Tubulointerstitial Uveitis

Tubulointerstitial Uveitis is known as tubulointerstitial nephritis and uveitis (TINU) syndrome—a disorder where the kidneys’ tubules/interstitium are inflamed (tubulointerstitial nephritis) and the eye’s uveal tract is inflamed (uveitis).

Tubulointerstitial nephritis and uveitis (TINU) syndrome is an immune-mediated illness that affects two organs:

• Kidneys: the tiny tubes (tubules) and the tissue between them (interstitium) become inflamed. This can reduce the kidney’s ability to filter blood, balance salts, and control water—sometimes causing acute kidney injury. People may feel tired, thirsty, need to urinate often, or have lab changes like high creatinine, but sometimes the kidney problem is silent. A kidney biopsy—if done—shows inflammatory cells around the tubules while the filtering units (glomeruli) are relatively spared. NCBIEyeWiki

• Eyes: the uveal tract (mainly the front chamber—anterior uveitis) becomes inflamed, causing redness, pain, light sensitivity, blurred vision, and floaters. The eye inflammation is usually non-granulomatous anterior uveitis, often in both eyes. MDPI

Tubulointerstitial uveitis most often refers to TINU syndrome—short for Tubulointerstitial Nephritis and Uveitis. It is an auto-immune inflammatory disease that affects two places at the same time:

1. The eyes (uveitis): The uvea is the middle, blood-rich layer of the eye (iris, ciliary body, and choroid). When it gets inflamed, you may notice eye pain, redness, light sensitivity, blurry vision, or floaters. Doctors call this inflammation uveitis. In TINU, uveitis is usually anterior (front of the eye, involving the iris), but it can sometimes be intermediate or posterior.

2. The kidneys (tubulointerstitial nephritis): The kidneys contain tiny filters and tubes. The tubules help fine-tune salt, acid–base balance, and water; the interstitium is the supporting tissue around those tubules. Tubulointerstitial nephritis means this tubule-interstitium unit is inflamed. People may feel fatigued, have fever, loss of appetite, weight loss, nausea, or flank discomfort. Lab tests can show abnormal kidney function, protein in urine, or white blood cells in urine.

The two parts (kidney and eye) do not always flare at the same time. Uveitis can appear months before or up to a year after the kidney inflammation. Because they can be out of sync, TINU is easy to miss unless clinicians think about both organs together and screen appropriately. Lippincott Journals

A very helpful lab clue is a high urinary β-2 microglobulin (Uβ2M). This protein leaks into urine when the tubules are inflamed. Uβ2M is often markedly elevated in TINU, can remain high even when creatinine is normal, and helps flag suspected cases in people with bilateral anterior uveitis. Still, definitive proof of tubulointerstitial nephritis comes from a renal biopsy (if it’s performed). PMC+1American Academy of OphthalmologyEyeWiki

Recent classification criteria combine anterior chamber inflammation with evidence of tubulointerstitial nephritis, shown either by a positive kidney biopsy or by abnormal kidney tests plus elevated urine β-2 microglobulin. PMCPubMedAjo

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Types

These “types” aren’t official subtypes with different names; they’re practical ways clinicians group real-world presentations:

1. By timing of eye vs kidney disease

   • Uveitis first (weeks–months before nephritis)

   • Simultaneous onset

   • Nephritis first (the most common pattern in case series) Lippincott Journals

2. By eye inflammation pattern

   • Acute bilateral non-granulomatous anterior uveitis (classic)

   • Recurrent or chronic anterior uveitis

   • Intermediate/posterior/panuveitis (less common but reported) MDPIAmerican Academy of Ophthalmology

3. By kidney severity

   • Mild, self-limited tubulointerstitial nephritis (improves with or without short steroids)

   • Moderate to severe acute kidney injury needing prolonged therapy and close monitoring

   • Relapsing or persistent tubulointerstitial nephritis (uncommon but described) ScienceDirect

4. By trigger/association

   • Idiopathic/autoimmune-predominant

   • Drug-associated (e.g., certain antibiotics, NSAIDs, others)

   • Infection-associated or systemic disease-associated (ruled out before labeling as TINU) EyeWikiNCBI

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Causes

TINU is immune-mediated. Often, no single cause is found, but several triggers/associations are reported. Below are 20 potential causes/associations or pathways; clinicians must exclude mimics before diagnosing TINU:

1. Autoimmune tubulointerstitial nephritis – the immune system mistakenly attacks kidney tubules; uveitis occurs as a related immune reaction. MDPI

2. Drug-induced immune reaction – after exposure to medications (e.g., some antibiotics like rifampin; NSAIDs; proton pump inhibitors; anticonvulsants), a hypersensitivity reaction inflames tubules and can also trigger uveitis. NCBIEyeWiki

