A Case of Tubulointerstitial Nephritis with Uveitis

E. Houlihan, J. Holian

St. Vincent’s University Hospital


Dear Sir,

I would like to report a case of Tubulointerstitial Nephritis with Uveitis; a relatively uncommon multisystem disorder which requires a high index of suspicion for correct diagnosis and appropriate treatment.

A 50-year-old female presented to the Emergency Department with a six-week history of fatigue. She had no past medical history, although she was taking Naproxen for ten days for back pain. She complained of nausea, fatigue and “all-over-body pain”. On clinical examination, she was of increased BMI and abdominal striae were present. Investigations revealed deranged renal function – urea 12.1(4.5 in 2017), creatinine 318(76), eGFR 14ml/min, normal CK and an elevated CRP at 63. Urine dipstick revealed blood and protein. Renal ultrasound displayed normal kidney echotexture. Extended workup was non-contributory (thyroid function, haematinics, cortisol, vasculitis screen, anti-GBM <1.9; urine ACR, SPEP moderately elevated alpha and beta).

Initial management involved cessation of NSAID and intravenous fluids. During the first two days of her admission, she complained of blurred, painful vision. Her eyes became injected and erythematous. She was reviewed by ophthalmology who diagnosed bilateral anterior granulomatous uveitis. Topical dexamethasone and cyclopentolate was recommended.

Her renal function deteriorated despite rehydration; creatinine peaked at 427 giving an eGFR of 10ml/min (CrCl 20ml/min). The patient was transferred to the nephrology service who performed a renal biopsy showing atrophic tubules and diffuse moderate to severe mononuclear inflammation; findings suggestive of tubulointerstitial nephritis. She was diagnosed with tubulointerstitial nephritis with uveitis (TINU) and was commenced on high dose prednisolone 60mg. She improved biochemically and clinically over the following six weeks; the uveitis improving more rapidly than renal function. The steroid was tapered over two months (to 10mg of prednisolone), and the eGFR improved to 53ml/min (creatinine 101).

Acute interstitial nephritis is an inflammatory condition causing a decline in renal function. It is commonly caused by drugs, infection and autoimmune conditions. Five to ten percent of acute interstitial nephritis is caused by TINU syndrome1, first described by Dobrin in 1975. This autoimmune, multisystem disorder is relatively uncommon; about 200 cases have been reported. The underlying pathology is poorly understood; it is hypothesised that the inflammation is antibody and T-lymphocyte driven, and so is likely of immunological origin. No risk factors are identified in 50% of cases, however it is suggested that infectious triggers (e.g. EBV, TB), pharmacological triggers (NSAIDs) and genetic susceptibility (HLA) play a role2. The median age is 15 years, and there is a 3:1 female preponderance3. Nephritis precedes uveitis in 65% of cases, and 80% of uveitis affects only the anterior segment3. The differential diagnosis of interstitial nephritis with associated ocular involvement includes sarcoidosis, Sjogren’s syndrome, Wegener’s granulomatosis, Bechet’s syndrome1. Urinary beta2 microglobulin is a marker of interstitial nephritis and can remain elevated for months. Recommended treatment includes oral glucocorticoid for three to six months with a slow taper; the same treatment as acute interstitial nephritis with a longer course. Topical and systemic corticosteroids are used to treat uveitis. The prognosis is favourable; however, relapses are common, and steroid-sparing immunosuppression may be required i.e. cyclosporine, methotrexate. A Chinese study published in 2017 reported recurrent kidney injury observed in 51% of patients with TINU compare to 8% of patients with drug-induced acute interstitial nephritis4.  Scheduled follow-up for twenty-four months is recommended. A survey published in Elsevier in 2001 reviewed 133 patients with TINU and persistent renal dysfunction was reported in 11% of cases3.


Corresponding Author
Elaine Houlihan
St Vincent’s University Hospital.
Email: [email protected]


1. Glenner GG. Amyloid deposits and amyloidosis: the β-fibrilloses. N Engl J Med 1980;302:1283-92, 1333-43
2. Gillmore JD, Wechalekar A, Bird J, Cavenagh J, Hawkins S, Kazmi M, Lachmann HJ, Hawkins PN, Pratt G; BCSH Committee. Guidelines on the diagnosis and investigation of AL amyloidosis. Br J Haematol 2015;168:207-18.
3. Stoopler ET, Sollecito TP, Chen SY. Amyloid deposition in the oral cavity: a retrospective study and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003; 95: 674-80.
4. Mahmood S, Sachchithanantham S, Bridoux F, Lane T, Rannigan L, Foard D, Sayed R, Patel K, Fontanna M, Whelan C, Lachmann HJ, Gillmore JD, Hawkins PN, Wechalekar A. Risk of progression of localised amyloidosis to systemic disease in 606 patients over 30 years. Blood 2013;122: 3143.