Acute Interstitial Nephritis: Complete Etiology and Etiology-Directed Treatment
How to Read This Page — Evidence Provenance
Anchored to a named, citable source with a PMID, listed in Verified Sources. The claim came from the literature, not from habit.
Clinical experience and conventional nephrology teaching where the literature is thin or absent. Real and useful — but you should know which is which before you act on it.
The entire second-line drug literature in AIN rests on case series in the single digits. When a treatment recommendation below is tagged PRACTICE-BASED, that is not hedging — it is an accurate description of the state of the field.
1. Definition and Mechanism
EVIDENCE-BASED Acute interstitial nephritis is immune-mediated inflammation of the renal interstitium and tubules with the glomeruli spared, accounting for 5–15% of AKI among hospitalized patients and roughly 15–27% of biopsies performed for unexplained AKI1,3,4.
EVIDENCE-BASED The effector mechanism is T-cell mediated delayed-type hypersensitivity1,2. Drug or metabolite haptenizes native tubular protein, generating a neo-antigen; CD4+ helper T cells recognize the drug-laden tubular epithelium; a mixed infiltrate of T cells and eosinophils enters the interstitium; cytotoxic T cells attack tubular epithelium. Interstitial edema and infiltrate dominate, with minimal tubular necrosis — the key histologic separation from ATN.
Because the effector is a T cell, B-cell–directed therapy is mechanistically mismatched in ordinary drug-induced AIN. This is why rituximab — the most common second-line question — does not belong here, and why it does belong in the antibody-mediated variants. Hold this thought through Section 6.
EVIDENCE-BASED The reaction is not dose-dependent and recurs rapidly on re-exposure — both hallmarks of an allergic rather than toxic mechanism2,3.
2. Etiology I — Drugs
EVIDENCE-BASED Drug exposure accounts for roughly 70–75% of biopsy-proven AIN. Within that, pooled biopsy series place antibiotics at approximately 49%, PPIs at approximately 14%, and NSAIDs at approximately 11%, with omeprazole the most implicated single agent (approximately 12%) and amoxicillin second (approximately 8%)1,4.
Antibiotics 1–3 weeks · PPIs 3–6 months · checkpoint inhibitors 3–12 months · mesalamine months to years. The most commonly missed AIN in practice is a slow creatinine drift on a chronic PPI, written off as CKD progression.
2.1 Antibiotics EVIDENCE-BASED
| Class | Agents | Distinguishing features |
|---|---|---|
| Penicillins | Methicillin (historical), nafcillin, oxacillin, amoxicillin, ampicillin, piperacillin | Hapten mechanism. Methicillin/nafcillin historically produced the full triad at high frequency; modern agents rarely do2 |
| Cephalosporins | All generations | Cross-reactive with penicillins — avoid both classes after either |
| Sulfonamides | TMP-SMX, sulfadiazine | Frequent culprit; also a DRESS trigger. Governs the PJP prophylaxis choice in Section 7 |
| Fluoroquinolones | Ciprofloxacin (most reported), levofloxacin, moxifloxacin | Can follow a single dose; granulomatous variants described1,20 |
| Glycopeptides | Vancomycin | Overlapping AIN and ATN on the same biopsy; also a DRESS trigger |
| Rifamycins | Rifampin | Distinct mechanism — anti-rifampin antibodies, not classic haptenization. Flu-like syndrome, hemolysis, thrombocytopenia; often dialysis-requiring; typically after intermittent dosing or re-exposure19 |
| Others | Macrolides, tetracyclines (minocycline), linezolid, daptomycin | Minocycline also causes drug-induced lupus and DRESS |
2.2 Gastrointestinal agents EVIDENCE-BASED
Proton pump inhibitors — a class effect across omeprazole, esomeprazole, pantoprazole, lansoprazole, rabeprazole, and dexlansoprazole. Cross-reactivity is near-universal, so switching to a different PPI after PPI-AIN is not a solution; famotidine is the substitute when acid suppression is genuinely required. The presentation is insidious — sterile pyuria or a bland sediment with a creatinine that drifts rather than jumps. Population data link PPI exposure to incident CKD, and AIN is a principal proposed mechanism1,10.
