Tubular and Interstitial Diseases

Tubular and Interstitial Diseases

Tubular and Interstitial Diseases

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Acute Tubular Injury - Tube Shock Central

  • Most common cause of Acute Kidney Injury (AKI); reversible damage to tubular epithelial cells.
  • Etiology:
    • Ischemic (80%): Hypotension (shock), hypovolemia, sepsis. 📌 "Tube Shock Central".
    • Nephrotoxic (20%): Aminoglycosides, contrast, heavy metals (Pb, Hg), myoglobin, ethylene glycol.
  • Pathogenesis:
    • Ischemia → ↓ATP → cell injury/necrosis → tubular obstruction (casts) & backleak.
    • Nephrotoxins → direct tubular cell damage.
  • Phases:
    • Initiation (hours-days): Insult; ↓urine output, ↑BUN, ↑Cr.
    • Maintenance (1-3 weeks): Sustained ↓GFR. Oliguria (<400 mL/day), uremia, hyperkalemia, metabolic acidosis.
    • Recovery: Tubular regeneration; polyuria (risk of hypokalemia); GFR gradually normalizes.
  • Morphology:
    • Proximal convoluted tubules (PCT) & thick ascending limb (TAL) most vulnerable.
    • Loss of brush border, epithelial cell sloughing, tubular dilatation.
    • Interstitial edema. Acute Tubular Necrosis Summary

⭐ Muddy brown granular casts in urine sediment are pathognomonic for ATN.

Acute Interstitial Nephritis - Allergic Kidney Attack

  • Inflammatory infiltrate & edema in renal interstitium; tubules affected (tubulitis).
  • Etiology:
    • Drugs (Most common, >70%): Penicillins, NSAIDs, PPIs, Sulfonamides, Rifampicin. (📌 Think "P-DRUGS": PPIs, Penicillins, Painkillers (NSAIDs), Diuretics, Rifampicin, SUlfonamides)
    • Infections: Bacterial, Viral (CMV, EBV).
    • Systemic: Sarcoidosis, SLE, TINU syndrome.
  • Classic Triad (often incomplete, <10-30%): Fever, Rash, Eosinophilia.
    • Other: Arthralgia, AKI features (oliguria, ↑Cr).
  • Urinalysis: Eosinophiluria (Hansel/Wright stain), WBCs, WBC casts, sterile pyuria, mild proteinuria.
  • Biopsy: Interstitial edema & cellular infiltrate (lymphocytes, eosinophils); tubulitis. Acute interstitial nephritis with eosinophilic infiltrate
  • Management: Withdraw offending agent; Corticosteroids if severe/persistent.

⭐ NSAID-induced AIN can present with heavy proteinuria and features of minimal change disease, unlike typical drug-induced AIN where proteinuria is usually mild to moderate and glomerular changes are absent or minimal beyond foot process effacement in some cases of NSAID AIN.

Chronic Tubulointerstitial Nephritis & Pyelonephritis - Kidney's Long Haul

  • Chronic Tubulointerstitial Nephritis (CTIN): Persistent inflammation & fibrosis of renal tubules/interstitium, leading to chronic kidney disease.
    • Causes: Drugs (analgesics - phenacetin, NSAIDs; lithium), toxins (lead), metabolic (hypercalcemia, hypokalemia), immune (Sjogren's), infections, obstruction.
    • Patho: Interstitial fibrosis, tubular atrophy, mononuclear infiltrates. Often non-specific.
    • Features: Gradual ↓GFR, polyuria, nocturia (impaired concentrating ability), HTN, anemia. Sterile pyuria common.
    • Analgesic Nephropathy: Classic cause; papillary necrosis, cortical scarring. Risk: >1g/day phenacetin for >3yrs.
  • Chronic Pyelonephritis (CPN): Tubulointerstitial scarring from recurrent/persistent bacterial infection.
    • Key Associations: Vesicoureteral reflux (VUR) in children, chronic obstruction in adults.
    • Patho: Coarse, asymmetric renal scars, typically polar; blunted/deformed calyces.
    • Micro: "Thyroidization" of tubules (colloid-like casts).
    • Features: Insidious onset; may present with HTN, recurrent UTIs, flank pain, or progressive renal insufficiency.

    ⭐ Thyroidization of tubules (dilated tubules with eosinophilic casts resembling thyroid follicles) is a characteristic histological feature of chronic pyelonephritis.

Chronic Pyelonephritis: Diagram and Gross Pathology

High‑Yield Points - ⚡ Biggest Takeaways

  • Acute Tubular Necrosis (ATN): Most common AKI cause; muddy brown casts are key.
  • Acute Interstitial Nephritis (AIN): Often drug-induced (e.g., NSAIDs, penicillins); classic triad: fever, rash, eosinophilia.
  • Pyelonephritis: WBC casts indicate renal infection; E. coli is the most common pathogen.
  • Analgesic nephropathy: Chronic use leads to papillary necrosis and chronic interstitial nephritis.
  • Myeloma Kidney: Light chain casts (Bence Jones proteins) are directly toxic to renal tubules.
  • Chronic pyelonephritis: Shows cortical scars and thyroidization of tubules; often due to reflux nephropathy or obstruction.
  • Renal Tubular Acidosis (RTA): Suspect with normal anion gap metabolic acidosis; Type 1 (distal) has impaired H+ secretion, Type 2 (proximal) has impaired HCO3- reabsorption, Type 4 involves aldosterone deficiency/resistance causing hyperkalemia.

Practice Questions: Tubular and Interstitial Diseases

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Polyuria with low fixed specific gravity urine is seen in ?

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Flashcards: Tubular and Interstitial Diseases

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Hemolytic uremic syndrome, Graft rejection, Acute cortical necrosis, Chronic glomerulonephritis and Alport syndrome, all lead to _____ nephrocalcinosis

TAP TO REVEAL ANSWER

Hemolytic uremic syndrome, Graft rejection, Acute cortical necrosis, Chronic glomerulonephritis and Alport syndrome, all lead to _____ nephrocalcinosis

cortical

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