The patient was a 44-year-old man with mild kidney dysfunction and a serum creatinine (Cr) level of ~1 mg/dL [estimated glomerular filtration rate (eGFR) =65 mL/min/1.73 m2]. Blood and urine tests and diagnostic imaging had failed to reveal the cause, and renal biopsy had not been done. No proteinuria or occult hematuria was detected, only a slight decline in his renal function. While bicycling in 2017, he suffered a trochanteric fracture of left femur that was fixed by intramedullary nail. Quantitative bone mineral testing at that time indicated the onset of osteoporosis. However, there was no indication of a predisposing endocrine (i.e., diabetes mellitus) or hereditary disorder, nor was there a history of steroid use. He was diagnosed with primary (idiopathic) osteoporosis.
The intramedullary nail was removed on August 2018. Treatment with eldecalcitol, an active vitamin D analog, began end of September and was undertaken in conjunction with an over-the-counter calcium supplement. In middle of October, the patient was struck by another vehicle while driving, causing a cervical sprain. He used oral loxoprofen on three occasions for pain relief, eventually switching to a twice-daily patch. Serum Cr, calcium, and albumin levels on end of October (1.09, 8.9 and 3.5 mg/dL, respectively) rose sharply by end of November (5.16, 12.0, and 4.0 mg/dL, respectively), thus prompting immediate hospitalization. No allergic symptoms (i.e., rash or mild fever) or abnormal physical findings were evident. The laboratory test findings at the time of admission are shown in Table.
Following intravenous hydration and the withdrawal of the culprit medications (eldecalcitol, loxoprofen patch, and calcium supplement), serum calcium and albumin levels fell to 8.5 and 2.7 mg/dL, respectively; whereas serum Cr continued to climb, reaching 8.01 mg/dL in the absence of proteinuria or hematuria. The urinary levels of beta2-microglobulin and N-acetyl-beta-D-glucosaminidase were 21,075 mug/dL and 22.2 U/L, respectively.
A renal biopsy performed in early December, two days after transfer to our hospital, showed lymphocytic interstitial infiltrates with some plasma cells amidst a scattering of normal and sclerotic glomeruli. Tubular epithelial cells appeared to be swollen and they were also detached from the basement membranes or demonstrated atypical cytoplasmic blebs. The tubular lumens were obstructed by Tamm-Horsfall protein and necrotic debris (Fig. 1). There were no specific clues regarding the basis of mild kidney dysfunction. Our diagnosis was acute interstitial nephritis and acute tubular injury. Physical examination and laboratory diagnostics excluded any conditions predisposing to interstitial nephritis, such as sarcoidosis, Sjogren's syndrome, or infectious disease (e.g., tuberculosis). The presumptive cause of renal decompensation was thus the loxoprofen patch. The patient's kidney function spontaneously improved after its withdrawal.
The patient was discharged in middle of December with a serum Cr level of 2.74 mg/dL, which fell to 1.27 mg/dL by January 2019 and later stabilized at 1.1-1.3 mg/dL (Fig. 2).