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Erythropoietin is a 30.4 kDa glycoprotein produced by the kidney, which is mostly known for its physiological function in regulating red blood cell production in the bone marrow. Accumulating evidence, however, suggests that erythropoietin has additional organ protective effects, which may specifically be useful in protecting the brain and kidneys from injury. Experimental evidence suggests that these protective mechanisms are multi-factorial in nature and may include inhibition of apoptotic cell death, stimulation of cellular regeneration, inhibition of deleterious pathways and promotion of recovery. In this article we review the physiology of erythropoietin, assess previous work that supports the role of erythropoietin as a general tissue protective agent and explain the mechanisms by which it may achieve this tissue protective effect. We then focus on specific laboratory and clinical data that suggest that erythropoietin has a strong brain protective and kidney protective effect. In addition, we comment on the implications of these studies for clinicians at the bedside and for researchers designing controlled trials to further elucidate the true clinical utility of erythropoietin as a neuroprotective and nephroprotective agent. Finally, we describe EPO-TBI, a double-blinded multi-centre randomised controlled trial involving the authors that is being conducted to investigate the organ protective effects of erythropoietin on the brain, and also assesses its effect on the kidneys.

Acute kidney injury (AKI) is the new consensus term for acute renal failure. The term describes a continuum of kidney injury, a common condition in the critically ill and after major surgery, which is associated with increased mortality. The incidence of AKI in intensive care unit patients in Australia is >30% and sepsis is a major contributory factor. However, there is limited knowledge about its incidence after major surgery, except for cardiac surgery. The creation of staged AKI classification systems (RIFLE [Risk, Injury, Failure, Loss, End-stage], Acute Kidney Injury Network and the new Kidney Disease: Improving Global Outcomes criteria) has accelerated progress in critical care nephrology research by showing that even small changes in serum creatinine are associated with increased risk of death and that this risk increases progressively with severity of AKI. Recent thought and research has cast doubt over previously accepted pathophysiological views of AKI. Moreover, terms such as ‘prerenal azotaemia’ and ‘acute tubular necrosis’ are now being challenged as lacking validity, having little supportive evidence and carrying limited clinical utility. In this review, we explore the limitations of animal and human models of AKI and the implications of recent research on our current understanding of the pathophysiology of AKI. In addition, we describe conventional and novel diagnostic methods and therapies, and explore the clinical implications of the effect of fluid administration and perioperative management. Finally, we identify priorities for clinical investigations and future directions in AKI research.

Barrier islands in sheltered settings are rare coastal geomorphic features. Here we present a case study of controls on the evolution of Tapora Island, North Island, New Zealand. Tapora Island is an active barrier island located opposite the entrance to the Kaipara Harbour on a high-energy coast. Subsurface facies form an aggradational barrier island succession from subtidal to subaerial elevations. This facies succession, combined with surface samples and geomorphic and geologic relationships, indicates that Tapora Island is the most recent barrier island at this location in the estuary and forms part of a prograded coast opposite the entrance. Wave data indicate that ocean swell waves penetrate the inlet for approximately 2 hours either side of high tide and are capable of transporting sand onto the island. The combined effects of swell waves, abundant sediment supply, and exposed aspect are the critical factors that have formed the barrier island. Despite the “sheltered’ estuarine setting, Tapora Island has formed under conditions that are more akin to open ocean coasts. The origin and development of Tapora Island broadly conforms to the accumulating barrier island model.