scholarly journals Differential diagnosis of hypercalcemia in a patient with CKD G5D

2021 ◽  
Author(s):  
A. K. Eremkina ◽  
A. M. Gorbacheva ◽  
D. V. Lisina ◽  
A. A. Povaliaeva ◽  
E. A. Pigarova ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Differential Diagnosis ◽  
Secondary Hyperparathyroidism ◽  
Bone Mineralization ◽  
Intact Parathyroid Hormone ◽  
Adynamic Bone Disease ◽  
Vitamin D Metabolism ◽  
Adynamic Bone ◽  
Serum Pth

Patients with chronic kidney disease are characterized by the development of mineral disorders due to a decrease in the number of functioning nephrons. These changes manifest by the development of secondary hyperparathyroidism (the overproduction of intact parathyroid hormone (PTH) associated with the serum hypocalcemia, hyperphosphatemia), dysfunctional vitamin D metabolism, bone mineralization and also extraosseous calcifications. Decreased serum PTH levels associated with hypercalcemia are suspicious for adynamic bone disease, but at the same time requires an extended differential diagnostic search (e.g. metastatic processes). One of the rare causes of hypercalcemia is a defect in 24-hydroxylase (CYP24A1). We present a case of a patient on hemodialysis with atypical secondary hyperparathyroidism and an established CYP24A1 defect.

scholarly journals Problems in differential diagnosis of secondary hyperparathyroidism

2021 ◽  
Vol 38 (1) ◽  
pp. 161-167
Author(s):  
S. G. Shulkina ◽  
D. O. Sirin ◽  
E. N. Smirnova ◽  
V. G. Zhelobov ◽  
N. Yu. Kolomeets ◽  
...  
Keyword(s):  
Vitamin D ◽  
Differential Diagnosis ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Clinical Case ◽  
Kidney Diseases ◽  
Active Form ◽  
Renal Tubules ◽  
Vitamin D Metabolism

Hyperparathyroidism is an endocrine disease characterized by excessive production of parathyroid hormone in the main cells of the parathyroid glands. Depending on the cause of this disease, there are primary, secondary (SHPT) and tertiary hyperparathyroidism. The most common causes of SHPT are vitamin D deficiency and chronic kidney disease (CKD). Vitamin D is converted to its active form by hydroxylation in the renal tubules. Developmental abnormalities and chronic kidney diseases lead to atrophy of the tubular epithelial cells that causes a violation of vitamin D metabolism and the development of SHPT, which in turn are accompanied by a violation of calcium-phosphorus metabolism and a syndrome of musculoskeletal disorders. This article presents an analysis of a clinical case of a patient diagnosed secondary hyperparathyroidism against the background of vitamin D deficiency combined with polycystic kidney disease. This clinical case reflects the complexity of the differential diagnosis of the disease and the tactics of patient's management.

scholarly journals Vitamin D Metabolism and Its Role in Mineral and Bone Disorders in Chronic Kidney Disease in Humans, Dogs and Cats

Metabolites ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 499
Author(s):  
Fernanda C. Chacar ◽  
Márcia M. Kogika ◽  
Rafael V. A. Zafalon ◽  
Marcio A. Brunetto
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Comparative Studies ◽  
Mineral Metabolism ◽  
Vitamin D Metabolism ◽  
Bone Disorders

Some differences regarding Vitamin D metabolism are described in dogs and cats in comparison with humans, which may be explained by an evolutionary drive among these species. Similarly, vitamin D is one of the most important regulators of mineral metabolism in dogs and cats, as well as in humans. Mineral metabolism is intrinsically related to bone metabolism, thus disturbances in vitamin D have been implicated in the development of chronic kidney disease mineral and bone disorders (CKD-MBD) in people, in addition to dogs and cats. Vitamin D deficiency may be associated with Renal Secondary Hyperparathyroidism (RSHPT), which is the most common mineral disorder in later stages of CKD in dogs and cats. Herein, we review the peculiarities of vitamin D metabolism in these species in comparison with humans, and the role of vitamin D disturbances in the development of CKD-MBD among dogs, cats, and people. Comparative studies may offer some evidence to help further research about vitamin D metabolism and bone disorders in CKD.

