Extraosseous Calcification in End‐stage Renal Disease: From Visceral Organs to Vasculature

Abstract

In earlier days, periarticular accumulations of calcium phosphate causing tumor-like depositions were considered the result of passive precipitation and referred to as metastatic calcifications. From sophisticated computer tomographic studies and growing insight, we have learned that calcifications in the cardiovascular system are far more threatening and in fact one of the most important sequela of end-stage renal disease. The histologic characteristic of uremia-related calcification is arteriosclerosis of the media. In addition, there is atherosclerosis of the intima, due to the high prevalence of classic cardiovascular risk factors in renal disease. The two vascular features can frequently exist at different sites in the vasculature. Novel diagnostic techniques are helping to elucidate the pathogenetic mechanisms of active conversion of vascular smooth muscle cells to osteochondritic cells. Through this process, extensive calcification of the central and peripheral vasculature ensues, influenced by different promotors and inhibitors. Calciphylaxis is a special form of extraosseous calcification leading to skin necrosis. The factors that trigger the development of calciphylaxis are not completely understood, but this syndrome shares part of the pathophysiologic basis of extraosseous calcification in general. However, the therapeutic approach must be prompt and aggressive, because of the poor prognosis. Frequently, a fatal outcome cannot be avoided in calciphylaxis.

Blood pressure as prognostic marker for body condition, cardiovascular, and metabolic diseases in the common marmoset (Callithrix jacchus)

“…The underlying reason for the congested renal pelvis and ureter in patient 1712.1 could not be evaluated conclusively, but they could have been caused by ureteral calculi [38]. The secondary findings in patient 1712.1 (alterations in the ribs and calcification in aorta and bronchial tubes) were also typical for renal diseases, through which renal hyperthyroidism and metastatic calcification may occur [36].…”

Calcium phosphate bions: towards a pathogenetic concept

“…Вместе с тем было выявлено, что КФБ выделяются из приблизительно 75% атеросклеротических бляшек крупных артерий человека, оказывают прямое цитотоксическое действие на эндотелиальные клетки in vitro, стимулируют выделение ими провоспалительных цитокинов интерлейкина-6 и интерлейкина-8, а при предварительном повреждении интимы брюшной аорты крыс баллоном вызывают ее гипертрофию, являющуюся характерным признаком атеросклероза [30]. Таким образом, защищая организм от «большего зла» -быстрой и массивной кальцификации сосудов [31,32], КФБ тем не менее потенциально могут являться одним из триггеров атеросклероза.…”

Compressive myelopathy from diffuse spinal dural calcifications in a patient with end-stage renal disease: illustrative case

“…In the spine, these metabolic derangements can result in paradoxical responses, including weakened bones, aberrant calcium deposition, and other hallmarks of renal osteodystrophy. 1–5 …”