A 37-year-old man consulted due to jaundice, fever and abdominal pain in March 2006. He thought of an episode of cholangitis, suspected cholangiolithiasis because of endoscopic microlithiasis.
Endoscopic sphincterotomy was performed in May 2006.
Eight days later she presented a new episode of cholangitis.
A calcified cholecystopathy was proposed as an explanation for recurrent cholangitis; scintigraphy with recurrent cholangitis was compatible with the diagnosis and a laparoscopic cholecystectomy was performed, but after 15 days another episode of cholecystitis was presented.
A liver biopsy showed acute cholangitis with minimal foci of fibrosis.
At the beginning of 2007, magnetic resonance cholangiography showed constrictions compatible with CEP, with no possibility of intervention.
She was treated with ursodeoxycholic acid and low doses of antibiotics (ciprofloxacin), but continued to present episodes of cholangitis.
In October 2007 the patient consulted due to fever and abdominal pain. Treatment with ciprofloxacin was initiated and a contrasted abdominal CT was requested, with a previous creatinine level of 8.7 mg/dl. In May 2007 the creatinine level was 1.2 mg/dl.
The patient was evaluated by Nephrology, with mild stenosis as the only finding.
Blood urea nitrogen (BUN) 46, normal sodium and potassium, pH 7.32, bicarbonate 16, Hb: 9.7 g/dl, urine glucose (50 mg/dl).
Renal ultrasound showed normal size kidneys, increased bilateral echogenicity.
Acute renal failure secondary to tubulointerstitial nephritis due to quinolone consumption was diagnosed.
The next day, with antibiotic withdrawal and hydration, creatinine fell to 5.5 md/dl and BUN to 36 mg/dl. Serum creatinine was normal, antinuclear antibodies (ANdl serodeficiency 2,280) were negative for Syphilis virus.
Twenty days later she returned with fever, diarrhea and edema.
On admission she presented creatinine 15 mg/dl, potassium 5.8 mEq/L; urine cytochemical: leukocyturia, proteinuria (25 mg/dl), glycosuria (50 mg/dl), hematuria (erythrocytes 6 x ap).
Physical examination showed no pathological findings.
Acute renal failure was considered; due to suspicion of tubulointerstitial nephritis, management with prednisone was initiated and a renal biopsy was performed.
Renal biopsy reported: tubulointerstitial nephritis acute, M. immunofluorescence: IgG: ++ (interstice), IgA and IgM: ++++ (interstice), chains k and Cowmb
Established as histological changes compatible with acute tubulointerstitial nephritis due to drug hypersensitivity vs. autoimmune.
Management was continued with steroids and creatinine 3.6 mg/dl.
Since the beginning of the treatment there have been no episodes of cholangitis or cholangitis, so the patient developed sclerosing AP with tubulo-interstitial cholangitis and sclerosing cholangitis.
IgG4 levels were not determined because she was already receiving steroid treatment.
Primer outpatient control: creatinine 1.6 mg/dl. He was on steroids demonte and prednisone dose of 5 mg was left indefinitely interday.
Subsequent controls with creatinine between 1.7 and 1.4 mg/dl.
The last control was performed in December 2010 with creatinine of 1.43 mg/dl, without new episodes of cholangitis or pancreatitis.