5-aminosalicylates — mesalamine, sulfasalazine, balsalazide, olsalazine. A systematic review of 5-ASA–induced interstitial nephritis in IBD and a dedicated review of mesalamine and kidney disease both describe an insidious course over months to years that is frequently irreversible when recognized late, supporting baseline and periodic creatinine monitoring11,12.
2.3 NSAIDs EVIDENCE-BASED
All non-selective agents and COX-2 selective agents. Two features set this subtype apart1,13:
- It does not respond to glucocorticoids — the single most important treatment exception on this page.
- It may present with concurrent nephrotic-range proteinuria from minimal-change overlap, which is unusual for AIN generally.
PRACTICE-BASED Topical NSAIDs are systemically absorbed and are routinely discounted by patients and clinicians alike. Ask about gels and patches by name.
2.4 Immune checkpoint inhibitors EVIDENCE-BASED
PD-1 agents (pembrolizumab, nivolumab, cemiplimab), PD-L1 agents (atezolizumab, durvalumab, avelumab), and CTLA-4 agents (ipilimumab, tremelimumab). Multicenter clinicopathologic series established AIN as the dominant renal lesion, characterized the extended latency, and defined outcomes and rechallenge experience14,15,16.
Most patients on a checkpoint inhibitor are also on a PPI, and concurrent PPI exposure is a recognized confounder in attributing the lesion14,15. Before you stop a cancer drug the patient needs, account for the PPI they do not. Stopping the PPI is free. Stopping immunotherapy is not.
2.5 Allopurinol and urate-lowering therapy EVIDENCE-BASED
Allopurinol is among the most severe drug causes, typically presenting as full DRESS — fever, rash, eosinophilia, hepatitis, and AKI. Risk is concentrated in HLA-B*58:01 carriers (Han Chinese, Thai, Korean ancestry) and is further amplified by renal impairment, a combination directly examined in the dermatologic literature17. PRACTICE-BASED Concurrent thiazide use is conventionally cited as an additional risk multiplier; febuxostat is the usual alternative, though cross-reactivity is described.
2.6 Anticonvulsants and other agents PRACTICE-BASED
The aromatic anticonvulsants — phenytoin, carbamazepine, phenobarbital — cross-react with one another and usually present as anticonvulsant hypersensitivity syndrome rather than isolated AIN. Switch to a non-aromatic agent (levetiracetam, valproate, gabapentin). Also reported: thiazide and loop diuretics (both sulfonamide-based), hydralazine (which also causes drug-induced lupus and ANCA vasculitis — check ANCA and anti-histone), statins, and rarely ACE inhibitors and ARBs.
2.7 DRESS — the drugs that cause it EVIDENCE-BASED
Renal involvement in DRESS is AIN. The RegiSCAR prospective study characterized the syndrome, its validated scoring, its 2–8 week latency — longer than ordinary drug hypersensitivity — and its tendency to relapse during steroid taper18. High-risk agents cluster tightly:
Allopurinol · aromatic anticonvulsants · sulfonamides · vancomycin · minocycline · dapsone · abacavir · nevirapine
2.8 Aristolochic acid — not AIN, and it matters EVIDENCE-BASED
Aristolochic acid produces a relentlessly progressive fibrosing interstitial nephropathy with a high rate of upper-tract urothelial carcinoma. It is not steroid-responsive, and recognizing it changes surveillance rather than immunosuppression21. Ask about herbal and traditional preparations explicitly.
3. Etiology II — Infection, Autoimmune, Malignancy, Genetic
3.1 Infection PRACTICE-BASED
Roughly 5–10% of AIN. The therapeutic implication is inverted from drug-induced disease: treat the organism, and steroids are generally contraindicated.
- Bacterial: Streptococcus, Staphylococcus, Legionella, Brucella, Salmonella, Campylobacter, Yersinia, Mycoplasma, Leptospira, M. tuberculosis, syphilis, Coxiella burnetii
- Viral: EBV, CMV, HIV, hantavirus, BK polyomavirus (allograft), adenovirus, parvovirus B19, hepatitis B and C, SARS-CoV-2, dengue
- Fungal / parasitic: Histoplasma, Coccidioides, Leishmania, Toxoplasma, Schistosoma
EVIDENCE-BASED BK polyomavirus nephropathy is the exception that proves the rule: management is reduction of immunosuppression, not addition, and is governed by international consensus guidelines22.
