Resumo

OCHOA, Federico; SEYAHIAN, Abril  e  ZOTTA, Elsa. Hemolytic uremic syndrome and renal handling of proteins. Salud(i)ciencia [online]. 2018, vol.22, n.8, pp.743-748. ISSN 1667-8682.

Abstract Hemolytic uremic syndrome (HUS) is defined by the triad of hemolytic anemia microangiopathic, thrombocytopenia and acute renal failure. In Argentina it constitutes the first cause of acute renal failure in Pediatrics. Approximately 2-4% of patients die during the acute phase of the disease, and only a third of the remaining 96% survive with renal sequelae, such as the persistence of proteinuria. A healthy adult filters around 5000 mg/day of proteins, with an excretion in urine of 150 mg/day. The little quantity of proteins excreted indicates the presence of a reabsorption mechanism at the level of the proximal tubule. Therefore, the tubular reabsorption plays a very important role since it is the main mechanism responsible for preventing the depletion of protein. For approximately 30 years, it has been known that albumin is reabsorbed in the proximal tubule. Protein reabsorption occurs by a clathrin-dependent receptor mediated endocytosis mechanism and by fluid phase endocytosis. The basic mechanism of renal damage in typical and atypical HUS has been described as a thrombotic microangiopathy, but of different causes. However, the pathophysiology of this disease is more complex than what was believed since the emerging tubular alteration will ewvolve into failures of the protein endocytosis mechanism that are added to the alterations at the level of the glomerular filtration barrier.

Palavras-chave : atypic hus; cubilin; endocytosis; FCRN;; hemolytic uremic syndrome; megalin; podocyte; proteinuria; renal failure; slit diaphragm.

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