Epidemiology of calcium, phosphate, and parathyroid hormone disturbances in chronic kidney disease

2018 ◽  
Author(s):  
Patrick Biggar ◽  
Hansjörg Rothe ◽  
Markus Ketteler
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Calcium Phosphate ◽  
Kidney Disease ◽  
Bone Biopsy ◽  
Normal Population ◽  
Laboratory Parameter ◽  
Risk Indicator ◽  
Calcium Balance ◽  
Wide Range

Chronic kidney disease-mineral and bone disorders (CKD-MBD), calcium, phosphate, and parathyroid hormone are biomarkers of mortality and cardiovascular risk. Hyperphosphataemia is a prominent and pathophysiologically most plausible risk indicator. Calcium balance and load appear to be more important than serum concentrations. Parathyroid hormone is a less reliable marker with a relatively wide range extending above that applicable for a normal population especially when used as a singular laboratory parameter without additional assessment of bone metabolism, for example, bone-specific alkaline phosphatase and bone biopsy. There is not a single prospective controlled hard-outcome study that provides us with unequivocal evidence that such an isolated laboratory parameter-based treatment approach will lead to significant clinical improvements. As CKD-MBD is complex, clinical decisions would be made easier by informative prospective trials.

scholarly journals Parathyroid Hormone Measurement in Chronic Kidney Disease: From Basics to Clinical Implications

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Kittrawee Kritmetapak ◽  
Chatlert Pongchaiyakul
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Renal Osteodystrophy ◽  
Biologically Active ◽  
Intact Pth ◽  
Current Standard ◽  
Mineral And Bone Disorder ◽  
Wide Range ◽  
Serum Pth

Accurate measurement of parathyroid hormone (PTH) is crucial for therapeutic decision-making in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD). The second-generation PTH assays, often referred to as “intact PTH” assays, are the current standard and most available assays in clinical practice. However, intact PTH assays measure both full-length biologically active PTH and heterogeneous PTH fragments in the circulation, providing the equivocal value of PTH measurement in patients with CKD-MBD. Due to the variability of PTH assays, preanalytical sample errors, and the phenomenon of end-organ PTH hyporesponsiveness, current CKD-MBD guidelines recommend a wide range for serum PTH targets (2–9 the upper normal limit of the intact PTH assay) in dialysis patients to diminish the risk of developing adynamic bone disease. Nevertheless, a sizeable proportion of CKD patients still experience renal osteodystrophy despite having serum PTH levels within the recommended range. The primary cause of this inconsistency is the analytical interference of various PTH fragments and oxidized PTH forms that considerably accumulate in CKD patients. Therefore, a new mass spectrometry-based assay, which is capable of specifically measuring the whole spectra of PTH fragments, can potentially improve diagnostic accuracy for renal osteodystrophy. However, the effects of different PTH fragments on bone metabolism, vascular calcification, and mortality in CKD patients warrant further research.

scholarly journals Bone disease in patients with chronic kidney disease under conservative management

2005 ◽  
Vol 123 (2) ◽  
pp. 83-87 ◽  
Author(s):  
Carlos Perez Gomes ◽  
Maria Inês Barreto Silva ◽  
Maria Eugênia Leite Duarte ◽  
David Dorigo ◽  
Carla Cavalheiro da Silva Lemos ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Creatinine Clearance ◽  
Conservative Management ◽  
Bone Disease ◽  
Bone Biopsy ◽  
Case Series ◽  
Calcium Phosphorus

CONTEXT AND OBJECTIVE: Few studies have focused on bone disease in patients with chronic kidney disease under conservative treatment. The objective was to evaluate bone disease in patients with chronic kidney disease. DESIGN AND SETTING: Case series, at the Nephrology Division, Hospital Universitário Pedro Ernesto. METHODS: 131 patients with creatinine clearance from 10 to 60 ml/min/1.73 m² were followed up for at least one year. Serum creatinine, albumin, calcium, phosphorus, alkaline phosphatase, total CO2 (tCO2), intact parathyroid hormone (iPTH), and alkaline phosphatase were measured. Creatinine clearance was calculated from 24-hour urine creatinine measurements and protein ingestion estimates from urea assays. RESULTS: Patients presenting creatinine clearance < 30 ml/min/1.73 m² had higher iPTH values, but normal serum levels for calcium, phosphorus, alkaline phosphatase and tCO2. Patients presenting iPTH values of twice the normal upper limit (144 pg/ml) showed lower tCO2 values. Bone alkaline phosphatase was evaluated in 37 patients with creatinine clearance < 30 ml/min/1.73 m², showing correlation with alkaline phosphatase but not with parathyroid hormone. Bone biopsy on nine patients with creatinine clearance < 30 ml/min/1.73 m² and iPTH > 144 pg/ml showed osteitis fibrosa (4), mild lesion (4) and high turnover (1). CONCLUSION: The present data suggest the importance of early control for iPTH and metabolic acidosis, among patients under conservative management for chronic kidney disease, in order to prevent complications related to bone disease.

Mineral metabolism

2018 ◽  
pp. 297-329
Author(s):  
Helen E. Turner ◽  
Richard Eastell ◽  
Ashley Grossman
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Calcium Phosphate ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Treatment Options ◽  
Endocrine System ◽  
Hypophosphataemic Rickets ◽  
Serum Pth

This chapter discusses skeletal functions and interactions between the endocrine system and the body’s mineral store. It describes minerals like calcium, phosphate, and magnesium’s regulation by hormones like parathyroid hormone (PTH), vitamin D, and calcitonin. It also investigates mineral-related disorders, such as hypercalcaemia, hypocalcaemia, pseudohypoparathyroidism, and hypophosphataemic rickets, describing their relations with serum PTH, symptoms, genetic causes, and treatment options. Separating disorders of phosphate homeostasis into hypophosphataemia, hyperphosphataemia, and chronic kidney disease, this chapter offers clinical advice on treating mineral–hormonal disorders and describes the symptoms and causes of disruptions in mineral homeostasis.

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