Mineral and Bone Disorders in Chronic Kidney Disease

Cannata-Andía, Jorge B.; Carrillo-López, Natalia; Rodriguez-García, Minerva; Torregrosa, José-Vicente

doi:10.1007/978-3-031-42045-0_16

Cited by 1 publication

(2 citation statements)

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“…While FGF-23 may increase in concentration earlier than PTH on the scale of CKD progression, measurement of PTH is more reliable, cheaper, faster and available on a wider scale [42,46]. Therefore, PTH is deemed a powerful marker for the complication rate starting from stage G3 CKD, specifically when interpreted as the plasmatic trend in association with glomerular filtration rate and clinical presentation [19,51,110].…”

Section: Discussionmentioning

confidence: 99%

“…The frequency of monitoring the biochemical parameters and PTH levels should be based on the magnitude of detected abnormalities and the progression of renal function decline [19]. The diagnostic and management approach of MBD is based on the trend in changes in the relevant markers, with special emphasis on the PTH level [51]. There is a statistically significant relationship between the trend in multiple MBD markers and defined renal endpoints (>30% reduction in GFR, necessity for dialysis or transplantation).…”

Section: Biochemical Diagnosis Of Ckd-mbd: Focus On Pthmentioning

confidence: 99%

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The Molecular Mechanisms Underlying the Systemic Effects Mediated by Parathormone in the Context of Chronic Kidney Disease

Maranduca,

Cozma,

Clim

et al. 2024

CIMB

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Chronic kidney disease (CKD) stands as a prominent non-communicable ailment, significantly impacting life expectancy. Physiopathology stands mainly upon the triangle represented by parathormone–Vitamin D–Fibroblast Growth Factor-23. Parathormone (PTH), the key hormone in mineral homeostasis, is one of the less easily modifiable parameters in CKD; however, it stands as a significant marker for assessing the risk of complications. The updated “trade-off hypothesis” reveals that levels of PTH spike out of the normal range as early as stage G2 CKD, advancing it as a possible determinant of systemic damage. The present review aims to review the effects exhibited by PTH on several organs while linking the molecular mechanisms to the observed actions in the context of CKD. From a diagnostic perspective, PTH is the most reliable and accessible biochemical marker in CKD, but its trend bears a higher significance on a patient’s prognosis rather than the absolute value. Classically, PTH acts in a dichotomous manner on bone tissue, maintaining a balance between formation and resorption. Under the uremic conditions of advanced CKD, the altered intestinal microbiota majorly tips the balance towards bone lysis. Probiotic treatment has proven reliable in animal models, but in humans, data are limited. Regarding bone status, persistently high levels of PTH determine a reduction in mineral density and a concurrent increase in fracture risk. Pharmacological manipulation of serum PTH requires appropriate patient selection and monitoring since dangerously low levels of PTH may completely inhibit bone turnover. Moreover, the altered mineral balance extends to the cardiovascular system, promoting vascular calcifications. Lastly, the involvement of PTH in the Renin–Angiotensin–Aldosterone axis highlights the importance of opting for the appropriate pharmacological agent should hypertension develop.

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