ACUTE KIDNEY INJURY PANEL

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An Acute Kidney Injury (AKI) panel is a group of diagnostic tests used to assess kidney function and detect signs of acute kidney injury, which is a sudden decline in the kidneys' ability to filter waste from the blood. The panel typically includes a blood urea nitrogen (BUN) test and a serum creatinine test, both of which measure waste products that build up in the blood when the kidneys aren't working properly. Additionally, it may include an electrolyte panel to check levels of substances like potassium and sodium, which can become imbalanced with kidney dysfunction. Some advanced panels may also include newer biomarkers like neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C, which can detect kidney stress and damage earlier than traditional markers. Interpreting the results helps determine the presence and severity of AKI, guiding the appropriate medical treatment.


Included Tests

A creatinine serum test measures the level of creatinine, a waste product produced by muscle breakdown, in your blood.Creatinine is normally filtered from the blood by the kidneys and excreted in urine.Elevated creatinine levels can indicate impaired kidney function.This test is essential for assessing kidney health, diagnosing kidney disease, monitoring the progression of kidney conditions, and evaluating the effectiveness of kidney treatments.

Cystatin C is a small protein produced by most cells in the body.It is freely filtered by the kidneys, making it a reliable marker of kidney function, even in individuals with normal creatinine levels.Unlike creatinine, cystatin C production is not influenced by muscle mass or diet, providing a more accurate assessment of glomerular filtration rate (GFR), a measure of kidney function.Elevated cystatin C levels can indicate kidney damage or dysfunction, even in the early stages of chronic kidney disease.

NEUTROPHIL GELATINASE ASSOCIATED LIPOCALCIN (NGAL) IS A LEADING NEW BIOMARKER OF ACUTE KIDNEY INJURY (AKI). NGAL CAN BIND TO IRON SIDEROPHORE COMPLEXES AND MAY HAVE TISSUE PROTECTIVE EFFECTS IN THE PROXIMAL TUBULE. IT IS HIGHLY UPREGULATED AFTER INFLAMMATION AND KIDNEY INJURY AND CAN BE DETECTED IN URINE WITHIN 2 HOURS OF CARDIOPULMONARY BYPASS ASSOCIATED AKI. SPECIFICITY OF NGAL IN CASES OF SEPSIS AND PYURIA NEEDS TO BE ESTABLISHED.

FRACTIONAL EXCRETION OF SODIUM (FENA) IS THE FRACTION OF FILTERED SODIUM LOAD THAT IS REABSORBED BY THE TUBULES AND IS A MEASURE OF BOTH THE KIDNEYS ABILITY TO REABSORB SODIUM AS WELL AS ENDOGENOUS AND EXOGENOUS FACTORS THAT AFFECT TUBULAR REABSORPTION. WITH PRERENAL AZOTEMIA, FENA IS USUALLY <1% SUGGESTING AVID TUBULAR SODIUM REABSORPTION. LOW FENA IS OFTEN SEEN IN GLOMERULONEPHRITIS, HENCE SHOULD NOT BE CONSIDERED SYNONYMOUS WITH INTRAVASCULAR VOLUME DEPLETION AND SHOULD NOT BE USED AS A SOLE GUIDE FOR VOLUME MANAGEMENT. IN ISCHEMIC AKI, FENA IS FREQUENTLY >1% BECAUSE OF TUBULAR INJURY AND RESULTANT INABILITY TO REABSORB SODIUM.

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  • Free and On Schedule Sample Collection
  • 24/7 Service
  • Affordable
  • Quick and Accurate Reports

5 mL (3 mL min.) Serum from 1 SST AND 10 mL (5 mL min.) aliquot of random Urine in a sterile screw capped container. Ship refrigerated or frozen.

CLIA, Nephelometry, Jaffes reaction, Indirect ISE

No special preparation required.

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