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Tubulointerstitial Nephritis Associated with Autoimmune Pancreatitis
Lynn D. Cornell
Mayo Clinic
Rochester MN
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History
A 68-year-old woman underwent an abdominal CT scan to evaluate a previously detected
liver mass and was found to have bilateral renal masses. On follow-up scans, the renal masses had become
larger, prompting three renal biopsies over one year's time. The patient's creatinine at the time of the
third biopsy was 0.9 mg/dl. Over several months following the third renal biopsy, the creatinine had
slowly increased and ranged from 1.1 to 1.6 mg/dl. The patient's medical history was significant for
hypertension, hyperlipidemia, type II diabetes mellitus, Crohn's disease, sclerosing cholangitis, and
bilateral orbital inflammatory lesions. The patient had intermittent pancreatic insufficiency, and an
endoscopic ultrasound done three years previously showed sclerosing pancreatitis.
On physical examination, the patient weighed 99 pounds, her blood pressure was 160/60, the lungs were
clear, she had normal cardiac sounds, and she had a benign abdominal examination without palpable
masses. She did not have edema. Medications were alendronate, pravastatin, hydrochlorothiazide,
lisinopril, atenolol, ursodiol, insulin, iron, calcium carbonate (TUMS), a multivitamin, and Ensure.
Other laboratory values included serum albumin 3.2 g/dL, hemoglobin 11.4 g/dL, hematocrit 35.2%, white
blood cell count 6x109/L, and platelet count 234,000/L. She had a positive anti-nuclear
antibody with a titer of 1:80, and normal serum C3 and decreased serum C4 levels. She did not have
significant proteinuria or hematuria.
The two previous renal biopsies showed arteriosclerosis and scant areas of inflammation consisting of
mononuclear cells, plasma cells, and eosinophils; these specimens were considered nondiagnostic.
Slide 1
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Slide 2
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Figure 1
A CT scan reveals a renal mass that was biopsied.
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Figure 2
This low-magnification image shows widespread interstitial inflammation (H&E).
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Figure 3
A PAS stain shows a normal glomerulus and interstitial inflammation with destruction of the tubules.
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Figure 4
The infiltrate is composed of plasma cells, mononuclear cells, and many eosinophils (H&E).
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Figure 5
The interstitium is expanded and contains plasma cells and prominent fibroblasts (H&E).
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Figure 6
Tubular basement membranes are thickened and contain granular deposits (trichrome).
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Figure 7
Electron-dense deposits are present within tubular basement membranes (electron microscopy).
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Figure 8
Some tubules show massive deposits of electron-dense material. These deposits did not show substructure on higher magnification (electron microscopy).
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Figure 9
Deposits are also present in the interstitium (electron microscopy). No electron-dense deposits were identified within glomeruli.
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