A. P. K. Lee

Bio: A. P. K. Lee is an academic researcher from University of Antwerp. The author has contributed to research in topics: Hantavirus & Nephropathia epidemica. The author has an hindex of 1, co-authored 1 publications receiving 5 citations.

Acute hantavirus infection presenting as haemolytic-uraemic syndrome (HUS): the importance of early clinical diagnosis.

Abstract: The European prototype of hantavirus, Puumala virus (PUUV), isolated from a common wild rodent, the bank vole (Myodes glareolus), causes nephropathia epidemica (NE). NE can perfectly mimic haemolytic-uraemic syndrome (HUS), progressing from an aspecific flu-like syndrome to acute kidney injury with thrombocytopaenia, and presenting with some signs of haemolytic anaemia and/or coagulopathy. Moreover, both NE and HUS can occur in local outbreaks. We report an isolated case of NE, initially referred for plasmapheresis for suspected HUS, although signs of overt haemolysis were lacking. Early suspicion of hantavirus infection, later confirmed by serology and reverse transcription polymerase chain reaction (RT-PCR), prevented subsequent excessive treatment modalities.

Clinical Characteristics of Ratborne Seoul Hantavirus Disease

Abstract: Although Seoul orthohantavirus is the only globally spread hantavirus pathogen, few confirmed human infections with this virus have been reported in Western countries, suggesting lower medical awareness of the milder, transient, and often chameleon-like symptoms of this zoonosis. We describe lesser known clinical and laboratory characteristics to help improve underreporting of this virus.

Molecular epidemiology of rodent-, shrew- and bat-borne hantaviruses in Mbeya region, Tanzania

Abstract: A Thesis Submitted in Partial Fulfilment for the Requirements of the Master’s in Life Sciences of the Nelson Mandela African Institution of Science and Technology

Hanta hemorrhagic fever with renal syndrome: A pathology in whose diagnosis kidney biopsy plays a major role (Review).

Abstract: Hantavirus infection belongs to a group of zoonoses rare in the Balkan Peninsula, causing two major syndromes, depending on the viral serotype involved: Hemorrhagic fever with renal syndrome (HFRS) also known as endemic nephropathy and cardiopulmonary syndrome (CPS). Because there is no specific treatment or vaccine for this condition approved in the USA or Europe, the key to minimizing the risk of adverse progression to chronic kidney disease, secondary hypertension or even death is primarily the recognition and early diagnosis of this condition with prompt therapeutic intervention. The aim of this study was to review the literature data on the epidemiology, pathogenesis and management of this disease and to identify several aspects related to the difficulties encountered in diagnosing this pathology, taking into consideration that the disease is not endemic in this geographical area.

Contemporary view about the pathogenesis of Hantavirus nephropathy (Literature rewiew)

Abstract: Hantavirus nephropathy (CVI) is considered to be acute kidney injury (AKI) associated with hantavirus infection (CVI). This infection in the countries of the European and Asian continents causes hemorrhagic fever with renal syndrome (HFRS). However, up to 60% of kidney damage is manifested by pathological changes in urinary sediment without signs of AKI, in connection with which the problems of terminology and diagnosis of kidney damage in HFRS were discussed. A review of the world literature of recent years, devoted to the study of modern data on the pathogenesis of CVI, is presented. The data were revealed that explain the organ specificity of the pathological process in different variants of CVI. The data were revealed that explain the organ specificity of the pathological process in different variants of CVI. The mechanisms related to various aspects of the pathogenesis of hantavirus nephropathy are considered. The factors that alter the functional activity of target cells through the direct action of the virus and the factors mediated by the immune response of the biological host to viral proteins in the form of the action of cytokines ("cytokine storm") causing damage to target organs (indirect factors) are listed. The influence of the hantavirus serotype, genetic factors, and the nature of the immune response of the biological host organism on the severity of renal dysfunction was shown. The concept of "acute damage to podocytes" is disclosed, which explains massive protein uria at the onset of the disease. The molecular and cellular mechanisms of damage to the main compartments of the kidney during hantavirus infection are presented. Disorders of hemostasis and mechanisms of hypercoagulation were demonstrated that underlie glomerular AKI due to acute microvascular syndrome, which is realized in the form of disseminated intravascular coagulation (DIC), hemolytic uremic syndrome (HUS), and thrombotic microangiopathy (TMA). The results of experimental data obtained on a laboratory model of infection and in cell culture, histological studies of autopsy material, and nephrobiopsy specimens from patients with hantavirus nephropathy are demonstrated.