hemoconcentration can cause creatinine concentration after diuresis
- related: Nephrology
- tags: #literature #nephrology
The case in this stem sounds all too familiar. This patient presented with an acute exacerbation of chronic heart failure. He has massive volume overload, and his treatment team begins aggressive diuresis. After diuresis of 16 L, the patient’s creatinine concentration has increased from 2.2 to 2.8 mg/dL (194.48-247.52 μmol/L).
Hemoconcentration is a common reason why creatinine concentration increases with diuresis, as the volume of distribution of creatinine is the total body water. It follows, then, that as body water decreases, creatinine concentration will increase. If we assume that 60% to 70% of this patient’s total body weight was water, then on admission, his total body water was between 66 and 77 L. After 16 L of diuresis, his total body water would have decreased to approximately 50 to 61 L. We can solve for his predicted postdiuresis creatinine concentration by using the following equation:
initial total body water ÷ follow-up body water = predicted follow-up creatinine ÷ initial creatinine
If the change was due to hemoconcentration and loss of body water alone (with no change in creatinine clearance), this equation predicts that his creatinine concentration would have increased to approximately 2.8 to 2.9 mg/dL (247.52-256.36 μmol/L).
Neither metolazone nor furosemide is directly nephrotoxic, but overdiuresis to the point of causing hypovolemia could potentially cause acute kidney injury. Not only was this patient’s increase in creatinine concentration appropriate for his diuresis, but he still had evidence of volume overload during examination at the time of his repeat creatinine concentration test. His very rapid diuresis put him at risk of electrolyte disturbances, but he did not undergo diuresis to the point at which his plasma blood volume would have been low enough to cause kidney injury. Although obstructive uropathy is a potential cause of increased creatinine concentration, the patient had been undergoing diuresis well, which rules this out.123456
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Footnotes
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Ahmad T, Jackson K, Rao VS, et al. Worsening renal function in patients with acute heart failure undergoing aggressive diuresis is not associated with tubular injury. Circulation. 2018;137(19):2016-2028. PubMed ↩
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El-Refai M, Krivospitskaya O, Peterson EL, et al. Relationship of loop diuretic dosing and acute changes in renal function during hospitalization for heart failure. J Clin Exp Cardiolog. 2011;2(10):1000164. PubMed ↩
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Joannidis M, Klein SJ, Ostermann M. 10 myths about frusemide. Intensive Care Med. 2019;45(4):545-548. PubMed ↩
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Liu KD, Thompson BT, Ancukiewicz M, et al; National Institutes of Health National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Network. Acute kidney injury in patients with acute lung injury: impact of fluid accumulation on classification of acute kidney injury and associated outcomes. Crit Care Med. 2011;39(12):2665-2671. PubMed ↩
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Rangaswami J, Bhalla V, Blair JEA, et al; American Heart Association Council on the Kidney in Cardiovascular Disease and Council on Clinical Cardiology. Cardiorenal syndrome: classification, pathophysiology, diagnosis, and treatment strategies: a scientific statement from the American Heart Association. Circulation. 2019;139(16):e840-e878. PubMed ↩