3.2 Systemic and autoimmune disease
| Disease | Renal signature | Anchor |
|---|---|---|
| Sarcoidosis | Granulomatous interstitial nephritis; hypercalcemia and hypercalciuria | EVIDENCE-BASED20,23 |
| Sjögren disease | Interstitial nephritis with distal (type 1) RTA, hypokalemia, nephrocalcinosis | EVIDENCE-BASED24 |
| IgG4-related disease | IgG4-rich plasma cell infiltrate, storiform fibrosis, mass-like lesions | EVIDENCE-BASED27,28 |
| TINU syndrome | Interstitial nephritis with bilateral anterior uveitis; young women; elevated urinary beta-2 microglobulin | EVIDENCE-BASED25 |
| Anti-brush border antibody (ABBA) disease | Antibodies to LRP2/megalin on the proximal tubular brush border; elderly, often progressive | EVIDENCE-BASED26 |
| SLE | Lupus interstitial nephritis; can occur isolated, without glomerular disease | PRACTICE-BASED |
| Anti-TBM antibody disease | Linear TBM staining on immunofluorescence | PRACTICE-BASED |
| Inflammatory bowel disease | Interstitial nephritis as an extraintestinal manifestation | EVIDENCE-BASED11,12 |
A Crohn or ulcerative colitis patient on mesalamine with interstitial nephritis has two candidate causes pointing in opposite therapeutic directions: mesalamine toxicity, where you stop the drug — or an extraintestinal manifestation of active IBD, where you intensify treatment11,12. Disease activity, timing relative to drug initiation, and biopsy separate them. Guessing wrong worsens the patient either way.
3.3 Malignancy and genetic disease
PRACTICE-BASED Lymphoma and leukemia infiltrate the interstitium and mimic inflammatory AIN; monoclonality on flow or immunohistochemistry makes the distinction, and the treatment is directed at the malignancy. Myeloma and monoclonal gammopathy require free light chains — and remember that a suppressed uninvolved chain is the clonal signal.
EVIDENCE-BASED Karyomegalic interstitial nephritis arises from biallelic FAN1 mutations and shows strikingly enlarged, hyperchromatic tubular nuclei; it presents in early adulthood with progressive CKD and has no role for immunosuppression29. PRACTICE-BASED Autosomal dominant tubulointerstitial kidney disease (UMOD, MUC1, REN, HNF1B) belongs in the differential of unexplained interstitial disease with a bland sediment and a family history.
4. Diagnosis
EVIDENCE-BASED The classic triad of fever, rash, and eosinophilia appears in under 10% of drug-induced AIN and is absent in over two-thirds of PPI-associated cases1,4. Its absence excludes nothing.
4.1 What helps — the sediment EVIDENCE-BASED
- Sterile pyuria with WBC casts — the most useful bedside finding1,3
- Sub-nephrotic proteinuria, usually under 1 g/day; nephrotic range points toward NSAID-associated minimal change13
- Cast logic: RBC casts = GN · WBC casts = AIN · muddy brown casts = ATN
4.2 What does not help — urine eosinophils EVIDENCE-BASED
Muriithi et al. compared 566 patients who had both a urine eosinophil test and a native kidney biopsy within a week of each other; 91 had AIN. At a 1% Hansel-stain cutoff: sensitivity 30.8%, specificity 68.2%, PPV 15.6%, NPV 83.7%5.
The likelihood ratios settle it: LR+ 0.97 and LR− 1.01. Both sit at 1.0, so the result moves post-test probability essentially nowhere in either direction. A test that cannot revise your estimate is not a diagnostic test. Raising the cutoff to 5% drops sensitivity to 19.8% while specificity rises to 91.2% — still not clinically useful. The test was also no better at separating AIN from ATN than from any other kidney disease.
