MO347: When Aki is Not Due to Rhabdomyolysis: A Rare Case of Nsaid-Related Rhabdomyolysis

Abstract

Abstract BACKGROUND AND AIMS Non-steroidal anti-inflammatory drugs (NSAIDS) have well-understood side effects. Rhabdomyolysis, though, is a rare adverse effect of NSAIDs and only a few cases have been reported. Here, we report a case of NSAID-related acute kidney injury (AKI) in an old diabetic woman who was found to have high muscle enzymes. METHOD A 75-year-old diabetic woman was referred to a nephrology clinic due to nausea, vomiting and high serum creatinine. She was a known case of type 2 diabetes that was well controlled by oral hypoglycemic agents (metformin, gliclazide and linagliptin). The patient was not known to have documented hypertension. She had never visited a nephrologist but her baseline creatinine was 1.2 mg/dL. Her family also admitted that she has frequently used different NSAIDs (celecoxib, diclofenac and ibuprofen) due to knee pain in the past few weeks. The patient had developed lower extremity weakness 3 days before referral followed by nausea and vomiting, 2 days later. Physical examination showed mild pitting edema of both feet. Her new data were as followings: Blood urea nitrogen: 85 mg/dL, creatinine: 7.5 mg/dL, uric acid: 4.5 mg/dL, sodium: 135 meq/L, potassium: 4.7 meq/L, hemoglobin 11.3 g/dL, white blood cells 5400 U/micL, platelets 186 000 U/micL, creatinine phosphokinase (CPK): 12730 U/L, lactate dehydrogenase (LDH) 1344 U/L, alanine transaminase (ALT) 78 U/L and aspartate transaminase (AST) 203 U/L. Urinalysis showed specific gravity 1.020, protein 4+, sugar 1+, blood trace, red blood cells (RBC) 2–4/hpf, white blood cells (WBC) 4–6 per hpf, and also, 2–4 granular casts per hpf were reported. Urine culture result was negative. 24-h urine specimen showed proteinuria of 7300 mg. Renal ultrasound showed normal-sized kidneys with increased corticomedullary differentiation and bilateral simple cortical cysts. Renal cortical thickness was >1 cm bilaterally, and there was no hydronephrosis or other pathologies. Hemodialysis was started for the patient and she underwent a kidney biopsy to define the cause of acute kidney injury (AKI). RESULTS Renal biopsy showed: membranous glomerulonephritis stage 2/4, severe acute tubulointerstitial nephritis, focal global glomerulosclerosis and vascular thickening. Interstitial fibrosis and tubular atrophy (IFTA) were reported to be about 20%. There was no sign of acute tubular necrosis. (pictures). Immunofluorescent (IF) study showed a 1+ granular pattern deposition of IgG along the glomerular basement membrane. CONCLUSION NSAID-related rhabdomyolysis is a rare side effect of this class of analgesics. Although any agent from this class can be causative, most reports involve the most widely used ones: diclofenac and Ibuprofen. AKI in the presented patient could have different etiologies regarding data and medical history. The value of renal biopsy is well depicted in this case. Although rhabdomyolysis seemed to be the principal etiology, at the first sight, NSAID-related interstitial nephritis played the main role in AKI. The patient was put on hemodialysis for 2 weeks. Any forms of NSAIDs were withheld. Acceptable renal recovery was achieved in 3 weeks; the patient was free from dialysis. Two months later, she has creatinine of 1.2 mg/dL and normal CPK and LDH levels. Angiotensin receptor blocker (ARB) was started as the beginning treatment of membranous nephropathy. Renal biopsy is of great value to differentiate causes of non-typical cases of AKI especially in rare cases where laboratory data may be confusing or misleading.