This case study involves a 27-year-old Caucasian male who developed a dull aching type of abdominal pain, fever, cough, and chest congestion with flu-like illness over the past 5 days. He used ibuprofen 200 mg 2 times a day for the past 2 days, with brief improvement in his symptoms. Subsequently, he experienced a focal to bilateral tonic-clonic seizure while working at a hardware store 1 day ago. He was initially brought to a nearby satellite facility. His biochemical profile was unremarkable, except for a deranged renal function. He was initiated on 500 mg levetiracetam twice daily, and magnetic resonance imaging of brain with gadolinium and electroencephalography were planned. He had been having occasional seizure episodes for the past 7 years, but he refused to start anticonvulsant therapy. He remained seizure-free for 24 hours after initiation of levetiracetam at the facility. The patient was then transferred to our hospital for further evaluation and management of his worsening renal function.
On detailed inquiry, he admitted having large amounts of daily intranasal cocaine 1 week ago, immediately preceding his clinical symptoms. He had been smoking marijuana and snorting cocaine 3 to 4 times per week for past several months but denied intravenous drug use. He chewed tobacco for 4 years but suspended its use 1 year ago. He also reported binge alcohol consumption. He denied stabbing chest or flank pain, nausea, vomiting, or change in bowel habits. There was no history of sore throat, joint swelling, skin rash, dysuria, or hematuria. Family history was negative for autoimmune diseases and tuberculosis. Abdominal examination was remarkable for diffuse tenderness with normal bowel sounds.
Laboratory evaluation revealed elevated serum creatinine levels, 2.8 mg/dL (baseline: 1.1 mg/dL), normal creatine phosphokinase, 226 U/L (39-308 U/L), and insignificant peripheral eosinophil count, 2%, consistent with acute kidney injury. The details of the laboratory studies are provided in Table 1. Urinalysis revealed pH 5.5, specific gravity 1.015, and proteinuria 30 mg/dL. A trace amount of blood was present, but ketones, nitrates, and leukocyte esterase were absent. Urine microscopy showed 4 to 5 white cells per high-power field and a few scattered red cells. It was negative for leukocytes, including eosinophils by special stain, pigmented granular casts, and bacteria. Urine culture also came out negative. Urine toxicology screen was positive for cocaine.
His hemoglobin A1c, serum lipase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total bilirubin were unremarkable for abnormalities. The measurements of serum complement levels were within normal limits. Tests for cytoplasmic-antineutrophil cytoplasm antibodies (c-ANCA), perinuclear-ANCA (p-ANCA), myeloperoxidase-ANCA (MPO-ANCA), and antiproteinase 3-ANCA (PR3-ANCA) were negative. Furthermore, rheumatoid factor, anti-glomerular basement membrane (anti-GBM), anti-Sjogren's-syndrome-related antigen A (anti-SSA), anti-apoptosis signal-regulating kinase 1 (anti-ASK1), anti-double stranded DNA (anti-dsDNA), anti-smooth muscle (anti-SM), anti-streptolysin O (ASO) titer, and anti-ribonucleoprotein particles (anti-RNP) antibodies were also negative. Serology for human immunodeficiency virus, and hepatitis B and C were negative for an active infectious process.
Computed tomography scan of the abdomen and pelvis without contrast showed nonspecific bilateral perinephric stranding, with a thickening along the anterior portion of the Gerota's fascia. Renal Doppler ultrasonography ruled out renal artery stenosis and aortic dissection. Transthoracic echocardiogram showed normal wall motion and ejection fraction. Electrocardiogram was also normal. Chest radiograph was negative for hilar nodules. Subsequently, an uneventful renal biopsy was performed. The histopathologic examination of the biopsy specimen revealed normocellular glomeruli (Figure 1). An interstitial inflammatory infiltrate composed of mononuclear cells was present, with no pathologic alterations in the arteries (Figure 2). Patchy interstitial edema along with inflammation was also identified (Figure 3). The biopsy findings ruled out the presence of mitotic figures and tubular necrosis, with no evidence of tubulitis or granulomas (Figure 4). The presence of eosinophils was confirmed, which was suggestive of acute interstitial inflammation (Figure 5).
In terms of possible causes of his acute kidney injury, certain etiologies related to cocaine use were high on the list that can cause rhabdomyolysis, vasculitis, renal infarction, and thrombotic microangiopathy. A variety of autoimmune disorders and infectious etiologies were also considered plausible. Based on the clinical history, extensive diagnostic workup, biopsy findings, and exclusion of the probable etiologies, the patient was diagnosed with acute interstitial nephritis secondary to cocaine use.