Limitations of Blood Urea Nitrogen as a Marker of Kidney Function in Malnourished Patients: A Case Report of Uremic Encephalopathy After Bariatric Surgery

Introduction: Blood urea nitrogen (BUN) is a clinical biomarker that quantifies the concentration of urea nitrogen, a metabolic waste product generated during the catabolism of proteins. Normal values typically range from 7 to 20 mg/dL. This parameter is frequently utilized as an indirect indicator of renal function, given that the kidneys play a central role in the excretion of urea. Impaired renal clearance leads to the accumulation of these nitrogenous waste products, which may precipitate uremic symptoms such as altered mental status (AMS) and asterixis. These manifestations can generally be seen with BUN >100 mg/dL. Case Description: A 49-year-old female with past medical history of gastric sleeve converted to roux-en-Y bypass 5 months prior, chronic kidney disease (CKD) stage 3, and hypertension presented with AMS and right-sided weakness. Patient underwent CT angiogram of the head and neck and MRI with no abnormalities. The patient was found to have uremic symptoms, weakness in upper extremities, slowed speech, and decreased cognition with a BUN of 31 mg/dL, serum creatinine of 4.39 mg/dL, eGFR of 11.7 ml/min/1.73m2, and albumin of 2 g/dL. Nutritional workup revealed multiple deficiencies. The patient underwent dialysis initiation with three sequential hemodialysis sessions and markedly improved during her third session, where she was able to speak and move her extremities at baseline with a BUN of 7 mg/dL. Discussion: BUN may not be sufficient as a standalone marker for kidney function. Given the complex medical histories including malnutrition, electrolyte imbalances, and altered protein metabolism often seen in patients with CKD, laboratory indicators of serum protein levels and other metabolites may not accurately reflect one’s true kidney function. In a patient with metabolic disturbances secondary to gastric surgery, the threshold for BUN levels leading to uremic encephalopathy may be altered, and so the contribution of malnourished states to kidney function must not be undermined. Therefore, diagnosis and treatment of uremic encephalopathy should be guided by clinical presentation rather than lab values. This case supports the significance of patient-centered assessment and the understanding that lab markers can be limited in atypical contexts, such as bariatric surgery patients.