Why older sources disagree: the four largest earlier series reported sensitivity 40–91% and specificity 52–95%, but none used kidney biopsy as the gold standard5. Those figures are an artifact of unvalidated reference standards, and they persisted in teaching material long after the biopsy-anchored data existed.
4.3 Biomarkers EVIDENCE-BASED
Urinary CXCL9 is the leading non-invasive discriminator, identified and validated for AIN diagnosis by Moledina et al.9. It is mechanistically coherent — tubular epithelium secretes CXCL9 in response to IFN-gamma from the infiltrating T cells that define the lesion — and it is stable at room temperature, unlike beta-2 microglobulin, which degrades at acidic pH and saturates in heavy proteinuria. The biomarker field was reviewed in 202631. PRACTICE-BASED Availability outside research and reference laboratories remains limited, so this rarely changes the biopsy decision today.
4.4 Biopsy — and what to demand from the report
PRACTICE-BASED Three items drive management more than the creatinine does:
- Degree of interstitial fibrosis and tubular atrophy (IFTA)
- Presence or absence of an active inflammatory infiltrate
- Granulomas — raising sarcoidosis, tuberculosis, fungal infection, PPIs, and fluoroquinolones20
5. Treatment — Sorted by Etiology
5.1 Universal first steps EVIDENCE-BASED
- Withdraw the offending agent — sequentially if AKI is mild, simultaneously if severe1,3
- Avoid the class and cross-reactive classes
- Hunt the over-the-counter exposures — PPIs and NSAIDs go unreported because patients do not classify them as medications
Withdrawal is reversible. The fibrosis from a two-week delay is not.
5.2 The etiology-directed table
PRACTICE-BASED except where a row carries a citation. The IgG4 row is the only one supported by randomized data.
| Etiology | First line | Then | Do NOT |
|---|---|---|---|
| Drug-induced (general) | Withdraw; prednisone 1 mg/kg/day if severe or not recovering6 | Extend steroids to 8–12 weeks if active infiltrate → MMF 1–2 g/day7 | Escalate when IFTA is heavy and infiltrate absent |
| NSAID-induced | Withdrawal and supportive care only13 | — | Give steroids — this subtype does not respond |
| PPI-induced | Withdraw; famotidine if acid suppression needed10 | Steroids if not recovering → MMF | Switch to another PPI |
| Mesalamine / 5-ASA | Withdraw permanently; steroids if inflammation active11,12 | — | Rechallenge; confuse with IBD-associated nephritis |
| Allopurinol / DRESS | Withdraw; prednisone 1 mg/kg/day, longer course, slow taper17,18 | MMF or cyclosporine if steroid-dependent | Rechallenge; use a 2-week taper — DRESS relapses |
| Checkpoint inhibitor | Hold the ICI; prednisone 0.5–1 mg/kg/day14,15,16 | MMF → infliximab or cyclophosphamide (case-level) | Stop the ICI before excluding a concurrent PPI |
| Infection-associated | Treat the organism | Supportive care | Give steroids — generally contraindicated |
| BK nephropathy (allograft) | Reduce immunosuppression22 | IVIG, leflunomide, cidofovir — all weak evidence | Add steroids for “rejection” without excluding BK |
| Sarcoidosis | Prednisone 0.5–1 mg/kg/day, slow taper over 6–12 months23 | Methotrexate, azathioprine, or MMF → infliximab | Reach for rituximab; overlook the hypercalcemia |
| Sjögren | Prednisone24 | MMF or azathioprine; hydroxychloroquine adjunct | Neglect the distal RTA — bicarbonate and potassium repletion are treatment |
| IgG4-related disease | Prednisone — but most flare on taper27 | Rituximab or inebilizumab; obexelimab28,30 | Expect steroids alone to hold remission; delay until fibrotic |
| TINU | Systemic steroids plus topical steroids for the uveitis25 | MMF or azathioprine for relapsing uveitis | Manage without ophthalmology — the courses run independently |
| Anti-TBM / ABBA disease | Prednisone | Rituximab — mechanistically rational, antibody-mediated26 | — |
| Lymphoma / myeloma | Treat the malignancy | — | Immunosuppress for “AIN” |
| Karyomegalic / genetic | Supportive; CKD management29 | Transplant | Immunosuppress — no role |