scholarly journals Treatment of mineral-bone disorders in chronic kidney disease

2020 ◽  
Vol 29 (4) ◽  
pp. 85-90
Author(s):  
I.T. Murkamilov ◽  
K.A. Aitbaev ◽  
V.V. Fomin ◽  
Zh.A. Murkamilova ◽  
F.A. Yusupov
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Ectopic Calcification ◽  
Serum Parathyroid Hormone ◽  
Adynamic Bone Disease ◽  
Bone Disorders ◽  
Increased Risk ◽  
Adynamic Bone

Mineral-bone disorders (MBD) in chronic kidney disease (CKD) manifest by hyperphosphatemia, vitamin D deficiency, overproduction of fibroblast growth factor-23, and secondary hyperparathyroidism. CKD-MBD also results in bone resorp-tion and ectopic calcification that is associated with an increased risk of cardiovascular events and mortality. Diet is the initial and obligatory approach to treatment for CKD-MBD. Sevelamer is frequently used for correction of hyperphosphatemia in patients with renal failure who present with calcification of arteries, adynamic bone disease and/or stably low serum parathyroid hormone levels. Calcimimetics, that is, cinacalcet and evocalcet, are widely used in hemodialysis patients who do not respond to treatment with vitamin D.

Vitamin D Deficiency and Intoxication - A concern either way

JMS SKIMS ◽  
2011 ◽  
Vol 14 (2) ◽  
pp. 40-42
Author(s):  
Muzafar Maqsood Wani ◽  
Imtiaz Ahmed Wani
Keyword(s):  
Vitamin D ◽  
Cell Growth ◽  
Bone Turnover ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Bone Mineralization ◽  
Normal Blood ◽  
Blood Levels ◽  
Calcium And Phosphorus ◽  
Biologic Function

Major biologic function of activated vitamin D is to maintain normal blood levels of calcium and phosphorus, thus regulating bone mineralization. Research suggests that vitamin D may help in immunomodulation, regulating cell growth and 1,4 differentiation as well as some diverse unspecified functions. Overt vitamin D deficiency leads to hypocalcaemia, secondary hyperparathyroidism and increased bone turnover, which in prolonged and severe cases may cause rickets in children and osteomalacia in elderly.... JMS 2011;14(2):40-42

FGF23, iron and vitamin D metabolism in chronic kidney disease

2016 ◽  
Author(s):  
Isabelle Piec ◽  
Allison Chipchase ◽  
Holly Nicholls ◽  
Jonathan Tang ◽  
Christopher Washbourne ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Metabolism

Vitamin D Metabolism and Potential Effects of Vitamin D Receptor Modulation in Chronic Kidney Disease

2017 ◽  
Vol 18 (7) ◽  
Author(s):  
Antonio Bellasi ◽  
Andrea Galassi ◽  
Michela Mangano ◽  
Luca Di Lullo ◽  
Mario Cozzolino
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Receptor ◽  
Vitamin D Metabolism ◽  
Receptor Modulation

scholarly journals Effects of Dietary Phosphate on Adynamic Bone Disease in Rats with Chronic Kidney Disease – Role of Sclerostin?

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79721 ◽  
Author(s):  
Juliana C. Ferreira ◽  
Guaraciaba O. Ferrari ◽  
Katia R. Neves ◽  
Raquel T. Cavallari ◽  
Wagner V. Dominguez ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Disease ◽  
Adynamic Bone Disease ◽  
Dietary Phosphate ◽  
Adynamic Bone

scholarly journals New Pathogenic Concepts and Therapeutic Approaches to Oxidative Stress in Chronic Kidney Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
José Pedraza-Chaverri ◽  
Laura G. Sánchez-Lozada ◽  
Horacio Osorio-Alonso ◽  
Edilia Tapia ◽  
Alexandra Scholze
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Cardiovascular Complications ◽  
Vitamin D Metabolism ◽  
Therapy Options ◽  
Mitochondrial Alterations ◽  
Inflammatory Processes ◽  
The Impact

In chronic kidney disease inflammatory processes and stimulation of immune cells result in overproduction of free radicals. In combination with a reduced antioxidant capacity this causes oxidative stress. This review focuses on current pathogenic concepts of oxidative stress for the decline of kidney function and development of cardiovascular complications. We discuss the impact of mitochondrial alterations and dysfunction, a pathogenic role for hyperuricemia, and disturbances of vitamin D metabolism and signal transduction. Recent antioxidant therapy options including the use of vitamin D and pharmacologic therapies for hyperuricemia are discussed. Finally, we review some new therapy options in diabetic nephropathy including antidiabetic agents (noninsulin dependent), plant antioxidants, and food components as alternative antioxidant therapies.

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