341.4 📋 章末速記 Summary

341.4.1 🔑 一句話總結

Tubulointerstitial diseases：(1) AIN (acute interstitial nephritis) — drug-induced most (PPI + NSAIDs + ICIs + penicillins + sulfonamides + ciprofloxacin + 5-ASA + allopurinol)、infectious、autoimmune (Sjögren, IgG4, sarcoidosis, TINU)；features = AKI + sterile pyuria + WBC casts + urine eosinophils (low sensitivity) ± hypersensitivity (rash + fever + eosinophilia in some)；treatment = hold offending drug + corticosteroids (prednisone 0.5-1 mg/kg) if severe/persistent；(2) chronic interstitial nephritis (CIN) — lithium, analgesics, calcineurin inhibitors, aristolochic acid (中草藥, Chinese herb nephropathy, Balkan endemic — urothelial cancer risk), reflux nephropathy, hereditary (ADPKD, NPHP, Alport), heavy metals (cadmium, lead, mercury), Mesoamerican nephropathy；(3) RTA (renal tubular acidosis): Type 1 distal (hypoK + non-AG acidosis + urine pH > 5.5 + Sjögren most common); Type 2 proximal (hypoK + variable urine pH + Fanconi syndrome often + MM + tenofovir + cystinosis); Type 4 hyperkalemic (hyperK + DKD + drugs — K-sparing/ACE/ARB/MRA/trimethoprim/calcineurin/NSAIDs/pentamidine — + hypoaldosterone); (4) Fanconi syndrome = proximal tubular dysfunction (glucosuria + aminoaciduria + phosphaturia + uricosuria + bicarbonaturia type 2 RTA); causes cystinosis (pediatric), MM, tenofovir, ifosfamide, heavy metals; (5) nephrogenic DI (polyuria + dilute urine + ADH resistance) — lithium most common acquired, hyperCa, hypoK, hereditary; treatment thiazide + amiloride; (6) ICI nephritis 2-5% — AIN typically, steroids + hold ICI; 2024 emerging recognition + treatment protocols。

341.4.2 💊 治療精要

• AIN：stop offending drug + corticosteroids if severe (prednisone 0.5-1 mg/kg × 4-6 wk → taper) + supportive (hydration, electrolytes) + avoid re-exposure
• ICI nephritis：hold ICI + prednisone 1 mg/kg × 4-6 wk → taper; can re-challenge after recovery in many
• CIN：remove offending agent + supportive CKD management + specific therapies (tolvaptan ADPKD, cysteamine cystinosis)
• RTA Type 1：potassium citrate or NaHCO3 + treat underlying (Sjögren management, autoimmune IS)
• RTA Type 2：high-dose bicarbonate + K + thiazide (paradoxical for some) + treat underlying (cystinosis, MM)
• RTA Type 4：address cause + fludrocortisone if true hypoaldosteronism + K restriction + loop diuretic (kaliuresis) + sodium bicarbonate + K binders (patiromer, SZC)
• Fanconi syndrome：replace losses (phosphate, bicarbonate, potassium, vit D)
• nephrogenic DI：thiazide diuretic (paradoxical effect) + amiloride (especially lithium-induced) + low Na diet + address cause (hold lithium, correct Ca/K)

341.4.3 🎯 盧醫師的考前提醒

1. AIN 經典 4 drug classes：PPIs (omeprazole, esomeprazole, pantoprazole — increasingly recognized) + NSAIDs + antibiotics (penicillins, sulfonamides, cipro) + ICIs (pembrolizumab, nivolumab — 2-5%) + 其他 (allopurinol, 5-ASA, anticonvulsants)
2. AIN 經典 features：AKI + sterile pyuria + WBC casts + urine eosinophils (low sensitivity ~ 25%) ± fever + rash + eosinophilia (classic hypersensitivity with penicillins, less with PPI/ICI)
3. AIN treatment：hold drug first + corticosteroids (prednisone 0.5-1 mg/kg × 4-6 wk) for severe/persistent; earlier initiation improves recovery
4. chronic interstitial nephritis causes：lithium、analgesics (NSAIDs)、calcineurin inhibitors、aristolochic acid (中草藥) — important in Taiwan + Balkan、reflux、heavy metals (Cd, Pb, Hg)、Mesoamerican (sugarcane workers heat stress)
5. aristolochic acid nephropathy：Chinese herb nephropathy + Balkan endemic；progressive interstitial fibrosis + urothelial carcinoma risk；某些 herbal remedies banned but exposure history important in Taiwan
6. RTA Type 1 distal：urine pH > 5.5 (cannot acidify) + hypoK + non-AG acidosis；Sjögren syndrome most common cause；treatment = potassium citrate or NaHCO3
7. RTA Type 2 proximal：variable urine pH + hypoK + Fanconi syndrome often + MM (multiple myeloma light chains) + tenofovir + acetazolamide + cystinosis；need high-dose bicarbonate
8. RTA Type 4 hyperkalemic：hyperK paradoxical + mild non-AG acidosis + DKD common + many drug culprits (K-sparing, ACE/ARB, MRA, trimethoprim, calcineurin inh, NSAIDs, pentamidine)
9. Fanconi syndrome：proximal tubular dysfunction with multiple defects — glucosuria (normal serum glucose) + aminoaciduria + phosphaturia (hypophosphatemia) + uricosuria + bicarbonaturia (type 2 RTA)；causes cystinosis, MM, tenofovir, ifosfamide, heavy metals
10. nephrogenic DI from lithium：most common acquired cause；polyuria + dilute urine + ADH resistance at collecting duct (aquaporin-2 dysfunction)；treatment thiazide + amiloride (paradoxical reducing UO) + low Na diet