A 64-year-old man comes to the hospital due to generalized weakness and fatigue for the past several weeks. He has a history of uncontrolled hypertension and nonadherence to medical therapy. Blood pressure is 160/100 mm Hg, pulse is 90/min, and respirations are 22/min. Oxygen saturation is 95% on room air. Physical examination shows elevated jugular venous pressure, bilateral crackles, and 3+ pitting edema in both legs. Laboratory results are as follows:
| Blood urea nitrogen | 82 mg/dL |
| Creatinine | 4.8 mg/dL |
Which of the following additional findings are most likely present in this patient?
Metabolic acidosis | ||
Type | Normal anion gap | Elevated anion gap |
Mechanism |
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Common |
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This patient's markedly elevated blood urea nitrogen (BUN) and serum creatinine in the setting of uncontrolled hypertension suggest advanced chronic kidney disease (CKD), a condition commonly presenting with fatigue, generalized weakness, and evidence of volume overload (eg, jugular venous distension, peripheral edema). Once CKD becomes advanced (eg, serum creatinine >3 mg/dL), anion gap metabolic acidosis with respiratory compensation is expected.
CKD involves a gradual decline in glomerular filtration rate (GFR), as evidenced by a slow increase in serum creatinine. Urea, which is formed in the liver from ammonia and other nitrogenous wastes derived from protein breakdown, is normally cleared by the kidneys and also accumulates as GFR declines. With advanced CKD, BUN levels become markedly elevated (eg, >60 mg/dL). Although urea is uncharged and does not contribute to acidemia or an elevation in the anion gap, elevated BUN (ie, uremia) is a marker for the reduced renal clearance and consequent accumulation of unmeasured acidic compounds (eg, hydrogen phosphate, hydrogen sulfate, uric acid). These compounds donate hydrogen ions (H+) to bind up bicarbonate (HCO3−) and acidify the blood, and the remaining anionic component increases the anion gap (normal: 10-14 mEq/L).
In response to the metabolic acidosis, the lungs compensate with hyperventilation to decrease PaCO2 and help normalize pH.
(Choice A) Low pH with low HCO3− and elevated PaCO2 represents mixed metabolic and respiratory acidosis. Such a scenario with an elevated anion gap may be seen with sepsis (ie, lactic acidosis) with acute respiratory failure.
(Choice C) Low pH with low HCO3− and slightly reduced PaCO2 represents metabolic acidosis with respiratory compensation. A normal anion gap is expected with metabolic acidosis that results from loss of HCO3− (eg, severe diarrhea). However, this patient with CKD will have accumulation of unmeasured acidic compounds, resulting in an elevated anion gap.
(Choice D) Low pH with elevated PaCO2 indicates respiratory acidosis. Minimal increase in HCO3- suggests acute respiratory acidosis (eg, acute opioid overdose) as there has not been time for metabolic compensation to occur (full metabolic compensation requires approximately 72 hours).
(Choice E) These acid-base and anion gap findings are within normal limits and indicate an absence of acid-base disturbance.
Educational objective:
Advanced chronic kidney disease typically involves the accumulation of unmeasured acidic compounds in the blood; therefore, anion gap metabolic acidosis with respiratory compensation is expected.