Practical approach to detection and management of acute kidney injury in critically ill patient

Abstract

Background: Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with high morbidity and mortality. This paper provides a critical review of the etiologies of AKI and a systematic approach toward its diagnosis and management with emphasis on fluid volume assessment and the use of urine biochemical profile and microscopy in identifying the nature and the site of kidney injury.

Materials and methods: The search of PubMed and selection of papers had employed observational designs or randomized control trials relevant to AKI.

Results: AKI is defined by the rate of rise of serum creatinine and a decline in urine output. The pathophysiology is diverse and requires a careful and systematic assessment of predisposing factors and localization of site of injury. The majority of AKIs are due to prerenal causes such as fluid volume deficit, sepsis, or renal as in acute tubular injury. The use of central venous and arterial blood pressure monitoring and inferior vena cava echocardiography complemented by urine analysis and microscopy allows assessment of fluid volume status and AKI etiology.

Conclusions: Timely intervention by avoidance of fluid volume deficit and nephrotoxic agents and blood pressure support can reduce the incidence of AKI in critically ill patients.

Keywords: Acute kidney injury; Critical illness; Fluid volume assessment; Urine microscopy.

Fig. 1

Urine microscopy for analysis of urine sediments. Renal tubular epithelial cell casts (a) and “Muddy” brown granular casts (b) suggest acute tubular injury/necrosis (ATN) as the etiology of AKI. White blood cell casts are generally seen in acute interstitial nephritis or acute pyelonephritis (c). Red cell cast denotes glomerular disease as in glomerulonephritis or small vessel vasculitis (d)