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Hemorrhagic fever with renal syndrome is an acute infectious illness characterized by fever, hemorrhage, and renal failure. Research over the last 40 years has led to the discovery and characterization of the causative viruses, detailed knowledge of the epidemiology of the disease, development of sensitive diagnostic assays, and improvements in patient management, which in turn have led to significant reductions in mortality. Considerable progress has also been made in elucidating the pathophysiology of the disease, although much more needs to be learned. Recent data show that hemorrhagic fever with renal syndrome has a wider geographic occurrence than previously thought. This syndrome must be considered in the differential diagnosis of acute renal failure of unknown cause.

Peculiarities of lesions of the cardiovascular system were studied in 332 patients with a grave course of hemorrhagic fever with the renal syndrome. Deep cardiovascular disorders manifesting themselves in low or high arterial pressure, ECG changes, hemodynamic disorders in the greater and lesser circulation, disorder of the morphological structure of the myocardium and small vessel walls were revealed.

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral fever which typically progresses through five stages: an acute grippe, followed by hemorrhage and shock, acute renal insufficiency from tubulo-interstitial nephritis, and recovery. Death from circulatory or renal failure occurs in 5%-15% of cases. In mild or abortive forms of the disease, associated with viral strains enzootic in Scandinavia the illness is milder. Hemorrhage and shock occur with lower frequency and the fatality rate is less than 1%. Pathologic examination of HFRS cases from Asia discloses generalized congestion, hyperemia, and hemorrhage, with scattered foci of necrosis in numerous organs. Congestion and hemorrhage are most evident in the kidney medulla. Widespread microscopic evidence of capillary and vascular dysfunction is found, with endothelial cell swelling, perivascular edema, diapadesis of erythrocytes and mononuclear cell infiltration. Hemorrhage and inflammation in the renal interstitium and tubular epithelial degeneration characterize the kidney pathology. Limited data indicate pathogenic roles for cell destruction from viral infection as well as immune mediated mechanisms. No specific therapy is available.

Survival, growth rates, body size and fertility of wild caught Norway rats (Rattus norvegicus), infected and uninfected with a Hantavirus (antigenically related to Seoul virus), were compared. No differences were found in the survival of seronegative versus seropositive rats, as measured by mark-recapture experiments. Growth rates, as measured by weight gain but not by increased body length, were slower in seropositive, sexually mature (greater than 200 g) rats, although no differences in the ultimate body size of infected versus uninfected rats were found. No differences in external measures of sexual maturity, or in embryo counts or testes sizes, were found for infected versus uninfected rats. We conclude that hantaviral infections have little or no impact on demographic processes in Norway rat populations.

A virus identical to or closely related to the viruses of the epidemic hemorrhagic fevers and/or nephropathia epidemica has been demonstrated serologically in rats from geographically separate areas of this country by three groups of investigators. This information suggests a previously unrecognized health threat that should be considered in the differential diagnosis of patients initially seen with febrile illnesses and acute renal failure. The salient features of these viral diseases and the clues that should alert the clinician to seek serologic confirmation of Hantaan or an immunologically related virus are discussed herein.

Hemorrhagic fever with renal syndrome (HFRS) came dramatically to the attention of Western medicine in 1951 with the "new" disease becoming a major source of morbidity and mortality in American troops in Korea. Known there as epidemic hemorrhagic fever (EHF) or Korean hemorrhagic fever (KHF), it became apparent that it was the same disease as the endemic (epidemic) hemorrhagic nephroso-nephritis of the Soviet Far East and Songo fever of the Japanese Army in Manchuria. The conjecture that the milder epidemic (endemic) nephropathy of Scandinavia and European Russia was the same or a related disease has now been substantiated with the demonstration of close serological relationship of the Bunyamwera-like virus causing KHF (Hantaan virus) to that of HFRS in Finland, Sweden, European Russia, Greece and Yugoslavia. In the past decade the disease has been recognized as a serious problem in 19 provinces of China and in Japan, where the virus is the Hantaan virus. The severe EHF (or KHF) has its silent reservoir in the wild mouse Apodemus agrarius or in laboratory rats while the less virulent European disease resides in the voles Clethrionomys sp. A mild nonhemorrhagic form of the East Asian nephropathy is carried to man by infected urban rats, Rattus rattus or Rattus norvegicus, in Japan and Korea. All forms are carried to man as a respiratory infection "when a mouse (or rat or vole) coughs". Antibodies to the Hantaan virus have been found in man in India, Iran, Central Africa, Alaska, Bolivia and in wild rodents and urban rats in the USA where human cases of muroid virus nephropathy have not been recognized. Antibody patterns to Hantaan virus and to Scandinavian nephropathia epidemica virus antigens found in human and rodent sera in America and in Sweden, Yugoslavia, and European Russia suggest the possibility of yet a third (or more) virus serotype(s), and also the possible presence of the East Asian type of virus in Europe.

The pattern of renal enhancement and washout of contrast medium was observed on sequential follow-up CT in 12 patients with Korean hemorrhagic fever, in which acute renal failure is one of the most important clinical features. Renal contrast enhancement and contrast medium washout were delayed longer in patients with severe oliguric renal failure. The delayed washout peaked at 4-5 days and did not return to normal until 8-9 days in the patients with severe oliguria; in the patients without severe oliguria the times were 1-2 days and 3-4 days, respectively. A characteristic "cart-wheel" pattern was observed during the washout stage in patients without severe oliguria. This "cart-wheel" pattern of washout is thought to result from relief of vasoconstriction and repair of tubular function. Multifocal "wedge-shaped" nonenhanced areas of the kidney, seen on the 2 week follow-up postcontrast CT, are thought to be ischemic zones due to persistent vasoconstriction. On the 6 week follow-up postcontrast CT in one patient, scarring of the kidney was detected in the same area that did not enhance on the 2 week CT. This scarring is thought to be a result of permanent vasoconstriction.