Autoimmune glycaemic dysregulation and hyperinsulinaemic hypoglycaemia mediated by insulin autoantibodies is an increasingly recognised but controversial phenomenon described in both exogenous insulin naïve (insulin autoimmune syndrome) and exposed (exogenous insulin antibody syndrome) individuals. There has been a significant proliferation of case reports, clinical studies and reviews in the medical literature in recent years which have collectively highlighted the discrepancy between experts in the field with regard to the nomenclature, definition, proposed pathophysiology, as well as the clinical and biochemical diagnostic criteria associated with the condition. The essential characteristics of the condition are glycaemic dysregulation manifesting as episodes of hyperglycaemia and unpredictable hyperinsulinaemic hypoglycaemia associated with high titres of endogenous antibodies to insulin. Although the hypoglycaemia is often life-threatening and initiation of targeted therapies critical, the diagnosis is often delayed and attributable to various factors including: the fact that existence of the condition is not universally accepted; the need to exclude surreptitious causes of hypoglycaemia; the diverse and often complex nature of the glycaemic dysregulation; and the challenge of diagnostic confirmation. Once confirmed, the available therapeutic options are expansive and the reported responses to these therapies have been variable. This review will focus on our evolving understanding, and the associated diagnostic challenges - both clinical and laboratory - of this complex condition.

Acute kidney injury (AKI) is a frequent complication in hospitalised patients and is diagnosed by urinary output and serum creatinine. Serum creatinine is an indirect marker for renal glomerular filtration, but lacks specificity for damage to kidney tissue and the relatively late response to injury precludes early recognition of AKI. Timely diagnosis of kidney injury using biomarkers that provide information about the aetiology of kidney injury is an unmet clinical need. To overcome the suboptimal performance of serum creatinine, injury biomarkers have been proposed that predict AKI in diverse clinical settings. The clinical performance of these markers is considered moderate due to the lack of specificity for kidney tissue or the underlying injury mechanisms, poor test specificity and confounding by interventions or comorbidities. Hence, it is not unequivocally beneficial to implement current kidney injury biomarkers in the clinical laboratory for diagnostic purposes. In this article we review biomarkers that might fulfil AKI-related unmet clinical needs in the academic hospital setting.