Search

Background. In COVID-19 patients, low serum vitamin D (VD) levels have been associated with severe acute respiratory failure and poor prognosis. In regular hemodialysis (HD) patients, there is VD deficiency and markedly reduced calcitriol levels, which may predispose them to worse outcomes of COVID-19 infection. Some hemodialysis patients receive treatment with drugs for secondary hyperparathyroidism, which have well known pleiotropic effects beyond mineral metabolism. The aim of this study was to evaluate the impact of VD status and the administration of active vitamin D medications, used to treat secondary hyperparathyroidism, on survival in a cohort of COVID-19 positive HD patients. Methods. A cross-sectional retrospective observational study was conducted from 12 March to 21 May 2020 in 288 HD patients with positive PCR for SARS-CoV2. Patients were from 52 different centers in Spain. Results. The percent of HD patients with COVID-19 was 6.1% (288 out of 4743). Mortality rate was 28.4% (81/285). Three patients were lost to follow-up. Serum 25(OH)D (calcidiol) level was 17.1 [10.6–27.5] ng/mL and was not significantly associated to mortality (OR 0.99 (0.97–1.01), p = 0.4). Patients receiving active vitamin D medications (16/94 (17%) vs. 65/191(34%), p = 0.003), including calcimimetics (4/49 (8.2%) vs. 77/236 (32.6%), p = 0.001), paricalcitol or calcimimetics (19/117 (16.2%) vs. 62/168 (36.9%), p &lt, 0.001), and also those on both paricalcitol and calcimimetics, to treat secondary hyperparathyroidism (SHPTH) (1/26 (3.8%) vs. 80/259 (30.9%), p &lt, 0.001) showed a lower mortality rate than patients receiving no treatment with either drug. Multivariate Cox regression analysis confirmed this increased survival. Conclusions. Our findings suggest that the use of paricalcitol, calcimimetics or the combination of both, seem to be associated with the improvement of survival in HD patients with COVID-19. No correlation was found between serum VD levels and prognosis or outcomes in HD patients with COVID-19. Prospective studies and clinical trials are needed to support these findings.

Pseudoxanthoma elasticum (PXE) is a rare genetic disorder characterized by calcification of elastic fibres, skin lesions, fundus lesions and systemic vascular complications. PXE affects approximately 1 in 160,000 people, typically appearing as a formation of yellow papules containing abnormally calcified elastic fibres. The renal involvement of PXE has been reported. Several factors are known to promote soft tissue and accelerated arterial calcification in chronic kidney disease, including systemic inflammation, altered calcium and phosphate homeostasis, hypertension and a deficiency of endogenous calcification inhibitors. Given the impact of this disease, nephrologists may seek additional supportive features to improve and avoid the risk of complications. Moreover, PXE per se represents an interesting model to evaluate vascular disease in the early stages of renal disease. LEARNING POINTS Pseudoxanthoma elasticum represents a rare disease that can involve renal problems. Vascular compromise in patients affected by pseudoxanthoma elasticum shares some components observed in patients with chronic kidney disease. Disorders of mineral and bone metabolism may coexist or be hidden in patients with pseudoxanthoma elasticum. Keywords: Pseudoxanthoma, chronic Kidney disease, cardiorenal INTRODUCTION Pseudoxanthoma elasticum (PXE) is a rare genetic disorder caused by mutations in the ABCC6 gene, which is characterized by calcification of elastic fibres, skin lesions, fundus lesions and systemic cardiovascular complications, including coronary artery lesions, lower-leg arterial lesions and gastrointestinal bleeding[1]. The mode of inheritance in most families is autosomal recessive, but PXE with autosomal dominant inheritance has also been reported. PXE affects approximately 1 in 160,000 people, typically appearing as a formation of yellow papules containing abnormally calcified elastic fibres. Cutaneous lesions are seen in the neck, axilla, cubital fossa, inguinal region and periumbilical area. Angioid streaks are typically seen in the fundus due to breaks in Bruch’s membrane. Thus, PXE represents a model disease for arteriosclerosis as it is thought to encompass an isolated arteriosclerotic type of arterial wall disease with relatively little interference by atherosclerotic arterial wall disease. Patients with PXE have low levels of inorganic pyrophosphate, a strong inhibitor of ectopic mineralization. This leads to a typical pattern of progressive calcification of elastic fibres in the skin, eyes and vasculature[2]. The renal involvement of PXE has been reported. Several factors are known to promote soft tissue and accelerated arterial calcification in chronic kidney disease (CKD), including systemic inflammation, altered calcium and phosphate homeostasis, hypertension and a deficiency of endogenous calcification inhibitors. Lau et al. reported for the first time that CKD results in acquired ABCC6 transporter deficiency which may contribute to CKD-associated vascular and soft tissue calcification[3]. On the contrary, although calciphylaxis most often occurs in patients with end-stage renal disease (ESRD) and secondary hyperparathyroidism, non-uremic calciphylaxis has been described in PXE-affected patients without several forms of CKD.