Role of renal biomarkers as predictors of acute kidney injury in cardiac surgery

Abstract

Cardiac surgery is unique in using cardiopulmonary bypass in various clinical scenarios. Injury of vital organs is unavoidable in the perioperative period. Acute kidney injury is a consequence of the systemic inflammatory response after bypass, emboli, ischemia, and low cardiac output states, reportedly occurring in 30%-40% of open heart surgeries. Acute kidney injury is associated with increased morbidity, mortality, and cost. Many preventive measures (off-pump procedures, decreased crossclamp time, pulsatile flow, adequate hydration) are taken in the perioperative period to avoid organ injury, but in vain. Traditionally, blood urea, serum creatinine, and creatinine clearance rate were applied for prediction of acute kidney injury. The recent emergence of biomarkers such as neutrophil gelatinase-associated lipocalin, cystatin C, liver-type fatty acid binding protein, interleukin-18, kidney injury molecule-1, and tetrahydrobiopterin have helped in detecting acute kidney injury long before the rise of serum creatinine. These biomarkers can also be used as tools for predicting therapeutic effects in acute kidney injury and for monitoring drug toxicity. This review consolidates the knowledge of biomarkers and their application in acute kidney injury management.

Biomarkers of acute kidney injury: the pathway from discovery to clinical adoption

“…In patients with congestive heart failure, Damman et al recently demonstrated that KIM-1 is an outstanding predictive marker for AKI detection [100]. Also, elevation of urinary KIM-1 levels was found to be correlated with increased risk of death or hospitalization among patients with congestive heart failure, independent of estimated glomerular filtration rate (GFR) [101]. In a study of 32 urinary biomarkers of AKI after cardiac surgery, incorporation of KIM-1 with IL-18 generated an AUC of 0.92, and the combination surpassed other biomarkers [99].…”

Acute kidney injury and tubular biomarkers after hematopoietic stem cell transplantation

“…Массивная гидратация, ле-карственное увеличение канальцевой секреции, потеря массы тела -не полный перечень обстоятельств, снижа-ющих эффективность применения обычных критериев ОПП для этого контингента больных [18]. Известны данные о клинической информативности определения БМ -молекул, экспрессируемых резидентными и им-мунными клетками почек в ответ на повреждение, при различных этиопатогенетических вариантах их повреж-дения [11][12][13][14][15][16]. Вместе с тем представлены только еди-ничные публикации, касающиеся сравнительного ана-лиза роли разных БМ в развитии ОПП, в том числе при ТГСК [17,20].…”

“…Из-вестно, что резидентными и иммунными клетками почки увеличивается экспрессия ряда молекул, которые могут служить биомаркерами (БМ) ранних стадий повреждения органа, когда изменения скорости клубочковой фильтра-ции (СКФ) и PCr еще отсутствуют [10][11][12]. Высокая эф-фективность определения БМ для прогнозирования не-которых этиопатогенетических вариантов ОПП показана в ряде исследований [13][14][15][16][17], однако подобные данные для ОПП при ТГСК ограничены.…”

Subclinical tubular epithelium damage and acute kidney injury following allogeneic hematopoietic stem cell transplantation

“…Massive infusion therapy, drug-enhanced tubular secretion, body mass losses may contribute to low efficiency of routine AKI criteria in patients following HSCT [11]. Some existing data presume potential clinical value of molecular markers, expressed by resident renal cells and local immune cell populations in certain types of kidney damage [5,6,13,[19][20][21]. Meanwhile, only scattered publications deal with comparative analysis of different MBMs in AKI following HSCT [17].…”

“…Both resident kidney cells and local immune cells are shown to enhance expression of some molecules, which may serve as biomarkers of early organ damage with still normal glomerular filtration rate (GFR) and P Cr values [19,20,22]. The efficacy of MBMs evaluation for the prediction of some etiological AKI variants has been already demonstrated [5,6,13,21]. There are, however, only scarce data concerning AKI associated with HSCT [17].…”