These studies suggest that the dis-regulated overproduction of interleukin 5 by blood mononuclear cells is an underlying cause of the eosinophilia found in at least some families with this disorder. Diagnosis
The diagnosis of familial eosinophilia rest upon a) familial clustering of the disorder; b) exclusion of "family acquired eosinophilia" (i.e. eosinophilia due to chronic parasite or other infestations that afflict multiple members of a family); c) lack of eosinophil-induced tissue destruction such as that which occurs in the hypereosinophilic syndrome; d) absence of signs or symptoms of other hereditary eosinophilias (e.g. hyperimmunoglobulin E syndrome, Omenn syndrome), Wiskott–Aldrich syndrome, and numerous other primary immunodeficiency syndromes); and d) lack of evidence for reactive eosinophilias (e.g. allergy-related), neoplastic eosinophilias (e.g. eosinophilic leukemia, clonal eosinophilia), or eosinophila associated with various hematological and non-hematological malignancies as outlined in causes of eosinophilia. Treatment
Since longitudinal data, including eosinophil counts obtained over a 20- to 30-year periods in some family members, show remarkable stability in the absolute eosinophil count with no evidence of disease   attributable to eosinophil-related tissue injury, therapy to lower eosinophil counts such as corticosteroids, tyrosine kinase inhibitors, and antibodies directed against interleukin 5 have in general not been used to treat familial eosinophilia. One patient with severe heart damage was treated with a corticosteroid but soon thereafter died. Familial eosinophilia unassociated with possible eosinophil-related tissue injuries may not require drug treatment, those cases with such tissue injuries, it is suggested, should be considered for such interventions. In all cases, however, regular follow-up of the disorder is strongly recommended.
According to a review article of 2015, there has been an increase in cases of acute kidney injury in the last 20 years which cannot be explained solely by changes to the manner of reporting. History
Before the advancement of modern medicine, acute kidney injury was referred to as uremic poisoning while uremia was contamination of the blood with urine. Starting around 1847, uremia came to be used for reduced urine output, a condition now called oliguria, which was thought to be caused by the urines mixing with the blood instead of being voided through the urethra.Acute kidney injury due to acute tubular necrosis (ATN) was recognized in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of kidney tubules, leading to a sudden decrease in kidney function. During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids. See also
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