Acute Kidney Injury (AKI) describes a sudden decline in kidney function, developing over hours or days. When kidneys are not working properly, waste products can build up in the body, leading to serious health issues. Urine studies offer a non-invasive and practical approach to assess kidney health and diagnose AKI by analyzing urine’s composition and characteristics. These analyses provide a direct window into the kidney’s filtering and reabsorption processes.
Fundamental Urine Tests
The initial assessment for suspected AKI often begins with a comprehensive urinalysis, which involves several components. A visual inspection of the urine can reveal abnormalities such as a dark or brown color, which might suggest the presence of blood or concentrated waste products. Cloudy urine could indicate the presence of cells, crystals, or bacteria, pointing towards inflammation or infection within the urinary tract.
Following visual inspection, a dipstick analysis provides a quick chemical screening. The dipstick is a small strip that changes color when dipped into urine, indicating the presence or absence of various substances. For instance, it can detect proteinuria, an excess of protein in the urine, often signaling damage to the kidney’s filtering units. The dipstick also checks for hematuria, or blood in the urine, and can measure glucose, pH, and specific gravity, with specific gravity reflecting the urine’s concentration.
The microscopic examination of urine sediment offers a more detailed look at cellular elements and other structures. Under a microscope, healthcare providers can identify red blood cells, suggesting bleeding from the kidneys or urinary tract, and white blood cells, indicating inflammation or infection. The presence of epithelial cells can point to damage within the kidney tubules.
Microscopic examination can reveal casts, which are cylindrical structures formed in the kidney tubules. Red blood cell casts suggest inflammation in the glomeruli, while white blood cell casts indicate inflammation in the kidney’s interstitial tissue. Granular and renal tubular epithelial cell casts are seen in acute tubular necrosis, representing damaged kidney cells or their breakdown products.
Electrolyte Ratios for Diagnosis
Beyond basic urinalysis, specific urine chemistry tests and calculated ratios provide deeper insights into the underlying cause of AKI, guiding appropriate treatment. Measuring urine sodium levels helps determine the kidney’s ability to conserve sodium. Low urine sodium, less than 20 milliequivalents per liter (mEq/L), suggests the kidneys are actively holding onto sodium and water due to reduced blood flow, a characteristic of pre-renal AKI. Conversely, higher urine sodium levels, exceeding 40 mEq/L, indicate the kidneys are unable to reabsorb sodium effectively due to tubular damage, seen in intrinsic kidney injury.
Urine creatinine, a waste product filtered by the kidneys, serves as a reference point for calculating various ratios. Its concentration helps normalize other measurements, providing a more accurate assessment of kidney function independent of urine volume. Urine osmolality measures the concentration of dissolved particles in the urine, reflecting the kidney’s concentrating ability. In pre-renal AKI, kidneys conserve water, leading to highly concentrated urine with an osmolality above 500 mOsm/kg. When kidney tubules are damaged in intrinsic AKI, their ability to concentrate urine is impaired, resulting in more dilute urine with an osmolality below 350 mOsm/kg.
The Fractional Excretion of Sodium (FeNa) compares the amount of sodium excreted in the urine to the amount filtered by the kidneys. It is calculated using urine and plasma sodium and creatinine levels. An FeNa value less than 1% suggests pre-renal AKI, indicating the kidneys efficiently reabsorb almost all filtered sodium to maintain circulating blood volume. In contrast, an FeNa greater than 2% points to intrinsic AKI, where tubular damage prevents adequate sodium reabsorption, leading to increased sodium excretion. This distinction guides fluid management, as pre-renal AKI responds to fluid resuscitation, while intrinsic AKI requires different interventions.
The Fractional Excretion of Urea (FeUrea) can complement or serve as an alternative to FeNa, particularly in patients receiving diuretics. Diuretics can increase sodium excretion, potentially confounding FeNa results. FeUrea is calculated similarly to FeNa but uses urea instead of sodium. An FeUrea less than 35% suggests pre-renal AKI, while values greater than 50% are consistent with intrinsic AKI. Both FeNa and FeUrea provide insights into the kidney’s tubular function and help differentiate the cause of AKI for targeted treatment.
Advanced Biomarkers
Newer urine biomarkers can detect kidney stress or damage earlier than traditional tests. These markers are specific proteins or molecules released into the urine when kidney cells are injured or under duress. They allow for more precise and timely identification of AKI, even before changes in traditional blood tests like creatinine become apparent. This early detection allows for quicker intervention, limiting the extent of kidney damage.
Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a biomarker that rises rapidly in the urine following acute kidney injury, particularly with tubular damage. Its early elevation makes it a tool for identifying AKI sooner than traditional markers. Kidney Injury Molecule-1 (KIM-1) is another specific protein found in the urine, associated with damage to the proximal tubules of the kidney, which reabsorb many filtered substances. Its presence indicates direct injury to these kidney structures.
Interleukin-18 (IL-18), a pro-inflammatory cytokine, is released into the urine during acute tubular necrosis, a common form of intrinsic AKI. Its appearance signals an inflammatory response within the kidney. The combination of Tissue Inhibitor of Metalloproteinase-2 (TIMP-2) and Insulin-like Growth Factor-binding Protein 7 (IGFBP7) has been identified as a marker for cell cycle arrest in kidney cells under stress. These two proteins are measured together to predict the risk of moderate to severe AKI. These advanced biomarkers can detect AKI earlier, help predict its severity, and guide treatment decisions, although their routine availability may vary across different clinical settings.