Urinary Biochemistry in the Diagnosis of Acute Kidney Injury

Abstract

Acute kidney injury (AKI) is a common complication, impacting short- and long-term patient outcomes. Although the application of the classification systems for AKI has improved diagnosis, early clinical recognition of AKI is still challenging, as increments in serum creatinine may be late and low urine output is not always present. The role of urinary biochemistry has remained unclear, especially in critically ill patients. Differentiating between a transient and persistent acute kidney injury is of great need in clinical practice, and despite studies questioning their application in clinical practice, biochemistry indices continue to be used while we wait for a novel early injury biomarker. An ideal marker would provide more detailed information about the type, intensity, and location of the injury. In this review, we will discuss factors affecting the fractional excretion of sodium (FeNa) and fractional excretion of urea (FeU). We believe that the frequent assessment of urinary biochemistry and microscopy can be useful in evaluating the likelihood of AKI reversibility. The availability of early injury biomarkers could help guide clinical interventions.

Baicalein protects renal tubular epithelial cells againsthypoxia-reoxygenation injury

“…The pathogenesis and prognosis of AKI have been studied more extensively in the past decade, which has revealed a series of biomarkers, the optimal dose and intensity of renal replacement therapy, and the effects of fluid management. Effective use of various drugs, including dopamine, atrial natriuretic peptide, and insulin-like growth factor, has been determined in animal trials, but not in clinical studies [ 3–6 ]. About 20–30% of AKI patients develop chronic kidney injury and eventually succumb to end stage kidney disease.…”

Acute Kidney Injury Definition and Diagnosis: A Narrative Review

“…With the enhanced understanding of the pathophysiology of AKI, novel biomarkers were identified, including proteins filtered by the glomerulus, enzymes released by tubular cells after injury, and inflammatory mediators [ 65 ]. These include Cys-C, neutrophil gelatinase associated lipocalin (NGAL), N-acetyl-glucosaminidase (NAG), kidney injury molecule 1 (KIM-1), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin 18 (IL-18), liver-type fatty acid-binding protein (L-FABP), calprotectin, urine angiotensinogen (AGT), urine microRNAs, insulin-like growth factor-binding protein 7 (IGFBP7), and tissue inhibitor of metalloproteinases-2 (TIMP-2), which have been evaluated in multiple settings, primarily on critically ill and surgical patients [ 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 ].…”

Diagnostik der akuten Organischämie

“…Zusätzlich kommt es z. B. während eines septischen Schocks infolge proinflammatorischer Mediatoren und neurohumeraler Aktivierung zu einer Erhöhung der tubulären Natriumresorption und einer falsch-tiefen FeNa [38]. Alle diese Aspekte CME Abb.…”