341.3 🏥 內科專科考前版

341.3.1 Mechanistic Deep Dive

341.3.1.1 AIN Pathophysiology

  • T-cell mediated hypersensitivity (Type IV)
  • Drug-T-cell interaction → activation
  • Cytokine release
  • Interstitial inflammation
  • Tubular damage (tubulitis)

341.3.1.2 PPI-Induced AIN

  • Mechanism: drug-T-cell interaction
  • Hypersensitivity may not be apparent
  • Often subtle Cr rise
  • Increasing recognition; long-term PPI exposure

341.3.1.3 Lithium Nephrotoxicity

  • Cellular damage to collecting duct cells
  • Inhibits aquaporin-2 insertion
  • Impaired urine concentration
  • Chronic interstitial nephritis

341.3.1.4 Aristolochic Acid Mechanism

  • DNA adduct formation
  • Tubular cell apoptosis
  • Progressive interstitial fibrosis
  • AA-DNA adducts in renal tissue
  • Promotes urothelial carcinoma

341.3.2 Recent Trials & Updates

341.3.2.1 ICI Nephritis Increasing

  • 2-5% of ICI patients
  • More with combination ICI
  • Earlier ICI use → earlier nephritis
  • Outcomes generally good with treatment

341.3.2.3 Sjögren Renal Treatment

  • HCQ
  • Steroids for active
  • Rituximab + MMF for refractory

341.3.2.4 Lithium Alternative

  • For NDI from lithium
  • Amiloride mechanism
  • May allow continued lithium

341.3.3 High-Yield Specialist Points

341.3.3.1 ICI-Associated AIN

  • Typically 2-3 months after ICI start
  • May have multi-organ irAEs
  • Treatment: hold ICI + prednisone 1 mg/kg
  • Re-challenge possible after recovery (Cr improvement)
  • Steroid taper over 4-6 weeks

341.3.3.2 Drug-Induced Crystals

  • Acyclovir crystals
  • Methotrexate crystals
  • Sulfa crystals
  • Indinavir crystals
  • Reversible with hydration + dose adjustment

341.3.3.3 Vancomycin AKI

  • Trough > 20 increases risk
  • Concurrent nephrotoxins worsen
  • AUC-based dosing newer recommended

341.3.3.4 Aminoglycoside Toxicity

  • Cumulative dose + duration
  • Once-daily extended-interval dosing reduces
  • Monitor: peak + trough
  • Renal recovery often

341.3.3.5 Pigment Nephropathy

  • Rhabdomyolysis (myoglobin)
  • Hemolysis (Hb)
  • ATN + tubular obstruction
  • Aggressive fluids

341.3.3.6 Crystal Nephropathy Workflow

  • Identify crystal type
  • Hydration
  • Specific treatment (e.g., rasburicase for TLS)

341.3.3.7 Mesoamerican Nephropathy

  • Sugarcane / agricultural workers
  • Heat stress + dehydration + occupational toxins
  • Central American epidemic
  • Multifactorial

341.3.3.8 Chronic Lithium Management

  • Monitor renal function annually
  • Switch if Cr rises
  • Amiloride for NDI
  • Lower lithium levels may help

341.3.3.9 Sjögren Renal Workup

  • Anti-SSA / Ro, anti-SSB / La
  • Schirmer test
  • Lip biopsy
  • Manage symptomatic
  • IS for severe

341.3.3.10 Cystinosis (Hereditary)

  • Pediatric
  • Cystine accumulation in lysosomes
  • Multisystem (kidney, eye, thyroid, gonads)
  • Treatment: cysteamine + supportive
  • Eventual transplant

341.3.3.11 Heavy Metal Workup

  • Lead, cadmium, mercury, arsenic
  • Occupational history
  • Whole blood + urine levels
  • Specific chelation if severe

341.3.4 Pearls

  • AIN: drug-induced most common; PPI, NSAID, ICI, penicillins
  • CIN: chronic; lithium, analgesics, aristolochic acid, reflux, hereditary
  • RTA Type 1: distal, Sjögren most common
  • RTA Type 2: proximal, Fanconi often, MM
  • RTA Type 4: hyperK, DKD, drug-induced
  • Fanconi syndrome: proximal tubular dysfunction (cystinosis, MM, tenofovir)
  • Nephrogenic DI: lithium, hyperCa, hypoK
  • ICI nephritis: 2-5%, AIN typically, steroid responsive
  • Aristolochic acid: 䞭草藥 history (Taiwan); urothelial cancer risk