Haemolytic Uraemic Syndrome (HUS): Clinical Medicine versus Clinical Anatomy

SN Muhammad , E Abdel Meguid, Robert Novo's

Research output: Contribution to journalArticlepeer-review

2894 Downloads (Pure)

Abstract

Haemolytic Uraemic Syndrome (HUS) is an acquired disorder affecting mainly infants and children. The triad of this clinical syndrome is defined by: 1) Thrombotic or Microangiopathic Haemolytic Anaemia with schistocytes 2) Thrombocytopenia and 3) Acute Renal Failure (ARF) which can develop into Chronic Kidney Disease (CKD). The aim of this article is to provide an editorial/commentary on the Clinical Medicine versus Clinical Anatomy of HUS.
HUS is the most common cause of Acute Renal Failure (ARF) in children with an equal sex incidence (Sherbotie et al., 2000). The annual incidence of VTEC infection varies geographically; it can range from 1 to 30 cases per 100,000 in industrialized countries. It is a rare syndrome post-puberty but it is also closely related to Thrombotic Thrombocytopenia (TTP) which is common in adults. The annual incidence of the Verocytotoxin-producing Esherichia coli (VTEC) infection varies geographically from year to year, ranging from 1-30 cases per 100,000 in industrialized countries and is associated with HUS. HUS occurs in sporadic
cases epidemics; between 1st January (2009) and 31st December (2012) in England, a total of 3717 cases were reported with evidence of Shiga toxin-producing E.coli (STEC) infection; sometimes following outbreaks. In
Hamburg (2011), there was an outbreak with more than 900 cases. The disease has seasonal variation, being more common in the warmer months in children. Renal histopathology is characterized by abnormal morphology applicable to afferent arterioles and glomeruli. The glomeruli show evidence of global sclerosis and glomerular thrombotic microangiopathy endothelial cell
swelling; capillary wall thickening and glomerular basement membranes also evident. Interstitial fibroedematous change and tubular atrophy are marked. Arterial, arteriolar and capillary lumina are narrow with obstruction and intimal thickening. The nature of vascular involvement in the kidneys supports the hypothesis that HUS is mediated by systemic toxemia and endothelial cells are the primary target cells owing to action of Verocytotoxin. Histopathological findings provide clues not only to the diagnosis but also in the support of
prognosis. Diffuse tubular interstitial change and global sclerosis indicate the degree of blood flow obstruction and prognosis. Renal blood flow obstruction caused by diffused arterial and arteriolar luminal stenosis may lead to irreversible changes in renal pathology
Original languageEnglish
Number of pages4
JournalAustin Journal of Anatomy
Volume4
Issue number(1)
Publication statusPublished - 16 Feb 2017

Fingerprint

Dive into the research topics of 'Haemolytic Uraemic Syndrome (HUS): Clinical Medicine versus Clinical Anatomy'. Together they form a unique fingerprint.

Cite this