3. Recent viral illness – viral antigens may provoke a cross-reactive immune response affecting kidney tubules and the uvea (association reported; specific virus varies). PubMed

4. Bacterial infections – post-infectious immune mechanisms (e.g., after streptococcal illness) can inflame the interstitium; uveitis linkage is rare but possible and must be excluded. NCBI

5. Autoimmunity in genetically predisposed hosts – HLA backgrounds may shape risk (reported in small series), priming an overactive response in kidney and eye. PubMed

6. Environmental exposures – less common but suspected triggers (e.g., heavy metals, herbal remedies) may cause interstitial nephritis, with uveitis as part of the immune cascade. NCBI

7. Sarcoid-like immune activation – granulomatous diseases can cause uveitis and interstitial nephritis; these must be ruled out to secure TINU diagnosis. NCBI

8. Autoimmune thyroid disease context – autoimmune clusters sometimes coexist; thyroid autoimmunity can accompany uveitis; not a cause of TINU per se but a red flag for autoimmunity. NCBI

9. Inflammatory bowel disease milieu – extra-intestinal eye inflammation is known in IBD; kidney interstitial inflammation can also occur; differential diagnosis overlaps with TINU. NCBI

10. Juvenile systemic autoimmune tendency – TINU is seen in adolescents/young adults, suggesting age-linked immune features. PubMed

11. Molecular mimicry after infections – an immune response targets a microbe and accidentally hits kidney/uveal antigens with similar structures. PubMed

12. Hypersensitivity to over-the-counter pain relievers (NSAIDs) – classic cause of interstitial nephritis; eye inflammation may co-occur. NCBI

13. Antibiotic-triggered reaction – several antibiotics can drive interstitial nephritis and, rarely, a full TINU picture. NCBI

14. Immune activation during steroid taper – in some cases, uveitis appears after nephritis when systemic steroids are tapered, hinting at unmasked ocular inflammation. BioMed Central

15. Allergic interstitial nephritis – eosinophil-rich kidney inflammation from an allergic drug reaction can coexist with uveitis. NCBI

16. Autoimmune anti-tubular basement membrane responses – rare antibody-mediated processes can target tubules; uveitis relationship is conceptual and part of differential. StatPearls

17. Systemic granulomatous diseases (e.g., sarcoidosis) misclassified – important mimics rather than true TINU; ruling them out is part of the “cause” hunt. NCBI

18. IgG4-related disease (differential) – can cause tubulointerstitial nephritis and eye disease; must be excluded before labeling as TINU. NCBI

19. Autoimmune rheumatic disease context – e.g., lupus, Sjögren’s, or vasculitis can involve kidney interstitium and eye; these are alternate causes that clinicians exclude. NCBI

20. Idiopathic (no trigger found) – in many patients, no clear cause is identified; the pattern still fits TINU after other conditions are excluded. PubMed

(Important note: By definition, TINU is a diagnosis of exclusion. Doctors first rule out infections (TB, syphilis), sarcoidosis, HLA-B27 disease, Behçet disease, and other uveitis-kidney links.) Archives of Rheumatology

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Symptoms

Kidney-related symptoms/signs

1. Tiredness and low energy from reduced kidney function or inflammation. NCBI

2. Nausea or poor appetite during acute kidney stress. NCBI

3. Increased thirst and frequent urination (tubules can’t concentrate urine well). Orpha

4. Flank or back discomfort (non-specific). NCBI

5. Swelling of ankles or around eyes (if kidney function is reduced). NCBI

6. Dark or foamy urine (from blood or protein in urine). EyeWiki

7. No symptoms at all—only abnormal labs (creatinine, β-2 microglobulin) reveal kidney involvement. PMC

Eye-related symptoms/signs

8. Eye redness (inflammation in the front of the eye). MDPI

9. Eye pain or ache (from anterior uveitis). MDPI

10. Photophobia (light hurts the eyes) due to inflamed iris and ciliary body. American Academy of Ophthalmology

11. Blurred vision from cells and protein in the anterior chamber, or related swelling. MDPI

12. Floaters (specks or threads in vision) when inflammatory cells drift in the vitreous. WebEye

13. Tearing and discomfort (irritation from inflammation). American Academy of Ophthalmology

14. Headache around the brow (from ciliary spasm). NCBI

15. Symptoms that come and go—uveitis can recur even after kidney tests improve. ScienceDirect

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Diagnostic tests

Below are 20 tests, grouped the way clinicians think about them. The goal is to prove there is uveitis and tubulointerstitial nephritis, while excluding other diseases that can look similar.