| Aristolochic acid | Cease exposure; urothelial cancer surveillance21 | — | Expect steroids to work |
5.3 Glucocorticoids — the evidence genuinely conflicts EVIDENCE-BASED
| Study | Design | Finding |
|---|---|---|
| González 20086 | Retrospective multicenter, n=61 (52 treated, 9 untreated) | Dialysis 4% vs 44%; creatinine 2.1 vs 3.7 mg/dL at 18 months; steroids within 7 days OR 6.6 (95% CI 1.3–33.6) |
| Muriithi 20144 | Retrospective, n=95 (83 prednisone, 12 not) | No difference in recovery at 6 months |
| Fernández-Juárez 20188 | Retrospective, treatment-duration analysis | Examined corticosteroid duration against recovery |
The nominal arithmetic gives ARR 40% and NNT 2.5. Do not quote that NNT. The control arm is nine patients, allocation was not randomized, and confounding by indication runs both directions — sicker patients get treated, and patients already improving do not. A confidence interval spanning 1.3 to 33.6 is the study telling you how little it knows. Hypothesis-generating, not an effect estimate. The negative studies are thought to reflect more severe disease and inclusion of steroid-unresponsive NSAID cases1,13.
6. The Non-Responder, and Where Rituximab Belongs
If the patient has not recovered 3–4 weeks after withdrawal plus steroids, work it in this order. PRACTICE-BASED
- Question the diagnosis. Consider alternative AKI etiologies, particularly if no biopsy was done. Biopsy now if feasible.
- If biopsy-confirmed, read the chronicity. This is the decision point.
- If there is an active infiltrate — extend the steroid course to a total of 8–12 weeks. Do not add a second agent yet.
Severe chronic changes (heavy IFTA) with no acute inflammatory infiltrate: the patient will not improve. Taper and stop the glucocorticoids. Adding immunosuppression here purchases infection risk, not GFR.
6.1 Mycophenolate EVIDENCE-BASED
Dose: 1 g/day orally in divided doses, titrated to 2 g/day if tolerated. The evidence is Preddie et al.7 — n=8, treated 13–34 months. Those patients had responded to steroids but could not tolerate withdrawal after six months: steroid-dependent, not steroid-resistant. All were able to discontinue glucocorticoids; two failed to improve creatinine.
The limitation that governs how far you can generalize: only two of the eight had drug-induced AIN. Applying this series to classic drug AIN is a genuine extrapolation, not an established indication.
6.2 Rituximab — where it belongs and where it does not
Not for ordinary drug-induced AIN — that lesion is T-cell mediated, so B-cell depletion targets the wrong compartment, and the major drug-induced AIN reviews do not list it1,2,3.
Rational when the driver is antibody- or B-cell-mediated: IgG4-related disease, where it has the strongest support28; anti-TBM disease; and ABBA disease26.
Not standard for sarcoid, where the pathway runs methotrexate, azathioprine, or MMF, then anti-TNF23.
6.3 IgG4-related disease — the one randomized exception EVIDENCE-BASED
Most patients respond to glucocorticoids but flare during or after taper, so additional therapy is usually required. Rituximab's historical basis is an open-label, single-arm trial of 30 patients — no control group28. That changed with obexelimab, a bifunctional anti-CD19/FcγRIIb antibody that inhibits rather than depletes B cells, reported in NEJM 202630: among 194 patients undergoing protocolized glucocorticoid withdrawal by week 8, disease flare over 52 weeks was 26.8% versus 54.6% with placebo.
| Obexelimab, 52-week flare | Value |
|---|---|
| Control event rate | 54.6% |
| Treatment event rate | 26.8% |
| RRR | approximately 51% |
| ARR | 27.8% |
| NNT | 4 over 52 weeks |
Randomized, double-blind, placebo-controlled — a genuine methodological step up from the single-arm rituximab data. Two caveats to carry: the endpoint is disease flare, an intermediate outcome rather than organ survival or mortality; and the trial enrolled patients undergoing protocolized steroid withdrawal, which elevates the control-arm event rate and therefore inflates the absolute difference relative to ordinary practice.
