Visualization of microcirculatory disorders in haemorrhagic fever with renal syndrome.

Haemorrhagic fever with renal syndrome (HFRS) is a severe virus-induced disease with renal involvement, first described in 1935 in the Far East of Russia. It is a zoonosis, with humans being affected by contact with animals (or their excretions) carrying the virus. While it was originally thought that the disease was unique to the Asian part of Russia, more recently epidemic outbreaks as well as sporadic cases of HFRS were also noted in Eastern Europe, Scandinavia, or even Western Europe [1,2]. The Hantavirus has by now been well characterized on a molecular level and it has become apparent that Hantavirus strains causing disease with more adverse prognosis prevail in the Far East of Russia, whereas strains causing more benign disease are found in Western Europe. According to our experience, in the Far East of Russia the incidence varies from 18 to 60 per 100000 of population, with a mortality rate of 1-6.5% [3]. Clinically the disease is characterized by haemorrhagic lesions, circulatory disturbances, and renal involvement presenting as acute renal failure and characterized by interstitial nephritis. Vascular injury is the hallmark of pathomorphology. It appears as if the virus has a specific affinity to endothelial cells, i.e. endothelial tropism; the earliest, most characteristic and most severe lesions concern the vascular wall. Such lesions include oedema of the vessel wall, regressive lesions terminating in necrosis of the wall microvessels, i.e. arterioles, capillaries, and venules [4]. The functional counterparts are increased vascular permeability and haemorrhage. Vascular injury will ultimately lead to stasis and arteriolar or venular thrombosis [5].