A) Physical examination

1. Vital signs and general exam
   The clinician checks heart rate, blood pressure, temperature, and looks for dehydration or swelling. High blood pressure can accompany kidney disease; fever might suggest infection (which would push doctors away from TINU and toward an infectious cause). A normal temperature and non-toxic appearance favor non-infectious inflammation. NCBI

2. Eye inspection at the slit lamp (anterior segment exam)
   A slit-lamp microscope lets the ophthalmologist see cells and protein (“flare”) in the front chamber, ciliary flush (a ring of redness around the cornea), and small deposits on the inner corneal surface (keratic precipitates). In TINU, the pattern is usually non-granulomatous anterior uveitis, often both eyes. MDPI

3. Fundus examination (back of the eye)
   Through dilated pupils, the doctor inspects the vitreous and retina. Although TINU is mainly an anterior uveitis, some people have intermediate or posterior involvement. Looking at the back of the eye helps detect macular edema (fluid in the central retina) or vitritis (inflammatory cells in the gel). American Academy of Ophthalmology

4. Focused kidney exam
   The clinician gently taps the flanks for tenderness and looks for ankle swelling. Findings are often subtle in TINU, so this exam mainly complements lab tests. NCBI

B) Manual/office eye tests

5. Visual acuity
   Reading the eye chart measures how much the inflammation is affecting sight. Changes help track response to therapy over time. NCBI

6. Intraocular pressure (IOP) measurement
   Inflammation or steroid treatment can change eye pressure. Measuring IOP warns clinicians about steroid-related pressure rise (steroid response) or pressure drops in acute inflammation. NCBI

7. Pupil tests and photophobia testing
   Bright light shining between the two eyes can trigger pain in an inflamed iris (consensual photophobia), a classic uveitis sign. NCBI

8. Color vision and Amsler grid (when appropriate)
   These quick checks help detect macular involvement or optic nerve issues if vision remains reduced despite a clear anterior chamber. NCBI

C) Laboratory and pathological tests

9. Serum creatinine and blood urea nitrogen (BUN)
   These are core kidney function tests. In TINU, creatinine may be elevated (indicating reduced filtration), but can normalize while urinary β-2 microglobulin remains high (ongoing tubular injury). EyeWikiPMC

10. Urinalysis with microscopy
    Doctors look for protein, blood, white cells, white cell casts, and glucose with normal blood sugar (tubular glucosuria). This pattern points to tubular injury rather than glomerular disease. EyeWiki

11. Urinary β-2 microglobulin (Uβ2M)
    This is a key screening test for TINU in patients with bilateral anterior uveitis or suspected tubulointerstitial nephritis. Uβ2M is usually very high and can stay high for months after creatinine improves. A useful positive test supports the diagnosis but does not replace biopsy. PMC+1JAMA Network

12. Electrolytes and acid–base tests
    Tubular dysfunction can cause low potassium, acidosis, or other salt imbalances. These abnormalities, if present, strengthen the case for tubular injury. NCBI

13. Inflammatory markers (ESR/CRP) and CBC
    These general markers may be elevated but are non-specific. CBC can show eosinophilia in drug-allergic interstitial nephritis. NCBI

14. Autoimmune and infectious exclusion panel
    Tests for ANA, ANCA, ACE (sarcoid), HLA-B27, syphilis serology, TB testing, and others are used to rule out mimics (e.g., sarcoidosis, syphilis, TB, HLA-B27 uveitis) before confirming TINU. NCBI

15. Renal biopsy (pathology)
    This is the definitive test for tubulointerstitial nephritis: it shows interstitial inflammatory infiltrates (often with eosinophils and mononuclear cells) and relative glomerular sparing. Biopsy is not always required but secures the diagnosis when the picture is unclear. EyeWiki

16. Urine protein quantification and β-2 microglobulin trend
    Following protein levels and Uβ2M over time shows whether tubular injury is improving or persisting. Persistent Uβ2M elevation can outlast creatinine changes and helps guide follow-up. PMC

D) Electrodiagnostic or functional eye tests

17. Optical coherence tomography (OCT) (functional/structural imaging with quantitative output)
    Although an imaging modality, OCT provides a functional readout of macular thickness and can detect cystoid macular edema, a vision-threatening complication even when anterior uveitis is controlled. NCBI

18. Visual field testing
    If inflammation or treatment affects the optic nerve or macula, automated perimetry can show blind-spot changes or peripheral vision defects, tracking eye function over time. NCBI

E) Imaging tests

19. Renal ultrasound
    A quick, non-invasive scan to look at kidney size and structure, exclude obstruction, and assess echogenicity. TINU usually shows normal-sized kidneys without obstruction, supporting an inflammatory (not obstructive) cause. NCBI

