Biomarkers and

Antibodies
Development
for Acute
Kidney Injury
Introduction of Acute Kidney Injury

Acute kidney injury (AKI, formerly known as acute renal failure), is common in
hospital patients, particularly in critically ill patients, and costly surgical
complication. It is typically defined as a clinical syndrome characterized by a
rapid failure or damage in renal excretory function and diagnosed by the
accumulation of end products of nitrogen metabolism (urea and creatinine) or
decreased urine output, or both. AKI is thought to be an independent risk factor
with high mortality rates estimated to range between 45-70% and has remained
a great healthcare concern. This kidney disease may be observed in up to 5%
of inpatient, and a diagnosis of it increases the risk of mortality 5.5 to 6.5-fold
as compared to similarly ill patients without AKI. In addition, AKI is supposed to
a potential cause of chronic kidney disease (CKD), as a significant number of
patients may need continued dialytic therapy, or reveal a decrease in function
following discharge.
 Fig.1 Evolution of acute kidney injury. (Bellomo, 2012)

AKI can be classified based on the genesis of the disorder as pre-renal, renal
or post-renal, which provides a convenient partition, but doesn't always obey
the definitions strictly. AKI brings a build-up of waste products in blood and
makes it hard for kidneys to keep the original balance of fluid in one's body. Co-
morbidities are important risk factors for AKI in patients who are in the hospital,
in intensive care units. The surgery in itself, especially emergency and major
surgery in the critically ill, is associated with a high incidence of AKI. Certain
types of surgeries, just like cardiac and transplantation surgeries, require
special attention due to a higher occurrence of AKI. Here, AKI may lead to a
great many complications, such as metabolic acidosis, high potassium levels,
uremia, and effects on other organs including brain, heart, and lungs, finally
death.
 Fig.2

AKI-induced distant organ effects. (Scheel, 2008)

Pathogenesis of AKI

The pathogenesis of AKI is very complex and multifactorial. Generally, it occurs

because of the damage to a kidney tissue caused by decreased kidney blood
flow from any cause (low blood pressure), exposure to substances harmful to
the kidney, an inflammatory process in the kidney, or an obstruction of the
urinary tract that impedes the flow of urine. In simple terms as follows:

 Decreased blood flow (kidney ischemia);

 Direct damage to the kidneys;
 Blockage of the urinary tract.
Drug nephrotoxicity was found to be responsible for 19% of AKI cases in a
recent epidemiological survey performed on critically ill patients. Incidentally,
AKI is usually diagnosed through laboratory findings, such as elevated blood
urea nitrogen and creatinine, or inability of the kidneys to produce sufficient
urine.

Fig.3
Schematic representation of factors contributing to the development of AKI in the
perioperative period and the risk associated with fluid overload. (Legrand, 2013)

Treatment of AKI

No specific therapy has emerged that can attenuate AKI or expedite recovery,
thus, treatment is backup, for example, renal replacement therapy. Current
efforts to understand and control AKI in surgical patients is focusing on
prevention, mitigation of further injury when AKI has occurred, treatment of
associated conditions and facilitation of renal recovery. Recently, major
advances suggest that biomarkers might be fast and accurate predictors of AKI
and help to detect AKI early, identify the etiology, predict outcomes, and tailor
specific therapies.
Creative Biolabs works as an outstanding expert at in vitro diagnostics (IVD)
market and experienced scientists of us are good at offering IVD antibody and
related technical services of diverse targeting AKI biomarkers. Meanwhile,
welcome consulting our IVD antibody platform, which including but not limited
to kidney diseases.

The IVD antibodies for diagnosis of acute kidney injury available in Creative
Biolabs include:

Fetuin-A
ATF 3
KIM-1
Cystatin C
NGAL
IGFBP-7
TIMP-2
IL-18
NAG
Creatinine
Chac1

References
1. Bellomo, R., (2012). “Acute kidney injury.” Lancet, 380(9843), 756-766.
2. Scheel, P.J., (2008). “Uremic lung: new insights into a forgotten
condition.” Kidney Int, 4(7), 849-851.
3. Legrand, M., (2013). “Case scenario: Hemodynamic management of
postoperative acute kidney injury.” Anesthesiology, 118(6), 1446-1454.