![]() There is a need for studies to help understand new knowledge about the incidence of AKI and its epidemiology. With that said, azotemia is quite common, responsible for 8% to 16% of hospital admissions and more so associated with a significantly higher risk of mortality. Interestingly, many aspects of the natural history of azotemia remain unclear to this day. With these labs, the clinician can discern the classification and etiology of the AKI, which guides clinical management.Īzotemia becomes manifested with a constellation of clinical signs and symptoms along with biochemical abnormalities it is termed uremia. This diagnosis is made with urinalysis (UA), urine electrolytes, metabolic panel (CMP/BMP), and a renal ultrasound (US). AKI is generally diagnosed by an increase in creatinine (Cr) by 0.3 mg/dL, Cr increase greater than 1.5%, or even less than 0.5 mL/kg per hr. There are multiple classification systems use to define AKI: The RIFLE criteria of 2004, AKIN criteria in 2007, and the KDIGO system in 2012. It is a typical feature of both acute and chronic kidney injury.Īzotemia is important when discussing the precipitant syndrome of acute kidney injury (AKI) there are three subtypes, prerenal, intrinsic, and post-renal azotemia. ![]() Raising the level of nitrogenous waste is attributed to the inability of the renal system to filter (decreased glomerular filtration rate-GFR) such as waste products adequately. Azotemia is a biochemical abnormality, defined as elevation, or buildup of, nitrogenous products (BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body. ![]()
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