From the Guidelines
A blood urea nitrogen (BUN) level of 70 mg/dL is significantly elevated and indicates impaired kidney function, which can be caused by various factors including acute kidney injury, chronic kidney disease, dehydration, or congestive heart failure, as suggested by studies such as 1. The most common causes of elevated BUN levels include:
- Acute kidney injury
- Chronic kidney disease
- Dehydration
- Gastrointestinal bleeding
- High-protein diet
- Certain medications (such as NSAIDs, aminoglycosides, or diuretics)
- Urinary tract obstruction
- Congestive heart failure, which is strongly linked to increased morbidity and mortality, as noted in 1. Immediate medical evaluation is necessary as this level suggests moderate to severe kidney dysfunction. Treatment depends on the underlying cause but may include:
- Intravenous fluids for dehydration
- Medication adjustments
- Dialysis in severe cases
- Addressing the primary condition affecting kidney function, such as optimizing hydration status and evaluating renal function before initiating potentially toxic drug therapy, as recommended in 1. This elevation occurs because the kidneys are unable to effectively filter urea, a waste product from protein metabolism, from the bloodstream. The BUN level should be interpreted alongside creatinine levels and other clinical findings to determine the specific cause and appropriate treatment approach, considering the potential for renal dysfunction to be reversible, as highlighted in 1.
From the Research
Possible Causes of Elevated BUN
- Acute kidney injury (AKI) can cause a rapid decline in glomerular filtration rate, leading to the accumulation of metabolic waste products, including blood urea nitrogen (BUN) 2
- Prerenal, intrinsic renal, and postrenal etiologies of AKI can contribute to elevated BUN levels 2
- Dehydration, volume depletion, and nephrotoxic medications can also contribute to elevated BUN levels 2
Biomarkers of Acute Kidney Injury
- Biomarkers such as kidney injury molecule-1 (KIM-1), liver-type fatty acid binding protein (L-FABP), insulin-like growth factor-binding protein-7 (IGFBP-7), and tissue inhibitor of metalloprotease-2 (TIMP-2) can be used to localize specific segments of injured tubules and predict the transition to chronic kidney disease (CKD) 3
- These biomarkers can also guide AKI management, improve diagnosis of diseases such as acute interstitial nephritis (AIN), and differentiate between kidney dysfunction and injury 3
Clinical Implications
- Accurate diagnosis of the underlying cause of AKI is key to successful management, and includes a focused history and physical examination, serum and urine electrolyte measurements, and renal ultrasonography when risk factors for a postrenal cause are present 2
- General management principles for AKI include determination of volume status, fluid resuscitation with isotonic crystalloid, treatment of volume overload with diuretics, discontinuation of nephrotoxic medications, and adjustment of prescribed drugs according to renal function 2