Your BUN/Creatinine ratio helps characterize the etiology of renal dysfunction when creatinine is elevated. A normal ratio of 10–20:1 suggests that BUN and creatinine are rising proportionally, which is typical of intrinsic renal disease where glomerular filtration is impaired but tubular function is relatively preserved. A ratio greater than 20:1 suggests pre-renal azotemia — the kidneys are underperfused, and urea is being disproportionately reabsorbed in the proximal tubule due to slow tubular flow and increased sodium and water reabsorption.

A ratio below 10:1 is less common and may indicate conditions where BUN production is decreased (liver disease, malnutrition, low-protein diet) or creatinine is disproportionately elevated (rhabdomyolysis, where massive muscle breakdown releases creatinine into the bloodstream). An elevated ratio above 20 can also be seen in upper GI bleeding, where digested blood protein increases BUN production, and with high-protein diets, corticosteroid use, or catabolic states.

Use the BUN/Creatinine ratio as part of the initial evaluation of a patient with acute kidney injury or unexplained elevation in serum creatinine. It is one of the first and simplest tests to help differentiate pre-renal from intrinsic renal causes of AKI, and it can be calculated from routine laboratory values that are almost always available.

The ratio is especially useful in the emergency department and inpatient settings when triaging the cause of AKI. It is commonly used alongside urinalysis, FENa, and renal ultrasound to build a clinical picture. It can also raise suspicion for upper GI bleeding in patients with an elevated ratio and no other obvious cause of pre-renal azotemia — particularly in patients with cirrhosis or on anticoagulation.

The BUN/Creatinine ratio is a screening tool with limited specificity. BUN is influenced by many factors beyond renal function, including dietary protein intake, liver synthetic function (urea is synthesized in the liver), GI bleeding, catabolic state, corticosteroid use, and tetracycline antibiotics. These confounders can elevate or lower the ratio independently of renal perfusion status.

The ratio also provides limited information in patients with chronic kidney disease, where baseline BUN and creatinine are already elevated and the ratio may not reliably distinguish between acute pre-renal insults and chronic disease progression. Additionally, the ratio does not differentiate between specific causes of pre-renal azotemia (dehydration vs. heart failure vs. hepatorenal syndrome) or intrinsic renal disease (ATN vs. glomerulonephritis vs. interstitial nephritis). It should be interpreted alongside FENa, urinalysis with microscopy, renal ultrasound, and the overall clinical picture.