20. OCT of the macula
    High-resolution cross-sections of the retina detect macular edema or subtle structural changes from inflammation—important because macular edema worsens vision and needs prompt treatment. NCBI

21. Fluorescein angiography (when posterior segment is involved)
    Dye is injected into a vein, and photos of the retina show leakage from inflamed vessels or macular edema, guiding therapy intensity. NCBI

22. Fundus photography
    Standardized photos document vitritis, optic disc edema, or vascular sheathing and help monitor change over time. NCBI

23. Chest imaging (X-ray or CT if sarcoidosis suspected)
    If blood tests or symptoms raise concern for sarcoidosis (a key mimic), chest imaging may show hilar lymphadenopathy—which would push the diagnosis away from TINU. NCBI

24. MRI brain/orbits (only if atypical visual symptoms)
    Rarely needed; considered if there’s optic nerve involvement, severe posterior disease, or neurologic signs suggesting an alternate diagnosis. NCBI

Non-pharmacological treatments

Each item includes a description, purpose, and simple mechanism.

1. UV-blocking eyewear

   • Description: Wear quality sunglasses (UV-A/UV-B) and a brimmed hat outdoors.

   • Purpose: Reduce light sensitivity and glare; protect the inflamed iris and retina.

   • Mechanism: Filters high-energy light that worsens photophobia and may aggravate inflammation.

2. Rest the eyes during flares

   • Description: Short breaks from screens, bright rooms, and intense near work.

   • Purpose: Lessen strain, pain, and photophobia.

   • Mechanism: Reduces ciliary muscle spasm and sensory irritation.

3. Warm eyelid hygiene (if blepharitis coexists)

   • Description: Gentle warm compress and clean lids with diluted baby shampoo or lid wipes.

   • Purpose: Improve tear film, comfort, and reduce surface irritation that can worsen symptoms.

   • Mechanism: Unclogs meibomian glands and stabilizes the tear layer.

4. Cold compress for acute soreness

   • Description: Clean cold pack over closed lids for 5–10 minutes.

   • Purpose: Ease pain and a feeling of “hot, irritated eyes.”

   • Mechanism: Mild vasoconstriction and sensory dampening reduce discomfort.

5. Hydration and kidney-friendly habits

   • Description: Adequate fluids (unless your doctor limits them), limit salt, avoid dehydration.

   • Purpose: Support kidney recovery and stable blood pressure.

   • Mechanism: Proper volume and reduced sodium lower tubular stress.

6. Avoid nephrotoxic exposures

   • Description: Be cautious with unnecessary NSAIDs, certain antibiotics, contrast dyes, and herbal blends that can stress kidneys (only use if your doctor approves).

   • Purpose: Protect tubular cells during healing.

   • Mechanism: Reduces toxic or ischemic injury to tubules.

7. Adequate sleep routine

   • Description: 7–9 hours for adults; consistent schedule.

   • Purpose: Supports immune balance and healing.

   • Mechanism: Sleep regulates inflammatory cytokines and hormonal repair signals.

8. Gentle aerobic activity (once cleared)

   • Description: Walking, cycling, swimming at low–moderate intensity.

   • Purpose: Improve circulation, mood, and metabolic health.

   • Mechanism: Exercise reduces systemic inflammation and oxidative stress over time.

9. Stress-reduction practice

   • Description: Breathing exercises, mindfulness, guided imagery, or yoga (eye-safe).

   • Purpose: Lower flare triggers linked to stress.

   • Mechanism: Calms the hypothalamic–pituitary–adrenal axis and sympathetic tone, reducing pro-inflammatory signals.

10. Anti-inflammatory meal pattern (dietary style)

• Description: Emphasize vegetables, fruits, legumes, whole grains, nuts, seeds, olive oil, oily fish; reduce ultra-processed foods, excess sugar, and high sodium.

• Purpose: Complement medicines, support kidney and eye tissues.

• Mechanism: Antioxidants and omega-3s dampen inflammatory pathways.

11. Blue-light moderation for screens

• Description: Blue-light filter/app or glasses if screens trigger symptoms.

• Purpose: Reduce photophobia and eye fatigue.

• Mechanism: Lowers short-wavelength strain on sensitive eyes.

12. Adherence coaching and written plan

• Description: Keep a medication schedule, reminders, and a flare diary.

• Purpose: Prevent rebound inflammation from missed drops or pills.

• Mechanism: Consistent dosing maintains immunomodulation.

13. Infection prevention hygiene

• Description: Handwashing, avoiding eye rubbing, proper contact lens hygiene (or avoid lenses during flares).

• Purpose: Lower risk of secondary eye infection during steroid use.

• Mechanism: Limits pathogen exposure when local immunity is suppressed.

14. Smoking cessation and smoke avoidance

• Description: Stop tobacco and avoid secondhand smoke.

