[Uremic calciphylaxis].

Uremic calciphylaxis is a rare disease that affects patients with chronic end-stage renal disease. It is a pathology of the microvessels of the dermis and hypodermis which are calcified and whose thrombosis leads to skin necrosis. Calciphylaxis lesions can be distal and axial.

Bone Fragility in Chronic Kidney Disease Stage 3 to 5: The Use of Vitamin D Supplementation.

Frequently silent until advanced stages, bone fragility associated with chronic kidney disease-mineral and bone disease (CKD-MBD) is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. Altogether, these factors contribute firstly to secondary hyperparathyroidism, and ultimately, to micro- and macrostructural bone changes, which lead to low bone mineral density and an increased risk of fracture.

The Use of Imaging Techniques in Chronic Kidney Disease-Mineral and Bone Disorders (CKD-MBD)-A Systematic Review.

Although frequently silent, mineral and bone disease (MBD) is one of the most precocious complication of chronic kidney disease (CKD) and is omnipresent in patients with CKD stage 5. Its pathophysiology is complex, but basically, disturbances in vitamin D, phosphate, and calcium metabolism lead to a diverse range of clinical manifestations with secondary hyperparathyroidism usually being the most frequent. With the decline in renal function, CKD-MBD may induce microstructural changes in bone, vascular system and soft tissues, which results in macrostructural lesions, such as low bone mineral density (BMD) resulting in skeletal fractures, vascular and soft tissue calcifications.

A Novel Heterozygous Deletion Variant in Gene Leading to Haploinsufficiency and Impairment of Fibroblast Growth Factor 23 Signaling Pathway.

Hyperphosphatemia is commonly present in end-stage renal disease. Klotho (KL) is implicated in phosphate homeostasis since it acts as obligate co-receptor for the fibroblast growth factor 23 (FGF23), a major phosphaturic hormone. We hypothesized that genetic variation in the KL gene might be associated with alterations in phosphate homeostasis resulting in hyperphosphatemia.

Novel insights into parathyroid hormone: report of The Parathyroid Day in Chronic Kidney Disease.

Chronic kidney disease (CKD) is often associated with a mineral and bone disorder globally described as CKD-Mineral and Bone Disease (MBD), including renal osteodystrophy, the latter ranging from high bone turnover, as in case of secondary hyperparathyroidism (SHPT), to low bone turnover. The present article summarizes the important subjects that were covered during 'The Parathyroid Day in Chronic Kidney Disease' CME course organized in Paris in September 2017. It includes the latest insights on parathyroid gland growth, parathyroid hormone (PTH) synthesis, secretion and regulation by the calcium-sensing receptor, vitamin D receptor and fibroblast growth factor 23 (FGF23)-Klotho axis, as well as on parathyroid glands imaging.

Bone, inflammation and the bone marrow niche in chronic kidney disease: what do we know?

Recent improvements in our understanding of physiology have altered the way in which bone is perceived: no longer is it considered as simply the repository of divalent ions, but rather as a sophisticated endocrine organ with potential extraskeletal effects. Indeed, a number of pathologic conditions involving bone in different ways can now be reconsidered from a bone-centred perspective. For example, in metabolic bone diseases like osteoporosis (OP) and renal osteodystrophy (ROD), the association with a worse cardiovascular outcome can be tentatively explained by the possible derangements of three recently discovered bone hormones (osteocalcin, fibroblast growth factor 23 and sclerostin) and a bone-specific enzyme (alkaline phosphatase).

[Utilization of alfacalcidol and active vitamin D analogs in chronic kidney disease].

Secondary hyperparathyroidism (SHPT) is one of the most frequent and deleterious complication of chronic kidney disease (CKD). SHPT is also one of the principal components of the now called CKD-mineral and bone disorders (MBD) syndrome. It is usually prevented and treated by vitamin D derivatives.

[Strategies aiming to control hyperphosphatemia in chronic kidney disease].

Chronic kidney disease is known to be associated with phosphate retention. The mechanisms are complex and the early increase in serum phosphate levels in chronic kidney disease is not strictly related to the dietary phosphate load or to the degree of phosphate retention. It also implicates the activity of intestinal sodium-phosphate cotransporters, the degree of bone turnover and the retention and/or phosphate release from the skeleton, and the feedback mechanisms regulating the phosphaturia.

Iron-based phosphate binders: do they offer advantages over currently available phosphate binders?

Increased cardiovascular morbidity and mortality has been associated with the hyperphosphatemia seen in patients with end-stage chronic kidney disease (CKD). Oral phosphate binders are prescribed in these patients to prevent intestinal absorption of dietary phosphate and reduce serum phosphate. In prospective observational cohorts they have shown to decrease all-cause and cardiovascular mortality risk.

Protocol adherence and the progression of cardiovascular calcification in the ADVANCE study.

Background: The ADVANCE study assessed the progression of vascular and cardiac valve calcification in 360 hemodialysis patients with secondary hyperparathyroidism (sHPT) assigned randomly to treatment either with cinacalcet plus low-dose vitamin D (≤ 6 µg/week of intravenous paricalcitol equivalent) or with varying doses of vitamin D alone for 52 weeks. The primary efficacy endpoint was progression of coronary artery calcification (CAC).

Methods: In this post-hoc analysis, we compared CAC progression among 70 protocol-adherent subjects given cinacalcet and low doses of vitamin D (CPA) as specified in the study protocol and 120 control subjects given vitamin D sterols.

Calcium-sensing receptor, calcimimetics, and cardiovascular calcifications in chronic kidney disease.

Renal function impairment goes along with a disturbed calcium, phosphate, and vitamin D metabolism, resulting in secondary hyperparathyroidism (sHPT). These mineral metabolism disturbances are associated with soft tissue calcifications, particularly arteries, cardiac valves, and myocardium, ultimately associated with increased risk of mortality in patients with chronic kidney disease (CKD). sHPT may lead to cardiovascular calcifications by other mechanisms including an impaired effect of parathyroid hormone (PTH), and a decreased calcium-sensing receptor (CaR) expression on cardiovascular structures.

Three feedback loops precisely regulating serum phosphate concentration.

Parathyroid hormone (PTH) and vitamin D were considered the major factors regulating phosphate homeostasis. Now, with the identification of fibroblast growth factor 23 (FGF23), a phosphaturic molecule inhibiting calcitriol and PTH, they need to be integrated into three feedback loops involving parathyroid, bone, and kidney. PTH and calcitriol are required for the appropriate synthesis of FGF23 by bone cells.