Abstract: PUB009
Myoglobin-Induced Acute Tubular Injury
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Ramrattan, Amit, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Shah, Syed Muhammad Obaida M, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Shafiq, Ihtesham, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Wall, Barry M., The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Vo, Hieu Q., The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Adeboye, Adedamola M., The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
Introduction
Rhabdomyolysis, if severe enough, can result in acute kidney injury from either fluid sequestration and consequential volume depletion or as a sequela of myoglobin induced nephrotoxicity and tubular injury. One would expect marked elevation of creatinine phosphokinase (CPK) and/or the presence of urine myoglobin, however, this was not demonstrated in this case.
Case Description
Our patient is a 66-year-old female with a past medical history of morbid obesity, type 2 diabetes mellitus, hypertension, and microcytic anemia with a baseline creatinine of 0.67mg/dl. One month prior, she had a routine visit to her Primary Care Physician (PCP), and received Seqirus Influenza Flucelvax 0.5ml after which she developed generalized myalgia for two weeks. Her myalgia improved but she then experienced weakness, described "beer" colored, foamy urine and endorsed decreased output for the following two weeks. When she presented to the Emergency Department, she had normal vital signs and physical examination except for mucosal palor. Imaging was negative for obstruction, and investigations showed an admission creatinine of 9.1mg/dl, negative Anti-GBM antibody, anti-nuclear antibody, double-stranded DNA antibody, p and c-ANCA, normal CPK and urine myoglobin. Routine urinalysis revealed 3+ hematuria, 3+ proteinuria and her urine protein:creatinine ratio was 7g/g. A renal biopsy was performed which showed acute tubular injury with positive staining myoglobin casts. She required 3 sessions of hemodialysis after which she begins to recover renal function, and her creatinine had stabilized at 6.3mg/dl. Three weeks after hospital discharge, she was able to remain off dialysis and her creatinine improved to 1.66mg/dl.
Discussion
Rhabdomyolysis can have a delayed presentation and can present as an AKI of unknown etiology. Myoglobin is well known for its cytotoxic effects but as shown in this case, can persist in the renal tubules in the setting of normal CPK and urine myoglobin. We should always consider rhabdomyolysis in the differential and diagnostic workup of AKI with appropriate staining of renal biopsy samples.