• Purpose: Improve outcomes and reduce relapse risk.

• Mechanism: Smoke increases oxidative stress and pro-inflammatory mediators.

15. Protective eyewear during dusty/irritant exposure

• Description: Wrap-around glasses at work or outdoors in dust or wind.

• Purpose: Reduce surface irritation that worsens symptoms.

• Mechanism: Physical barrier limits tear film disruption and reflex inflammation.

16. Blood pressure and glucose control (if applicable)

• Description: Regular home checks and follow clinician advice.

• Purpose: Protect kidney microcirculation and retinal health.

• Mechanism: Stable hemodynamics prevent microvascular damage.

17. Sunrise-to-noon outdoor timing

• Description: If you need sun exposure, prefer early morning when light is gentler.

• Purpose: Less photophobia and less UV load.

• Mechanism: Minimizes UV-related irritation.

18. Low-vision aids (if chronic changes exist)

• Description: Magnifiers, high-contrast settings, large fonts, task lighting.

• Purpose: Preserve function during recovery or in chronic cases.

• Mechanism: Enhances visual input when acuity/contrast are reduced.

19. Patient education and emergency plan

• Description: Learn red flags and whom to call urgently.

• Purpose: Faster treatment at first sign of a flare.

• Mechanism: Early intervention breaks inflammatory cascades before damage accrues.

20. Co-management (eye–kidney–primary team)

• Description: Ophthalmologist, nephrologist, and primary clinician share updates.

• Purpose: Align eye and kidney therapy and medication safety.

• Mechanism: Reduces drug conflicts, monitors labs, and times tapering safely.

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Drug treatments

Doses are typical adult starting ranges—your clinician may adjust for age, kidney function, severity, and other conditions.

1. Topical corticosteroid (ocular anti-inflammatory)

   • Class: Corticosteroid eye drop.

   • Examples & dosing: Prednisolone acetate 1%—1 drop 6–8×/day, then taper; Difluprednate 0.05%—1 drop 4×/day, then taper.

   • Purpose: Rapidly calm anterior uveitis.

   • Mechanism: Blocks phospholipase A2 and downstream prostaglandins/cytokines.

   • Side effects: ↑Intraocular pressure (steroid response), cataract with long use, infection risk.

2. Cycloplegic/mydriatic drops (pain relief & synechiae prevention)

   • Class: Anticholinergic.

   • Examples & dosing: Cyclopentolate 1%—1 drop 2–3×/day; Atropine 1%—1 drop 1–2×/day.

   • Purpose: Relieve ciliary spasm pain and prevent iris sticking to lens (posterior synechiae).

   • Mechanism: Temporarily paralyzes ciliary muscle and dilates pupil.

   • Side effects: Blurry near vision, light sensitivity, rare systemic anticholinergic effects.

3. Periocular steroid injection (for stubborn local inflammation)

   • Class: Corticosteroid (sub-Tenon’s or periocular).

   • Example: Triamcinolone acetonide 40 mg periocular as a single dose, repeat per specialist.

   • Purpose: Strong local control when drops are not enough.

   • Mechanism: Concentrated local immunosuppression.

   • Side effects: IOP rise, cataract progression, rare globe perforation (procedure-related).

4. Systemic corticosteroid (whole-body control & kidney protection)

   • Class: Oral corticosteroid.

   • Example & dosing: Prednisone 0.5–1 mg/kg/day (e.g., 30–60 mg daily), then slow taper over weeks as inflammation quiets.

   • Purpose: Treat both uveitis and tubulointerstitial nephritis when indicated.

   • Mechanism: Broad suppression of inflammatory gene transcription.

   • Side effects: Weight gain, mood shift, high blood sugar/pressure, infection risk, stomach upset, bone loss (with prolonged use).

5. Methotrexate (steroid-sparing immunomodulator)

   • Class: Antimetabolite DMARD.

   • Example & dosing: 7.5–25 mg once weekly PO/SC + folic acid 1 mg daily.

   • Purpose: Maintain control and reduce steroid dose in recurrent or chronic cases.

   • Mechanism: Inhibits dihydrofolate reductase; down-modulates T-cell activity and cytokines.

   • Side effects: Nausea, mouth sores, liver enzyme elevation, cytopenias (needs lab monitoring); avoid in pregnancy.

6. Mycophenolate mofetil (steroid-sparing)

   • Class: Antimetabolite.

   • Example & dosing: 500 mg–1 g twice daily.

   • Purpose: Alternative to methotrexate for long-term control.

   • Mechanism: Inhibits inosine monophosphate dehydrogenase → suppresses lymphocyte proliferation.

   • Side effects: GI upset, infections, leukopenia; teratogenic—reliable contraception required.

