[Hantavirus causing fatal haemorrhagic fever in the Czech Republic]. / Hantavirus jako puvodce smrtelné hemoragické horecky v Ceské republice.

Hantaviruses are RNA viruses of the family Bunyaviridae. Their hosts are mammals of the orders rodents (voles, rats, mice), insectivores (shrews, moles), and chiroptera (bats). Hantaviruses are present in many areas of Europe, the Americas, Asia, and Africa. In the Czech Republic, the occurrence of five species of hantaviruses has been reported (Dobrava/Belgrade, Puumala, Tula, Seewis, and Asikkala), with the first three of them causing human diseases. Although the course of hantavirus infections can be very serious, there is a low awareness of these diseases, even among health professionals, and hantavirus is often not considered in the diagnosis. A case history is reported of a patient who developed hantavirus haemorrhagic fever with renal syndrome (HFRS) with fatal outcome. The patient presented with typical clinical signs, but the correct diagnosis was only made at post mortem.

Effect of kidney transplantation on bone.

A broad range of different factors aggravates renal osteodystrophy, which is present in virtually all patients with chronic kidney disease and after successful kidney transplantation. Altered hormonal status, including sex hormones and parathyroid hormone (PTH), a deficit of 1,25(OH)(2) vitamin D(3) (calcitriol), immunosuppressive therapy and post-operative immobilization contribute to a progressive loss of bone density and structure. The decrease of bone mass is particularly prominent during the first 6 months after kidney transplantation and is associated with an increased number of fractures, both compared with the normal population as well as with dialysis patients. At particular risk are patients with a history of diabetes, long duration of haemodialysis and post-menopausal women. To prevent post-transplant bone loss prescription of steroids should be minimized and withdrawn as early as possible. Additional intake of alpha-calcidol [25(OH) vitamin D(3)] or calcitriol, despite normal serum levels, reduces persistent hyperparathyroidism after kidney transplantation, improves intestinal calcium absorption and activates osteoblasts. Inhibition of osteoclasts by biphosphonate therapy seems to effectively reverse bone loss during the early and late course of kidney transplantation. However, as the majority of transplant recipients have a low-turnover bone disease, inhibition of osteoclasts, through which bone turnover is impaired, might further reduce osteoblast activity and promote osteoid synthesis. Most investigations were small-scale studies with 10-100 participants and a follow up of only 12 months. This makes conclusions on the effect of any intervention on the fracture rate impossible. Larger, randomized multicentre studies investigating bone-sparing therapy on hard end points are therefore advocated.