A 49-year-old female presented to the emergency room with lumbar pain, transitory dark urine, asthenia, anorexia, weight loss, and leg and periorbital edema (Table 1). She referred chronic use of a proton pump inhibitor and had been consuming a nonsteroidal anti-inflammatory drug (NSAID) for the previous month.
Laboratory evaluation showed elevation of the erythrocyte sedimentation rate (ESR) 140 mm/first hour and C-reactive protein (CRP) 7.75 mg/dL, normocytic and normochromic anemia (Hb 10.1 g/dL), and increased serum creatinine (3.96 mg/dL) and urea (103 mg/dL). Urinalysis showed hematuria and proteinuria (1044 mg/24 h) without cellular casts. Additional investigations were unremarkable. She underwent a kidney biopsy for declining kidney function despite intravenous hydration and discontinuation of nephrotoxins that showed, on light microscopy, normal glomeruli and diffuse mononuclear cell interstitial infiltrates, consistent with acute TIN, which was initially deemed pharmacologic.
She started systemic corticosteroids (oral prednisolone 1 mg/kg/day) with clinical improvement and full renal function recovery in 6 months. However, at 8 months after the initial presentation, while on the final phase of steroid tapering (prednisolone 2.5 mg every other day), she presented with ciliar hyperaemia and pain in the right eye (Table 1) and unilateral anterior nongranulomatous uveitis was detected (Figure 1).
Based on the presence of uveitis and TIN, the diagnosis of TINU syndrome was confirmed. Further clinical investigation was made to rule out the main infection and inflammatory diseases considered for differential diagnosis, including hepatitis B and C, Toxoplasma gondii, Mycobacterium tuberculosis, Epstein-Barr, syphilis, cytomegalovirus, and brucellosis infections, sarcoidosis, and Behcet's disease. Examination for human leukocyte antigen (HLA) alleles showed HLADQ B1*02*06 HLADR B1*02*06 positivity. Systemic corticosteroids were optimized to 0.5 mg/kg/day, and azathioprine 2 mg/kg/day was associated, beyond topical corticosteroids, with achieved uveitis control (Table 1). Six years after being diagnosed, the patient is clinically stable under immunosuppressive therapy with prednisolone 5 mg/day and azathioprine 1 mg/kg/day.