7. Supportive Care and the Prophylaxis Trap
PRACTICE-BASED PJP prophylaxis applies at prednisone 20 mg/day or above for four or more weeks, particularly alongside MMF.
- Sulfonamides are a classic AIN trigger. If sulfa is anywhere on the suspect list, do not use it.
- Trimethoprim inhibits tubular creatinine secretion, raising creatinine 0.1–0.3 mg/dL with no change in true GFR — contaminating the exact measurement you are using to judge treatment response.
Atovaquone 1500 mg daily avoids both. Dapsone requires G6PD testing and is itself a DRESS trigger18.
PRACTICE-BASED Before rituximab: HBsAg and anti-HBc (reactivation risk) and a baseline quantitative IgG. Also address bone protection for prolonged steroid courses, gastric protection without a PPI if the AIN was PPI-induced, and vaccination status before immunosuppression.
8. Prognosis
PRACTICE-BASED Complete recovery in roughly 50–75% with prompt withdrawal; partial recovery 20–30%; progression to ESKD 5–10%, higher with delayed recognition.
EVIDENCE-BASED Predictors of poor recovery are consistent across series1,3,4:
- Kidney failure lasting more than three weeks before treatment
- NSAID as the causative agent
- Interstitial granulomas, fibrosis, and tubular atrophy on biopsy
- Mesalamine as the agent — frequently irreversible11,12
Time-to-withdrawal is the dominant modifiable variable. Steroids may accelerate recovery when started early; nothing rescues a kidney that has already fibrosed. When deciding whether to escalate immunosuppression, the biopsy chronicity — not the creatinine — casts the deciding vote.
Verified Sources
Every PMID below was verified individually against the PubMed E-utilities API on 2026-07-30 — title, journal, and year confirmed against the cited identifier. Reference 5 was additionally verified full-text against the source PDF. Claims tagged PRACTICE-BASED are deliberately not anchored here; they represent conventional teaching and clinical experience, and are labeled so readers can weigh them accordingly.
- Moledina DG, Perazella MA. Drug-induced acute interstitial nephritis. Clin J Am Soc Nephrol. 2017. PMID: 28893923
- Perazella MA, Markowitz GS. Drug-induced acute interstitial nephritis. Nat Rev Nephrol. 2010. PMID: 20517290
- Praga M, González E. Acute interstitial nephritis. Kidney Int. 2010. PMID: 20336051
- Muriithi AK, Leung N, Valeri AM, et al. Biopsy-proven acute interstitial nephritis, 1993-2011: a case series. Am J Kidney Dis. 2014;64(4):558-566. PMID: 24927897
- Muriithi AK, Nasr SH, Leung N. Utility of urine eosinophils in the diagnosis of acute interstitial nephritis. Clin J Am Soc Nephrol. 2013;8(11):1857-1862. PMID: 24052222 — verified full-text; source of the LR 0.97 / 1.01 figures.
