Visualization of microcirculatory disorders in haemorrhagic fever with renal syndrome

Abstract

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]. These vascular changes are prominent in visceral organs, particularly the kidney, the pitiutary and adrenal glands, the right atrium, and the central nervous system [6]. Their occurrence in the skin and conjunctiva as well opens a fascinating possibility to visualize the sequence of events leading to vascular necrosis and haemorrhage. Starting in 1950, we have tried to document microcirculatory changes in Khabarovsk, a region endemic for

Platelet glycoprotein IIb/IIIa (HPA-1 and HPA-3) polymorphisms in patients with hemorrhagic fever with renal syndrome

“…The underlying pathophysiologic changes of HFRS are vascular endothelial cell injury, increased capillary permeability, acute renal failure, and abnormal coagulation [7][8][9]. The mechanisms by which pathogenic hantaviruses induce the pathophysiologic changes in HFRS are not well understood.…”

Low levels of serum vitronectin associated with clinical phases in patients with hemorrhagic fever with renal syndrome

“…Formation of VN-TAT may occur in HFRS due to activation of coagulation, fibrinolysis, and complement systems. Impairments of capillary and small vessels as well as abnormal coagulation are fundamental pathological changes in HFRS patients [22,23]. Therefore, deposition in injured tissues and endothelial cells and incorporation into complexes during the course of HFRS may be major factors related to the increased consumption of VN during the acute phase of HFRS.…”