini, M., Ottolini, D., Calì, T., & Carafoli, E. (2013). Calcium in health and disease. Interrelations between essential metal ions and human diseases, 81-137.
[9] Deluque, A. L., Dimke, H., & Alexander, R. T. (2025). Biology of calcium homeostasis regulation in intestine and kidney. Nephrology Dialysis Transplantation, 40(3), 435-445.
[10] Liu, J., Tio, M. C., Verma, A., Schmidt, I. M., Ilori, T. O., Knauf, F., ... & Waikar, S. S. (2022). Determinants and outcomes associated with urinary calcium excretion in chronic kidney disease. The Journal of Clinical Endocrinology & Metabolism, 107(1), e281-e292.
[11] Rastogi, A., Bhatt, N., Rossetti, S., & Beto, J. (2021). Management of hyperphosphatemia in end-stage renal disease: a new paradigm. Journal of Renal Nutrition, 31(1), 21-34.
[12] Cano, A., Chedraui, P., Goulis, D. G., Lopes, P., Mishra, G., Mueck, A., ... & Lambrinoudaki, I. (2018). Calcium in the prevention of postmenopausal osteoporosis: EMAS clinical guide. Maturitas, 107, 7-12.
[13] Stremke, E. R., & Hill Gallant, K. M. (2018). Intestinal phosphorus absorption in chronic kidney disease. Nutrients, 10(10), 1364.
[14] Khundmiri, S. J., Murray, R. D., & Lederer, E. (2016). PTH and vitamin D. Comprehensive Physiology, 6(2), 561.
[15] Michels, T. C., & Kelly, K. M. (2013). Parathyroid disorders. American family physician, 88(4), 249-257.
[16] Felsenfeld, A. J., Levine, B. S., & Rodriguez, M. (2015, November). Pathophysiology of calcium, phosphorus, and magnesium dysregulation in chronic kidney disease. In Seminars in dialysis (Vol. 28, No. 6, pp. 564-577).
[17] Portales-Castillo, I., & Simic, P. P. T. H. (2022). PTH, FGF-23, Klotho and Vitamin D as regulators of calcium and phosphorus: Genetics, epigenetics and beyond. Front Endocrinol 2022; 13: 992666.
[18] Hart, N. H., Newton, R. U., Tan, J., Rantalainen, T., Chivers, P., Siafarikas, A., & Nimphius, S. (2020). Biological basis of bone strength: anatomy, physiology and measurement. Journal of musculoskeletal & neuronal interactions, 20(3), 347.
[19] Goldstein-Fuchs, J., & Fouque, D. (2009). The ubiquitous nature and elusive role of phosphorus and vascular calcification. American Journal of Kidney Diseases, 53(3), 363-365.
[20] Almquist, M., Isaksson, E., & Clyne, N. (2020). The treatment of renal hyperparathyroidism. Endocrine-related cancer, 27(1), R21-R34
[21] Makras, P., Yavropoulou, M. P., Kassi, E., Anastasilakis, A. D., Vryonidou, A., & Tournis, S. (2020). Management of parathyroid disorders: recommendations of the working group of the Bone Section of the Hellenic Endocrine Society. Hormones, 19(4), 581-591.
[22] Naveh-Many, T., & Volovelsky, O. (2020). Parathyroid cell proliferation in secondary hyperparathyroidism of chronic kidney disease. International journal of molecular sciences, 21(12), 4332.
[23] Brandenburg, V., & Ketteler, M. (2022). Vitamin D and secondary hyperparathyroidism in chronic kidney disease: a critical appraisal of the past, present, and the future. Nutrients, 14(15), 3009.
[24] L. Hu et al., “Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic,” Oct. 01, 2022, MDPI. doi: 10.3390/ijms232012223.
[25] Hou, Y. C., Lu, C. L., & Lu, K. C. (2018). Mineral bone disorders in chronic kidney disease. Nephrology, 23, 88-94.
[26] M. van Driel and J. P. T. M. van Leeuwen, “Vitamin D and Bone: A Story of Endocrine and Auto/Paracrine Action in Osteoblasts,” Feb. 01, 2023, MDPI. doi: 10.3390/nu15030480.
