How Can Urine Microscopy Influence the Differential Diagnosis of AKI?

Abstract

Acute kidney injury (AKI), which is associated with increased morbidity and mortality, is a relatively common complication in hospitalized patients (1–3). The most common cause of AKI in hospitalized patients is acute tubular necrosis (ATN) followed by prerenal azotemia (4). Because therapies and prognoses for prerenal azotemia and ATN differ substantially, early clinical differentiation is desirable to assist the clinician in patient treatment. For example, an early diagnosis of prerenal azotemia would facilitate early treatment to correct volume status and potentially prevent ATN. Also, in the setting of AKI from ATN, it would avoid worsening of the clinical course with incorrect therapies such as excessive volume resuscitation leading to pulmonary edema and other untoward end organ effects. Presently, the diagnosis of AKI is primarily based on changes in serum creatinine concentration, blood urea nitrogen, and urine output. These biomarkers are very helpful in diagnosis of AKI but rarely help in discriminating between ATN and prerenal azotemia. Urine biochemistry measures, such as fractional excretion of sodium and urea, also provide important information in the differentiation of AKI into traditional categories of prerenal azotemia and ATN (5–9) when the patient is not on diuretics or does not have underlying chronic kidney disease. Urinalysis and urine microscopy are also commonly used to differentiate these two causes of AKI and are generally accepted as critical for the evaluation of patients with kidney disease. Urine microscopy is the best surrogate for the histologic state of the kidney and is not affected by underlying chronic kidney disease or presence of medications. As a result, urine sediment analysis is considered an integral part of the clinical workup of kidney disease in hospitalized patients with AKI. Urinary microscopy in patients with ATN classically is described as containing renal tubular epithelial cells, renal tubular epithelial …