7. Azathioprine (steroid-sparing)

   • Class: Purine analog immunosuppressant.

   • Example & dosing: 1–2.5 mg/kg/day.

   • Purpose: Another option to reduce steroid reliance.

   • Mechanism: Inhibits purine synthesis → dampens T/B-cell proliferation.

   • Side effects: Bone marrow suppression, liver enzyme elevation; check TPMT activity if available.

8. Calcineurin inhibitors (for refractory cases)

   • Class: T-cell pathway inhibitors.

   • Examples & dosing: Cyclosporine 2–5 mg/kg/day in divided doses; Tacrolimus 0.05–0.1 mg/kg/day (oral).

   • Purpose: Control difficult uveitis while sparing steroids.

   • Mechanism: Blocks IL-2 transcription and T-cell activation.

   • Side effects: Kidney toxicity (monitor closely), hypertension, tremor, gum changes.

9. Biologics—anti-TNF (for refractory or systemic disease)

   • Class: Monoclonal antibodies against TNF-α.

   • Examples & dosing: Adalimumab 40 mg SC every 2 weeks; Infliximab 5–10 mg/kg IV at weeks 0, 2, 6, then every 4–8 weeks.

   • Purpose: Strong control for non-infectious uveitis not responding to other agents.

   • Mechanism: Neutralizes TNF-α, a key driver of ocular inflammation.

   • Side effects: Infection risk (screen TB/hepatitis), infusion reactions, rare demyelination.

10. Topical or oral NSAIDs (adjunct only, with kidney caution)

• Class: Non-steroidal anti-inflammatory drugs.

• Examples & dosing: Topical ketorolac 0.5% 1 drop 3–4×/day (adjunct for cystoid macular edema); Oral NSAIDs only if nephrologist approves.

• Purpose: Supplemental pain/inflammation control.

• Mechanism: COX inhibition → lower prostaglandins.

• Side effects: Kidney stress, stomach upset/ulcer, bleeding risk—often avoided in active nephritis unless the kidney specialist agrees.

Important: Drug choices are individualized. Infectious causes of uveitis must be ruled out before using immunosuppressive therapy.

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Dietary molecular supplements

Always discuss with your clinician—quality varies and some interact with medicines. Doses are typical study/in-practice ranges for adults.

1. Omega-3 (EPA/DHA)

   • Dosage: 1–2 g/day combined EPA+DHA.

   • Function: Anti-inflammatory support; may help tear film and ocular surface comfort.

   • Mechanism: Shifts eicosanoid balance toward less-inflammatory mediators, produces resolvins/protectins.

2. Vitamin D3

   • Dosage: Commonly 1000–2000 IU/day; personalize after a blood test.

   • Function: Immune regulation; low D is linked with several autoimmune disorders.

   • Mechanism: Modulates T-cell differentiation and cytokines.

3. Curcumin (with piperine for absorption)

   • Dosage: 500–1000 mg/day standardized curcumin; if combined with piperine, lower doses may suffice.

   • Function: Adjunct anti-inflammatory.

   • Mechanism: Inhibits NF-κB and other inflammatory pathways.

4. Lutein + Zeaxanthin

   • Dosage: 10 mg lutein + 2 mg zeaxanthin/day.

   • Function: Macular antioxidant support, visual function.

   • Mechanism: Blue-light filtering and oxidative stress reduction in the retina.

5. Green tea extract (EGCG)

   • Dosage: 200–400 mg EGCG/day (avoid high doses; take with food).

   • Function: Antioxidant/anti-inflammatory adjunct.

   • Mechanism: Limits oxidative signaling and inflammatory cascades.

6. Quercetin

   • Dosage: 250–500 mg/day.

   • Function: Flavonoid with anti-inflammatory and mast-cell-stabilizing effects.

   • Mechanism: Inhibits NF-κB and reduces histamine release.

7. Resveratrol

   • Dosage: 100–250 mg/day.

   • Function: Antioxidant support.

   • Mechanism: Activates sirtuin pathways; reduces oxidative inflammation.

8. N-Acetylcysteine (NAC)

   • Dosage: 600–1200 mg/day.

   • Function: Replenishes glutathione (master antioxidant).

   • Mechanism: Direct free-radical scavenging and glutathione precursor.

9. Probiotics (lactobacillus/bifidobacterium blends)

   • Dosage: As per product (often 10–20 billion CFU/day).

   • Function: Gut–immune axis support.

   • Mechanism: Modulates mucosal immunity and systemic inflammatory tone.

10. Zinc (with copper balance)

• Dosage: 15–30 mg elemental zinc/day with 1–2 mg copper if used longer term.

• Function: Immune enzyme cofactor; supports healing.

