A 28-year-old male was admitted with lumbar fossa pain, fatigue and nausea, with preserved diuresis.
The patient had a history of intranasal cocaine consumption (1 g) five days before admission.
She reported eating nonsteroidal anti-inflammatory drugs or other drugs at all times.
Physical examination revealed good general health, with slightly elevated blood pressure of 147/97 mmHg, without fever, skin rash or arthralgia.
Cardiovascular and respiratory examinations were normal.
The abdomen was blade, depressible and painless, the liver was palpable 1 cm below the costal margin and presented mild pain at bilateral lumbar palpation.
Blood count showed normal levels of albumin and normal range; serum creatinine: 160 μmol/ l; urea: 7.5 mmol/ l; potassium: 3.9 mmol/ l.
Total creatine kinase was normal (3.3 μkat/l), with a normal MB fraction.
Urine sediment showed 2 leukocytes and 3 leukocytes per field and there were no signs of eosinophil dysfunction.
Urine chemistry: sodium: 46 mmol/l, potassium: 33 mmol/l and chloride: 63 mmol/l, protein: creatinine ratio in 5 g/mol; urine culture negative.
Protein electrophoresis, immunoglobulins, complement, levels of angiotensin converting enzyme and antinuclear antibody titers were normal.
Serology for human immunodeficiency virus, human immunodeficiency virus, cytomegalovirus, hepatitis A, B, and C and mycoplasma did not detect active infection.
Ultrasound showed a normal sized, diffusely echogenic kidney with appropriate arterial and venous flow.
The electrocardiogram was normal.
Chest X-ray showed a cardiothoracic index < 0.5 and pulmonary fields without infiltrates.
After admission, urine output was maintained at 50-75 ml/h and creatinine remained unchanged.
The patient underwent a renal biopsy.
Histological findings are as follows: optical coherence tomography showed a total of 13 glomeruli, all of them normal, nonspecific, proliferation or necrotic lesions.
Basal membranes and glomerular mesangium were normal.
The interstice showed moderate mononuclear inflammatory infiltrate with abundant eosinophils, with focal tubulitis and urticaria.
Arterilases showed no remarkable lesions and there were no deposits related to immunofluorescence.
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The findings were consistent with the pathological diagnosis of acute tubulointerstitial nephritis (AIN).
This fact, together with the clinical characteristics and recent cocaine consumption, led us to define this case as cocaine-induced AIN.
The patient obviously ignored the drug consumption and was treated with oral prednisone (1 mg/kg/day initial dose), which was progressively reduced and integrated after 12 weeks.
In the subsequent follow-up, the patient had a good evolution with progressive improvement in renal function until complete recovery one month after the start of treatment.
