Prerenal Azotemia: Differentiation of Hyperureagenesis from Renal Hypoperfusion Using Urinary Urea Nitrogen Data

Abstract

Blood urea nitrogen (BUN) rises disproportionately to serum creatinine in patients with prerenal azotemia whether due to impaired hemodynamics or excessive ureagenesis. To determine whether urinary urea nitrogen excretion rates can distinguish between these caused of hyperuremia we performed a cross-sectional observational study to compare urinary urea nitrogen excretion rates in a highly selected group of patients with prerenal azotemia. Patients who had stable serum creatinine levels, BUN: serum creatinine ratios exceeding 20:1, and progressive azotemia were identified from the hospital laboratory data base. Using conventional clinicolaboratory criteria, 27 patients were diagnosed with either renal hypoperfusion (group I; n = 17) or hyperureagenesis ((group II; n = 10). Random urine sampling for electrolytes, osmolality, creatinine, and urea nitrogen was followed by 24 h collection for creatinine clearance and urinary urea nitrogen. There were no significant differences in age, gender, absolute levels of BUN, or BUN: serum creatinine ratios between the groups. Creatinine clearance (ml/min/1.73 m2) (ml/s/1.73 m2) was lower in group I than in group II (21 +/- 16 vs 36 +/- 13; p < 0.05) (0.35 +/- 0.27 vs 0.60 +/- 0.22; p < 0.05). Twenty-four hour urinary urea nitrogen levels were significantly different (group I, 4.8 +/- 2.9 vs. group II, 13.6 +/- 3.2 gm; p < 0.001) (group I, 171 +/- 300 vs. group II, 486 +/- 114 mmol; p < 0.001). Random urine urea excretion indices were less discriminating but nevertheless still capable of separating the groups. Timed as well as random urine urea nitrogen determinations may assist in differentiating prerenal azotemia due to renal hypoperfusion from hyperureagenesis. Differentiation of these causes of prerenal azotemia might prevent iatrogenic overhydration of patients with azotemia incorrectly attributed to hemodynamic disturbances.