• Mechanism: Stabilizes cell membranes and immune signaling.

Safety notes: If you have kidney impairment, some supplements (e.g., high-dose vitamin A, high-dose vitamin C, certain minerals) may be inappropriate. Coordinate all supplements with your nephrologist and ophthalmologist.

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Advanced immunomodulatory or “regenerative” options

These are not first-line. Some are off-label for uveitis or investigational. Use only under experienced specialists after infections are excluded.

1. Tocilizumab (IL-6 inhibitor)

   • Dosage (common regimens): 8 mg/kg IV every 4 weeks or 162 mg SC weekly.

   • Function: Control refractory uveitis or macular edema in some cases.

   • Mechanism: Blocks IL-6 receptor, reducing inflammatory signaling.

   • Notes/risks: Infection risk, liver enzyme elevation, neutropenia; monitor labs.

2. Rituximab (anti-CD20)

   • Dosage: 1000 mg IV day 1 and day 15, then maintenance per response (specialist protocol).

   • Function: B-cell depletion for selected refractory autoimmune uveitis.

   • Mechanism: Targets CD20 on B cells → reduces autoantibody and antigen presentation.

   • Risks: Infusion reactions, infections, hypogammaglobulinemia.

3. Abatacept (T-cell co-stimulation blocker)

   • Dosage: Weight-based IV every 4 weeks or 125 mg SC weekly.

   • Function: Option in difficult non-infectious uveitis.

   • Mechanism: CTLA-4–Ig fusion protein prevents full T-cell activation.

   • Risks: Infection risk; monitor.

4. JAK inhibitors (e.g., Tofacitinib)

   • Dosage: 5 mg PO twice daily (or extended-release 11 mg once daily)—specialist discretion.

   • Function: Case-level evidence in refractory uveitis.

   • Mechanism: Inhibits JAK-STAT signals for multiple cytokines.

   • Risks: Infections, lipid changes, rare thrombosis—requires careful selection and monitoring.

5. Intravitreal corticosteroid implant (fluocinolone or dexamethasone)

   • Dosage: Implanted by a retinal surgeon (e.g., dexamethasone 0.7 mg implant every few months as needed; fluocinolone longer-acting).

   • Function: Long-term local control when topical/systemic therapy is inadequate or poorly tolerated.

   • Mechanism: Sustained local steroid delivery to the eye.

   • Risks: IOP rise, cataract; needs close follow-up.

6. Cell-based therapies (investigational)

   • Dosage: Not standardized; conducted only in clinical trials (e.g., mesenchymal stem cell infusions).

   • Function: Aim to re-tune the immune system or promote tissue repair.

   • Mechanism: Immunomodulation via paracrine anti-inflammatory signals.

   • Risks/notes: Experimental efficacy and safety; discuss only within formal research settings.

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Surgeries

1. Cataract surgery (phacoemulsification with IOL)

   • Procedure: Ultrasound breaks the cloudy lens; a clear artificial lens is placed.

   • Why: Long-standing inflammation and steroids can cause cataract, causing blurred vision, glare. Surgery is done when the eye is quiet and vision is significantly affected.

2. Glaucoma surgery (trabeculectomy or tube shunt)

   • Procedure: Create a new fluid outflow pathway (trabeculectomy) or place a drainage tube/plate to lower eye pressure.

   • Why: Steroids and inflammation may raise pressure, risking optic nerve damage.

3. Pars plana vitrectomy

   • Procedure: Microsurgery removes vitreous gel and inflammatory debris; may peel membranes and treat complications.

   • Why: Persistent vitreous haze, non-resolving floaters, traction, or to place drug implants.

4. Synechiolysis / pupillary membrane removal

   • Procedure: Mechanically break adhesions between iris and lens and remove membranes.

   • Why: Restore a round pupil, improve fluid flow, reduce risk of pressure rise and glare.

5. Intravitreal implant placement

   • Procedure: In-office or operating room placement of a sustained-release steroid implant.

   • Why: Long-term local control for recurrent macular edema or chronic uveitis.

Key surgical principle: Uveitic eyes do better when inflammation is quiet before surgery and kept controlled after.

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Prevention strategies

1. Follow-up on schedule with both ophthalmology and nephrology.

2. Take medicines exactly as prescribed; do not self-taper steroids.

3. Screen for infections (TB, hepatitis, etc.) as directed before strong immunosuppression.

4. Vaccinate appropriately (non-live during immunosuppression; coordinate with your clinicians).

5. Protect kidneys: avoid unnecessary nephrotoxic meds or dyes; stay hydrated if allowed.

6. Eye protection & UV filters to reduce light-driven irritation.

7. Quit smoking and avoid secondhand smoke.

8. Balanced anti-inflammatory eating pattern to support immune balance.

9. Manage comorbidities (BP, diabetes, autoimmune diseases) tightly.

10. Know red flags (sudden pain, vision drop, halos with headache, severe photophobia) and seek care promptly.

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When to see a doctor—urgent vs routine

• Seek urgent eye care now if you have:

  • Sudden severe eye pain, marked redness, light halos with headache, or rapid vision drop.

