Abstract | May 4, 2021

Clinical Utility of Serum Cystatin C to Avoid Misinterpreting Kidney Function by Using Serum Creatinine

Presenting Author: Kapila Patel, MS, Medical Student MS2, Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology, Hypertension and Kidney Transplantation, Department of Medicine, University of California Irvine School of Medicine, Irvine, California

Coauthors: Natsuki Eguchi, BS, Junior Specialist. Division of Nephrology, Hypertension and Kidney Transplantation, Department of Medicine, University of California Irvine School of Medicine, Orange, California, Hwakyung Seo, Undergraduate Researcher., University of California Irvine, Irvine, California, Ekamol Tantisattamo, MD, MPH, FASN, FAHA, Assistant Clinical Professor. Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology, Hypertension and Kidney Transplantation, Department of Medicine; Nephrology Section, Department of Medicine; Multi-Organ Transplant Center, Section of Nephrology, Department of Internal Medicine, University of California Irvine School of Medicine, Orange, California; Veterans Affairs Long Beach Healthcare System, Long Beach, California; William Beaumont Hospital, Oakland University William Beaumont School of Medicine, Royal Oak, Michigan

Learning Objectives

  1. In assessing kidney function, serum cystatin C is not confounded by patient characteristics such as race, gender, and muscle mass, and should be utilized in conjunction with serum creatinine.

Introduction:
While serum creatinine (SCr) remains the most common biomarker used to determine kidney function, it is affected by race, gender, and muscle mass. We present a case of a woman with focal segmental glomerulosclerosis (FSGS) who had acute kidney injury (AKI) of unclear etiology; however, estimated glomerular filtration rate (eGFR) by using serum cystatin C (SCc) showed improved kidney function.

Case Presentation:
The patient is a 45-year-old Hispanic woman with nephrotic-range proteinuric stage 2 chronic kidney disease (CKD) secondary to biopsy-proven primary FSGS. She was initially treated with tacrolimus and prednisone 20 mg daily. Lisinopril 20 mg daily was started for antiproteinuric effect. Urinary total protein/urinary creatinine (UPCR) was 9.4 g/g of Cr. She developed non-oliguric AKI with a SCr of 1.1 mg/dL from the baseline of 0.7 – 0.9 mg/dL. FENa and FEurea was 1.08% and 37.95% respectively. A 12-hour tacrolimus trough level had been in the therapeutic range of 1.5 to 4.7 ng/mL. She denied loss of appetite, vomiting, diarrhea, or lower urinary tract symptoms. She did not take over-the-counter medications. Vital signs were unremarkable. Over the past year, SCr has been at 1.2-1.4 mg/dL despite lisinopril dose being decreased. SCc initially increased from 1.57 mg/L to 1.67 mg/L during the period of acute rising of SCr, but trended down to 1.35 mg/L. UPCR has trended down to 0.17 g/g of Cr with a prednisone slowly tapered to 5 mg/day. Serum albumin improved from 2.4 to 4 g/dL, concomitant with improved subjective symptoms. She had no history of volume depletion, nor showed signs of urinary tract obstruction. FENa and FEurea did not clearly suggest prerenal or intrinsic renal causes. She was not exposed to nephrotoxic medications.

Final Diagnosis:
Though her rising SCr level met AKI criteria, her clinical picture was not consistent with AKI suggesting that her SCr levels were likely confounded by race, gender, and chronic steroid use.

Outcome:
SCc is a new biomarker of kidney function that is not affected by patient characteristics. Our case illustrates how SCc should be incorporated with SCr for interpretation of kidney function, particularly in patients with factors that affect SCr.

Timeline 1

Download Abstract
Back to Abstracts