Novel acute kidney injury biomarkers: their characteristics, utility and concerns

Abstract

Acute kidney injury (AKI) consists of a rapid renal function decline which usually increases serum urea and creatinine levels. Since kidney injury begins by inducing biological and molecular changes which evolve to cellular damage, biomarkers could be used as tools for monitoring early AKI appearance, and predicting its recovery. Among the main AKI biomarkers the neutrophil gelatinase-associated lipocalin, cystatin C, kidney injury molecule-1, monocyte chemotactic peptide-1, N-acetyl-β-D-glucosaminidase, interleukin-18, liver-type fatty acid-binding protein, netrin-1, cycle arrest markers, endogenous ouabain, selenium-binding protein 1, and BPIFA2 marker, have been described. Even though novel biomarkers seem to be more helpful to early detect AKI and/or predict the need for renal replacement, and mortality compared to serum creatinine, more comprehensive studies are still required to determine their clinical utility.

Age‐Dependent Changes of Kidney Injury Biomarkers in Pediatrics

“…It provides the estimated glomerular filtration rate and is based on the child's height and values of serum creatinine, a by‐product of muscle metabolism eliminated through glomerular filtration . Unfortunately, estimated glomerular filtration rate and serum creatinine are both unreliable and inaccurate markers for monitoring of kidney function and detecting KI in pediatric populations for the following reasons: (1) approximately 50% of renal parenchymal loss must occur before serum creatinine changes can be detected; (2) serum creatinine can be influenced by muscle mass variation, nutrition, age, and sex; (3) during the first days of life, serum creatinine rather reflects the maternal kidney function instead of the kidney function of the neonate; (4) overestimation of kidney function is possible in patients with cachexia; and (5) serum creatinine does not allow the exact localization nor the extent of KI …”

“…10 Unfortunately, estimated glomerular filtration rate and serum creatinine are both unreliable and inaccurate markers for monitoring of kidney function and detecting KI in pediatric populations for the following reasons: (1) approximately 50% of renal parenchymal loss must occur before serum creatinine changes can be detected; (2) serum creatinine can be influenced by muscle mass variation, nutrition, age, and sex; (3) during the first days of life, serum creatinine rather reflects the maternal kidney function instead of the kidney function of the neonate; (4) overestimation of kidney function is possible in patients with cachexia; and (5) serum creatinine does not allow the exact localization nor the extent of KI. [11][12][13][14][15][16][17][18][19][20][21][22][23] Understanding Age-Dependent Changes in Pediatrics Kidney function comprises 3 main processes: First, glomerular filtration is responsible for the filtration of the plasma across the glomerular membrane into the renal tubule. Second, tubular excretion transporters can increase the excretion of drug molecules by more actively transport from the plasma into the tubule.…”

Clinical Factors and Anticoagulation Level That Determine the Sudden Loss of Kidney Function in Patients Long-Taking Warfarin (A 5-Year Prospective, Observational Study)

“…Все это обусловливает актив-ный интерес к биомаркерам раннего поврежде-ния почки, которые отвечали бы требованиям высокой чувствительности и специфичности, будучи при этом простыми и неивазивными. Среди новых биомаркеров активно изучаются ассиметричный диметиларгинин, симметрич-ный диметиларгинин, уромодулин, молекула повреждения почки-1, липокалин, ассоцииро-ванный с нейтрофильной желатиназой [7][8][9][10][11][12][13][14][15]. Все они в наибольшей степени изучены как пре-дикторы острого почечного повреждения (ОПП).…”

Looking for a better definition and diagnostic strategy for acute kidney injury: a new proposal

“…1,3 Secondly, despite having described novel and earlier AKI biomarkers, they have reduced availability, low specificity, usefulness not in all causes of AKI, insufficient patient outcome and cost-effectiveness studies, and mainly they do not guarantee the immediate AKI detection since their request is subject to the clinical suspicion of this condition by the attending physician, which definitely depends on the AKI definition currently used. 5,6 In order to overcome these difficulties we present here the following proposals, valid for both the adult and pediatric patient.…”