CHARACTERISTICS OF ALTERATIONS IN PHOSPHORUS-CALCIUM METABOLISM IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND ARTERIAL HYPERTENSION

According to recent research, the number of patients with chronic kidney disease (CKD) — a significant cause of mortality — is increasing globally. Serious complications of CKD include disturbances in phosphorus-calcium metabolism and pathological changes in the cardiovascular system. Arterial hypertension is considered a primary risk factor for the progression of CKD and is present in 85–100% of patients with CKD. On one hand, declining renal function can contribute to the development of hypertension; on the other, arterial hypertension can mask the manifestations of the underlying disease. The objective of the study was to determine the interrelationships between serum phosphorus and calcium levels and urinary hydroxyproline levels in patients with various stages of CKD, depending on the presence of arterial hypertension. The study included 76 patients with CKD (mean age 36.5 ± 12.8 years). By CKD stage, patients were divided into four groups: Stage I — 22 (29%), Stage II — 28 (37%), Stage IIIA — 14 (19%), and Stage IIIB — 12 (15%). By the presence of arterial hypertension, two groups were formed: Group A — 42 patients with hypertension (55%), and Group B — 34 patients without hypertension (45%). The study revealed alterations in phosphorus-calcium metabolism in patients with stages I–III CKD, characterized by a tendency toward elevated phosphorus and decreased calcium levels, as well as alterations in collagen metabolism markers in both groups. The urinary content of total hydroxyproline and its free fraction in patients with CKD — both with and without hypertension — was statistically significantly higher than in healthy individuals (p < 0.05). In Group A, the total hydroxyproline fraction was 38.8 ± 3.7 mg/day, and in Group B, 37.3 ± 5.4 mg/day; the free fraction was 6.86 ± 1.02 mg/day in Group A and 4.04 ± 0.47 mg/day in Group B. It was concluded that disturbances of phosphorus-calcium metabolism accompany CKD and are associated with increased urinary excretion of the free hydroxyproline fraction, while the presence of arterial hypertension is associated with more pronounced disturbances of mineral and collagen metabolism in patients with CKD.References1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. (2024). KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney International, 105(4S), S117–S314. https://doi.org/10.1016/j.kint.2023.10.0182. Kovesdy, C. P. (2022). Epidemiology of chronic kidney disease: An update 2022. Kidney International Supplements, 12(1), 7–11. https://doi.org/10.1016/j.kisu.2021.11.0033. Centeno, P. P., Herberger, A., Mun, H. C., Tu, C., Nemeth, E. F., Chang, W., Conigrave, A. D., & Ward, D. T. (2019). Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion. Nature Communications, 10(1), 4693. https://doi.org/10.1038/s41467-019-12399-94. Duque, E. J., Elias, R. M., & Moysés, R. M. A. (2020). Parathyroid hormone: A uremic toxin. Toxins, 12(3), 189. https://doi.org/10.3390/toxins120301895. Gutierrez, O., Isakova, T., Rhee, E., Shah, A., Holmes, J., Collerone, G., Jüppner, H., & Wolf, M. (2005). Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. Journal of the American Society of Nephrology, 16(7), 2205–2215. https://doi.org/10.1681/ASN.20050100526. Natale, P., Green, S. C., Ruospo, M., Craig, J. C., Vecchio, M., Elder, G. J., & Strippoli, G. F. (2025). Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD). Cochrane Database of Systematic Reviews. https://doi.org/10.1002/14651858.CD006023.pub47. Torres Sánchez, M. J., et al. (2024). Hydroxyproline in urine microvesicles as a biomarker of fibrosis in the renal transplant patient. Biomedicines, 12(12), 2836. https://doi.org/10.3390/biomedicines121228368. Hsu, C. Y., Chen, L. R., & Chen, K. H. (2020). Osteoporosis in patients with chronic kidney diseases: A systematic review. International Journal of Molecular Sciences, 21(18), 6846. https://doi.org/10.3390/ijms211868469. Iwasaki, Y., Kazama, J. J., & Fukagawa, M. (2017). Molecular abnormalities underlying bone fragility in chronic kidney disease. BioMed Research International, 2017, 3485785. https://doi.org/10.1155/2017/348578510. Wang Q, Cui Y, Yogendranath P, Wang N. (2018) Blood pressure and heart rate variability are linked with hyperphosphatemia in chronic kidney disease patients. Chronobiol Int.;35(10):1329–34. https://doi.org/10.1080/07420528.2018.148685011. 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. https://doi.org/10.1053/j.jrn.2020.02.00312. Sidar Copur , Duygu Ucku , Mario Cozzolino , Mehmet Kanbay. (2022). Hypoxia-inducible factor signaling in vascular calcification in chronic kidney disease patients. Journal of Nephrology, Volume 35, Issue 9, 1 December 2022, Pages 2205–2213. https://doi.org/10.1007/s40620-022-01432-8