Something new is coming to Sketchy... ­čĹÇBe the first to know!

Renal Function Tests & Acute Kidney Injury (AKI)

No items found.



In evaluating renal function, creatinine, glomerular filtration rate (GFR), and blood urea nitrogen (BUN) serve as pivotal markers. Creatinine, a breakdown product of creatine from muscle cells, has a normal serum concentration around 1.0 mg/dL and is freely filtered at the glomerulus. It is neither reabsorbed nor substantially secreted in the nephron, making its clearance a useful proxy for GFR. The clearance formula, C=UV/P, allows clinicians to estimate GFR, which is normally > 100 ml/min in healthy individuals. In contrast, blood urea nitrogen (BUN), which originates from amino acid & pyrimidine metabolism in the liver, is actively reabsorbed in the PCT. The concentration and interrelationships of these markers offer valuable insights into renal function.

Acute kidney injury (AKI) is categorized into pre-renal, intrinsic renal, and post-renal types, each with specific diagnostic markers. Pre-renal AKI commonly results from hypoperfusion due to conditions such as hypovolemia or heart failure. It is characterized by an increased BUN/Cr ratio (>15) and decreased fractional excretion of sodium (FENa <1%). Intrinsic renal AKI often stems from acute tubular necrosis and is marked by a BUN/Cr ratio <15 and FENa >2%. Post-renal AKI, often arising from mechanical obstructions like nephrolithiasis or benign prostatic hyperplasia (BPH), initially presents with a high BUN/Cr ratio but can progress to a low BUN/Cr ratio in severe or prolonged disease.

Lesson Outline

Don't stop here!

Get access to 155 more Pathophysiology lessons & 13 more medical school learning courses with one subscription!

Try 7 Days Free


What is renal function testing and why is it important?

Renal function tests assess kidney performance through the analysis of blood and urine samples. Key parameters include estimated glomerular filtration rate (GFR), creatinine levels, and blood urea nitrogen (BUN). The ratios of these parameters (such as BUN/Cr ratio) can be utilized to further narrow the diagnosis These tests are indispensable for early detection of kidney damage, gauging the severity of renal diseases like acute kidney injury (AKI), and monitoring treatment efficacy.

How does creatinine serve as a diagnostic marker for acute kidney injury (AKI)?

Creatinine, a byproduct of muscle metabolism, is used as a clinical indicator of renal function, as it is freely filtered at the glomerulus and minimally secreted or reabsorbed in the nephron. Elevated serum creatinine levels can signify reduced GFR and potential renal dysfunction, such as AKI. Therefore, monitoring creatinine levels is integral to renal function assessment.

How are glomerular filtration rate (GFR) and creatinine clearance utilized to evaluate renal function?

GFR measures the volume of fluid filtered from the glomerular capillaries into Bowman's capsule per unit time. Creatinine clearance approximates GFR, as creatinine is freely filtered and minimally secreted or reabsorbed. A decline in GFR or creatinine clearance below the normal range (<100 ml/min mg/dL) can indicate renal dysfunction or AKI.

What is the role of blood urea nitrogen (BUN) in renal function tests?

BUN quantifies the nitrogen content in blood originating from urea, a waste product of protein metabolism. BUN is actively reabsorbed in the proximal convoluted tubule of the nephron. Elevated BUN levels can signify reduced GFR or renal injury, making it a valuable component of renal function tests.

What conditions are commonly associated with pre-renal AKI, intrinsic-renal AKI, and post-renal AKI respectively?

AKI can arise from various causes and is classified into pre-renal, intrinsic renal, and post-renal categories. Pre-renal AKI commonly results from renal hypoperfusion due to factors like hypovolemia or low cardiac output states. Intrinsic renal AKI is often due to direct renal tissue damage, as seen in acute tubular necrosis or acute interstitial nephritis. Post-renal AKI is usually caused by urinary tract obstructions, such as nephrolithiasis or benign prostatic hyperplasia.