Hospital-acquired acute kidney injury prevalence in in adults at a South African tertiary hospital.

BACKGROUND: Hospital Acquired Acute Kidney Injury (HA-AKI) prevalence has not been analysed in a South African setting. We investigated HA-AKI prevalence, using the KDIGO definition, with clinical characteristics and outcomes. The aim was to provide evidence for earlier treatment interventions to improve outcomes, such as recent UK NHS initiatives of automated electronic alerts in the laboratory information system. METHODS: Retrospective laboratory and clinical data was analysed for a 6-month period at Tygerberg Hospital, Cape Town. Serum creatinine results and clinical records were analysed and collated into gender and age group specific results. RESULTS: HA-AKI occurred in 6.2% of hospitalised patients for the period of analysis. The highest incident occurred in females aged 18-39 and males aged 40-59. The most common AKI stage reached was stage 1. HA-AKI increased length of stay by an average of 4.6 days and 20% of patients were readmitted at a later date with renal dysfunction. CONCLUSION: AKI prevalence is significant and associated with adverse patient outcomes. Initiatives that allow front-line healthcare professionals to treat and manage AKI, such as introduction of automated electronic alerts, should be considered. Similar initiatives have been implemented in UK NHS hospitals with positive impacts.

Deposition of amyloid ß in the walls of human leptomeningeal arteries in relation to perivascular drainage pathways in cerebral amyloid angiopathy.

Deposition of amyloid ß (Aß) in the walls of cerebral arteries as cerebral amyloid angiopathy (CAA) suggests an age-related failure of perivascular drainage of soluble Aß from the brain. As CAA is associated with Alzheimer's disease and with intracerebral haemorrhage, the present study determines the unique sequence of changes that occur as Aß accumulates in artery walls. Paraffin sections of post-mortem human occipital cortex were immunostained for collagen IV, fibronectin, nidogen 2, Aß and smooth muscle actin and the immunostaining was analysed using Image J and confocal microscopy. Results showed that nidogen 2 (entactin) increases with age and decreases in CAA. Confocal microscopy revealed stages in the progression of CAA: Aß initially deposits in basement membranes in the tunica media, replaces first the smooth muscle cells and then the connective tissue elements to leave artery walls completely or focally replaced by Aß. The pattern of development of CAA in the human brain suggests expansion of Aß from the basement membranes to progressively replace all tissue elements in the artery wall. Establishing this full picture of the development of CAA is pivotal in understanding the clinical presentation of CAA and for developing therapies to prevent accumulation of Aß in artery walls. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.