[27] Shifrin, A. (2020). Brief overview of calcium, vitamin D, parathyroid hormone metabolism, and calcium-sensing receptor function. Advances in Treatment and Management in Surgical Endocrinology, 63-70.
[28] Burnier, M., & Damianaki, A. (2023). Hypertension as cardiovascular risk factor in chronic kidney disease. Circulation research, 132(8), 1050-1063.
[29] Makris, K., Sempos, C., & Cavalier, E. (2020). The measurement of vitamin D metabolites: part I—metabolism of vitamin D and the measurement of 25-hydroxyvitamin D. Hormones, 19(2), 81-96.
[30] Moor, M. B., & Bonny, O. (2016). Ways of calcium reabsorption in the kidney. American Journal of Physiology-Renal Physiology, 310(11), F1337-F1350.
[31] Asaduzzaman, M., Shobnam, A., Farukuzzaman, M. D., Gaffar, A., Juliana, F. M., Sharker, T., ... & Islam, M. J. (2018). Assessment of red blood cell indices, white blood cells, platelet indices and procalcitonin of chronic kidney disease patients under hemodialysis. Int. J. Health Sci. Res, 8, 98-109.
[32] Levey, A. S., Inker, L. A., & Coresh, J. (2014). GFR estimation: from physiology to public health. American Journal of Kidney Diseases, 63(5), 820-834.
[33] R. M. Hanna, E. Streja, and K. Kalantar-Zadeh, “Burden of Anemia in Chronic Kidney Disease: Beyond Erythropoietin,” Jan. 01, 2021, Adis. doi: 10.1007/s12325-020-01524-6.
[34] Kurella Tamura, M., Vittinghoff, E., Yang, J., Go, A. S., Seliger, S. L., Kusek, J. W., ... & Yaffe, K. (2016). Anemia and risk for cognitive decline in chronic kidney disease. BMC nephrology, 17, 1-7.
[35] Zhong, H., Lin, W., & Zhou, T. (2020). Current and emerging drugs in the treatment of anemia in patients with chronic kidney disease. Journal Of Pharmacy & Pharmaceutical Sciences, 23, 278-288.
[36] Tervaert, T. W. C., Mooyaart, A. L., Amann, K., Cohen, A. H., Cook, H. T., Drachenberg, C. B., ... & Bruijn, J. A. (2010). Pathologic classification of diabetic nephropathy. Journal of the American Society of Nephrology, 21(4), 556-563.
[37] Rahhal, M. N., Gharaibeh, N. E., Rahimi, L., & Ismail-Beigi, F. (2019). Disturbances in insulin–glucose metabolism in patients with advanced renal disease with and without diabetes. The Journal of Clinical Endocrinology & Metabolism, 104(11), 4949-4966.
[38] Kreiner, F. F., Kraaijenhof, J. M., von Herrath, M., Hovingh, G. K. K., & von Scholten, B. J. (2022). Interleukin 6 in diabetes, chronic kidney disease, and cardiovascular disease: mechanisms and therapeutic perspectives. Expert review of clinical immunology, 18(4), 377-389.
[39] Groth, T., Stegmayr, B. G., Ash, S. R., Kuchinka, J., Wieringa, F. P., Fissell, W. H., & Roy, S. (2023). Wearable and implantable artificial kidney devices for end‐stage kidney disease treatment: current status and review. Artificial Organs, 47(4), 649-666.
[40] S. M. S Alfahdawi Babasaheb Ambedkar, “Biochemical Investigation to Determine the Factors Involved in Renal Failure Formation for Dialysis Patients.” [Online]. Available: https://www.researchgate.net/publication/357555820
[41] Muglia, L., Di Dio, M., Filicetti, E., Greco, G. I., Volpentesta, M., Beccacece, A., ... & Soraci, L. (2024). Biomarkers of chronic kidney disease in older individuals: navigating complexity in diagnosis. Frontiers in Medicine, 11, 1397160.
