Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the past, urine biochemistry was a major tool in acute kidney injury (AKI) management. Classic papers published some decades ago established the values of the urine indices which were thought to distinguish "pre-renal" (functional) AKI attributed to low renal perfusion and "renal" (structural) AKI attributed to acute tubular necrosis (ATN). However, there were a lot of drawbacks and limitations in these studies and some recent articles have questioned the utility of measuring urine electrolytes especially because they do not seem to adequately inform about renal perfusion nor AKI duration (transient vs. persistent). At the same time, the "pre-renal" paradigm has been consistently criticized because hypoperfusion followed by ischemia and ATN does not seem to explain most of the AKI developing in critically ill patients and distinct AKI durations do not seem to be clearly related to different pathophysiological mechanisms or histopathological findings. In this new context, other possible roles for urine biochemistry have emerged. Some studies have suggested standardized changes in the urine electrolyte composition preceding increases in serum creatinine independently of AKI subsequent duration, which might actually be due to intra-renal microcirculatory changes and activation of sodium-retaining mechanisms even in the absence of impaired global renal blood flow. In the present review, the points of controversy regarding urine biochemistry assessment were evaluated as well as future perspectives for its role in AKI monitoring. An alternative approach for the interpretation of measured urine electrolytes is proposed which needs further larger studies to be validated and incorporated in daily ICU practice.
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PMID:Urine biochemistry assessment in critically ill patients: controversies and future perspectives. 2703 61

A case of acute kidney injury (AKI) strongly suspected to be drug-induced (oxaliplatin and non-steroidal anti-inflammatory drug) is discussed regarding the mechanism of a reduced glomerular filtration rate responsible for the development of AKI. Urinary biochemical tests are useful for the differential diagnosis of pre- renal (functional) AKI and intrinsic (structural) AKI(so-called acute tubular necrosis). In this case, although a comprehensive differential diagnosis using these parameters supported intrinsic AKI, only one pa- rameter, fractional excretion of urea (FEurea), indicated the existence of prerenal AKI. As a result of treatment with the appropriate management of body fluid in addition to avoiding nephrotoxic medications, AKI rapidly improved. FEurea revealed the underlying mechanism of AKI. [Review].
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PMID:[Acute Kidney Injury in a Patient with Diarrhea and Vomiting Undergoing Chemotherapy for Colorectal Cancer]. 3069 74