- González E, Gutiérrez E, Galeano C, et al. Early steroid treatment improves the recovery of renal function in patients with drug-induced acute interstitial nephritis. Kidney Int. 2008;73(8):940-946. PMID: 18185501
- Preddie DC, Markowitz GS, Radhakrishnan J, et al. Mycophenolate mofetil for the treatment of interstitial nephritis. Clin J Am Soc Nephrol. 2006;1(4):718-722. PMID: 17699278
- Fernández-Juárez G, Pérez JV, Caravaca-Fontán F, et al. Duration of treatment with corticosteroids and recovery of kidney function in acute interstitial nephritis. Clin J Am Soc Nephrol. 2018;13(12):1851-1858. PMID: 30397027
- Moledina DG, Obeid W, Smith RN, et al. Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis. J Clin Invest. 2023. PMID: 37395276
- Lazarus B, Chen Y, Wilson FP, et al. Proton pump inhibitor use and the risk of chronic kidney disease. JAMA Intern Med. 2016;176(2):238-246. PMID: 26752337
- Moss JG, et al. 5-ASA induced interstitial nephritis in patients with inflammatory bowel disease: a systematic review. Eur J Med Res. 2022. PMID: 35488310
- Adiga A, Nugent K. The association of mesalamine with kidney disease. Adv Chronic Kidney Dis. 2020. PMID: 32147005
- Klomjit N, Manohar S. Acute kidney injury associated with non-steroidal anti-inflammatory drugs. Eur J Intern Med. 2022. PMID: 35534373
- Cortazar FB, Kibbelaar ZA, Glezerman IG, et al. Clinical features and outcomes of immune checkpoint inhibitor-associated AKI: a multicenter study. J Am Soc Nephrol. 2020;31(2):435-446. PMID: 31896554
- Cortazar FB, Marrone KA, Troxell ML, et al. Clinicopathological features of acute kidney injury associated with immune checkpoint inhibitors. Kidney Int. 2016;90(3):638-647. PMID: 27282937
- Barbir EB, et al. Immune checkpoint inhibitor-associated nephritis — treatment standard. Nephrol Dial Transplant. 2024. PMID: 39138117
- Ng CY, Yeh YT, Wang CW, et al. Impact of the HLA-B*58:01 allele and renal impairment on allopurinol-induced cutaneous adverse reactions. J Invest Dermatol. 2016;136(7):1373-1381. PMID: 26996548
- Kardaun SH, Sekula P, Valeyrie-Allanore L, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): an original multisystem adverse drug reaction. Results from the prospective RegiSCAR study. Br J Dermatol. 2013;169(5):1071-1080. PMID: 23855313
- De Vriese AS, Robbrecht DL, Vanholder RC, et al. Rifampicin-associated acute renal failure: pathophysiologic, immunologic, and clinical features. Am J Kidney Dis. 1998;31(1):108-115. PMID: 9428460
- Joss N, Morris S, Young B, Geddes C. Granulomatous interstitial nephritis. Clin J Am Soc Nephrol. 2007;2(2):222-230. PMID: 17699417
- Luciano RL, Perazella MA. Aristolochic acid nephropathy: epidemiology, clinical presentation, and treatment. Drug Saf. 2015;38(1):55-64. PMID: 25446374
- Kotton CN, Kamar N, Wojciechowski D, et al. The second international consensus guidelines on the management of BK polyomavirus in kidney transplantation. Transplantation. 2024. PMID: 38605438
- Calatroni M, Moroni G, Conte E, et al. Renal sarcoidosis. J Nephrol. 2023. PMID: 35761015
- Chatterjee R, et al. Renal involvement in Sjögren's syndrome: predictors and impact on patient outcomes. Rheumatol Int. 2023. PMID: 36650312
- Amaro D, Carreño E, Steeples LR, et al. Tubulointerstitial nephritis and uveitis (TINU) syndrome: a review. Br J Ophthalmol. 2020;104(6):742-747. PMID: 31719109
- Dvanajscak Z, Cossey LN, Larsen CP, et al. Anti-brush border antibody disease (anti-LRP2 nephropathy) associated with lupus nephritis. Kidney Int Rep. 2020. PMID: 32954086
- Sahutoglu T, et al. Update on acute tubulointerstitial nephritis: clinical features, immunologic insights, and diagnostic and treatment approaches. Kidney Int Rep. 2025. PMID: 40630288
- Carruthers MN, Topazian MD, Khosroshahi A, et al. Rituximab for IgG4-related disease: a prospective, open-label trial. Ann Rheum Dis. 2015;74(6):1171-1177. PMID: 25667206
- Isnard P, Rabant M, Labaye J, et al. Karyomegalic interstitial nephritis: a case report and review of the literature. Medicine (Baltimore). 2016;95(11):e3181. PMID: 27196444
- Della-Torre E, et al. Obexelimab for the treatment of IgG4-related disease. N Engl J Med. 2026. PMID: 42233621
- Sadarangani S, et al. Diagnosing acute tubulointerstitial nephritis: novel biomarkers address an important clinical challenge. Curr Opin Nephrol Hypertens. 2026. PMID: 41460039
Last updated: 2026-07-30 For questions or updates, contact: acbland@gmail.com