  • New flashing lights, curtain-like shadow, or dense floaters.

  • Painful eye with nausea/vomiting (possible pressure crisis).

• Call your kidney/primary team promptly if you notice:

  • Reduced urination, dark/foamy urine, swelling of legs/face, unusual fatigue, or rising blood pressure.

• Routine appointments: Keep all scheduled monitoring visits even if you feel well—uveitis and nephritis can smolder silently.

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What to eat and what to avoid

What to emphasize:

• Vegetables and fruits of many colors (antioxidants, fiber).

• Whole grains (oats, brown rice, whole-wheat).

• Legumes (lentils, chickpeas, beans).

• Nuts and seeds (handful/day if kidneys allow potassium/phosphorus).

• Olive oil as the main fat.

• Oily fish (salmon, sardines, mackerel) 2x/week for omega-3s.

• Adequate water unless your nephrologist limits fluids.

• Herbs/spices (turmeric/ginger/garlic) for flavor instead of excess salt.

What to limit or avoid:

• Ultra-processed foods high in salt, sugar, and additives.

• Excess sodium (aim for <2 g salt/day if your clinician agrees) to protect kidneys and blood pressure.

• Sugary drinks and refined snacks that fuel inflammation.

• Alcohol (especially if on methotrexate or with kidney strain).

• High-dose supplements not cleared by your clinicians—some can burden kidneys.

• Unregulated herbal blends with unknown nephrotoxic risks.

Personalized kidney diet needs may differ (e.g., potassium/phosphorus restrictions). Follow your nephrologist’s plan.

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Frequently asked questions

1. Is TINU the same thing as uveitis?
   No. TINU includes uveitis (eye inflammation) plus tubulointerstitial nephritis (kidney inflammation). Some people first show kidney signs; others first show uveitis.

2. Can TINU be cured?
   Many people achieve full remission with proper treatment and tapering. Some have relapsing uveitis requiring longer steroid-sparing therapy. Long-term outlook is usually good with close care.

3. How is TINU diagnosed?
   By eye exam (slit-lamp confirms uveitis) plus kidney evaluation (blood/urine tests, sometimes kidney biopsy). Doctors also exclude infections and other autoimmune diseases.

4. Why are steroids used so much?
   Corticosteroids are the fastest way to calm inflammation and protect vision and kidneys. Because of side effects, clinicians try to taper and may add steroid-sparing medicines.

5. Will eye drops alone be enough?
   For mild anterior uveitis, sometimes yes. If uveitis is severe, recurrent, or if kidney disease is active, you may need systemic therapy.

6. Are NSAIDs safe for pain?
   Not always in TINU—because kidneys are inflamed. Never start NSAIDs without nephrology approval. Safer alternatives may be chosen.

7. How long will treatment last?
   It varies—from a few months to a year or more. The aim is complete quiet of inflammation with the lowest medication exposure that keeps it quiet.

8. What are the main medication risks?
   Steroids: eye pressure, cataract, weight/mood/sugar changes.
   Immunomodulators/biologics: infections and lab abnormalities—hence regular monitoring.
   Calcineurin inhibitors: potential kidney toxicity—close labs are essential.

9. Can diet change the disease?
   Diet can support the immune system and kidneys but does not replace medical therapy. Think of food as complementary care.

10. Is vision loss permanent?
    Most vision changes improve when inflammation is controlled early. Delayed treatment or complications (like macular edema or glaucoma) can cause lasting changes, so early action matters.

11. Can I wear contact lenses?
    During active uveitis, avoid contact lenses. After the eye is quiet, your doctor may allow cautious use with strict hygiene.

12. What about pregnancy?
    Planning is crucial. Some drugs are unsafe in pregnancy (e.g., methotrexate, mycophenolate). Discuss family planning and safe alternatives with your care team before conception.

13. Will I need surgery?
    Only if complications occur (cataract, glaucoma, persistent vitreous haze). Surgeons prefer the eye quiet before operating.

14. Are vaccines allowed?
    Inactivated (non-live) vaccines are generally fine and encouraged; live vaccines are usually avoided during strong immunosuppression. Coordinate with your team.

15. How do I prevent flares?
    Keep appointments, take meds as prescribed, limit triggers (UV, smoke), protect kidneys, and seek care early at any sign of recurrence.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 29, 2025.