Abstract

Cystatin C has been suggested to be a more accurate glomerular filtration rate (GFR) surrogate than creatinine in patients with acquired immunodeficiency syndrome (AIDS) because it is unaffected by skeletal muscle mass and dietary influences. However, little is known about the utility of this marker for monitoring medications in the critically ill. We describe the case of a 64-year-old female with opportunistic infections associated with a new diagnosis of AIDS. During her course, she experienced neurologic, cardiac, and respiratory failure; yet her renal function remained preserved as indicated by an eGFR ≥ 120 mL/min and a urine output > 1 mL/kg/hr without diuresis. The patient was treated with nephrotoxic agents; therefore cystatin C was assessed to determine if cachexia was resulting in a falsely low serum creatinine. Cystatin C measured 1.50 mg/L which corresponded to an eGFR of 36 mL/min. Given the >60 mL/min discrepancy, serial 8-hour urine samples were collected and a GFR > 120 mL/min was confirmed. It is unclear why cystatin C was falsely elevated, but we hypothesize that it relates to the proinflammatory state with AIDS, opportunistic infections, and corticosteroids. More research is needed before routine use of cystatin C in this setting can be recommended.

Highlights

  • In critically ill patients, serum creatinine suboptimally predicts glomerular filtration rate (GFR) because of its delayed rise during acute injury and the myriad of confounders which influence its concentration including skeletal muscle mass, dietary intake, interactions with vasopressors, antibiotics, and bilirubin and fluid shifts [1,2,3,4]

  • We report our experience in a treatment-naıve patient with a new diagnosis of acquired immunodeficiency syndrome (AIDS) in whom cystatin C falsely underestimated GFR

  • Serum creatinine has historically been the standard to estimate GFR and optimize medication dosing in human immunodeficiency virus (HIV)-positive patients, but in recent years cystatin C has been shown to be an equivalent or more reliable alternative [1, 9, 12]

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Summary

Introduction

Serum creatinine suboptimally predicts glomerular filtration rate (GFR) because of its delayed rise during acute injury and the myriad of confounders which influence its concentration including skeletal muscle mass, dietary intake, interactions with vasopressors, antibiotics, and bilirubin and fluid shifts [1,2,3,4]. For this reason cystatin C, an alternate endogenous marker of GFR, may be more suitable. We report our experience in a treatment-naıve patient with a new diagnosis of acquired immunodeficiency syndrome (AIDS) in whom cystatin C falsely underestimated GFR

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