Abstract
In renal failure, blood urea nitrogen and serumcreatinine usually rise in tandem; the normalBUN : Cr ratio is 10–15 : 1. Disproportionate risesin BUN : Cr (> 20 : 1) often imply pre-renalazotemia but may be caused by increased proteincatabolism or an excessive protein load. Inthis study we looked at intensive care patientswho acutely developed markedly increased BUN(≥ 100 mg/dL) with only modestelevation of Cr (≤ 5 mg/dL) forpossible causes of the disproportionateazotemia. There were 19 such casescollected over 6 months, nine women andten men, with mean age 69.2 ± 4.4years (13/19 > 75 years). Peak BUN was 156 ± 11 mg/dL; peak Cr 4.3 ± 0.5 mg/dL.Eleven patients expired. Mean serum albuminat the time of consultation was 2.7 ± 0.2 g/dL; mean total lymphocyte count 1.0± 0.1/mm3. Of possible factors causing theazotemia, nine patients had documentedhypovolemia; eight had congestive heartfailure; six were in septic orhypovolemic shock, and two receivedhigh-dose steroids. As contributing factors,eight patients had Salb < 2.5 g/dL;eight were given a high protein intake ≥ 100 g/d; two had HIV, andtwo others had gastrointestinal bleeding.Infection was present in 14 patients;seven had sepsis (bacteremia withhypotension). All patients had at leastone of these factors present and 16/19 hadtwo or more. Fractional Na excretion was< 1% (consistent with pre-renal azotemia) inonly four of the 11 patients in whom itwas measured. We conclude that severelydisproportionate BUN : Cr is frequentlymultifactorial and is most common in theelderly, perhaps due to their lower musclemass, and in ICU patients given a high proteinintake. It is often not indicative ofuncomplicated renal hypoperfusion,although low renal perfusion (hypovolemia,shock, or heart failure) is common. Mortalityis high due to the severe illnesses, especiallyinfection, worsened by decreased renal functionand hypercatabolic state.
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Feinfeld, D.A., Bargouthi, H., Niaz, Q. et al. Massive and disproportionate elevation of blood urea nitrogen in acute azotemia. Int Urol Nephrol 34, 143–145 (2002). https://doi.org/10.1023/A:1021346401701
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DOI: https://doi.org/10.1023/A:1021346401701