[42] Ortiz, A., Ardiles, L., Pefaur, J., Goecke, H., Roessler, E., Elgueta, S., & Rosati, P. (2021). Nephrology in Chile. Nephrology Worldwide, 139-145.
[43] Zhang, X., Bansal, N., Go, A. S., & Hsu, C. Y. (2015). Gastrointestinal symptoms, inflammation and hypoalbuminemia in chronic kidney disease patients: a cross-sectional study. BMC nephrology, 16, 1-8.
[44] Alencar, S. B. D., de Lima, F. M., Dias, L. D. A., Dias, V. D. A., Lessa, A. C., Bezerra, J. M., ... & de Petribu, K. C. (2019). Depression and quality of life in older adults on hemodialysis. Brazilian Journal of Psychiatry, 42(2), 195-200.
[45] Izzo, C., Secondulfo, C., Bilancio, G., Visco, V., Virtuoso, N., Migliarino, S., ... & Vecchione, C. (2024). Chronic kidney disease with mineral bone disorder and vascular calcification: an overview. Life, 14(3), 418.
[46] Floege, J., Kim, J., Ireland, E., Chazot, C., Drueke, T., de Francisco, A., ... & ARO Investigators. (2011). Serum iPTH, calcium and phosphate, and the risk of mortality in a European haemodialysis population. Nephrology Dialysis Transplantation, 26(6), 1948-1955.
[47] Mazzaferro, S., de Martini, N., Cannata-Andía, J., Cozzolino, M., Messa, P., Rotondi, S., ... & ERA-EDTA CKD-MBD Working Group†. (2021). Focus on the possible role of dietary sodium, potassium, phosphate, magnesium, and calcium on CKD progression. Journal of clinical medicine, 10(5), 958.
[48] Xiao, W., Wang, Y., Pacios, S., Li, S., & Graves, D. T. (2015). Cellular and molecular aspects of bone remodeling. Frontiers of oral biology, 18, 9.
[49] Dedic, C., Hung, T. S., Shipley, A. M., Maeda, A., Gardella, T., Miller, A. L., ... & Rubinacci, A. (2018). Calcium fluxes at the bone/plasma interface: acute effects of parathyroid hormone (PTH) and targeted deletion of PTH/PTH-related peptide (PTHrP) receptor in the osteocytes. Bone, 116, 135-143.
[50] Hou, Y. C., Lu, C. L., & Lu, K. C. (2018). Mineral bone disorders in chronic kidney disease. Nephrology, 23, 88-94.
[51] Bacchetta, J., Bardet, C., & Prié, D. (2020). Physiology of FGF23 and overview of genetic diseases associated with renal phosphate wasting. Metabolism, 103, 153865.
[52] Gohil, A., & Imel, E. A. (2019). FGF23 and associated disorders of phosphate wasting. Pediatric endocrinology reviews: PER, 17(1), 17.
[53] Shroff, R. (2013). Phosphate is a vascular toxin. Pediatric nephrology, 28(4), 583-593.
[54] Lalayiannis, A. D. (2023). Bone mineral density and vascular calcification in children and young adults with chronic kidney disease (Doctoral dissertation, UCL (University College London)).
[55] Levassort, H., Boucquemont, J., Lambert, O., Liabeuf, S., Laville, S. M., Teillet, L., ... & Ckd-Rein Study Collaborators. (2024). Urea level and depression in patients with chronic kidney disease. Toxins, 16(7), 326.
[56] Cukor, D. (2021, December). Introduction: psychosocial issues in kidney disease. In Seminars in Nephrology (Vol. 41, No. 6, p. 485).
[57] Viaene, L., Behets, G. J., Heye, S., Claes, K., Monbaliu, D., Pirenne, J., ... & Evenepoel, P. (2016). Inflammation and the bone-vascular axis in end-stage renal disease. Osteoporosis International, 27, 489-497.
[58] Evenepoel, P., Dejongh, S., Verbeke, K., & Meijers, B. (2020). The role of gut dysbiosis in the bone–vascular axis in chronic kidney disease. Toxins, 12(5), 285.
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