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Block 2 PATH Exam -- Tubulointerstitial Disease Lecture


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Acute Interstitial (Hypersensitivity) Nephritis
ARF with interstitial inflammatory cells
Causes: idiopathic (no Ephils), drugs, infections, etc.
Drug causes include: NSAIDs, Methicillin, Anti-biotics, Diuretics
Mechanism is ALLERGIC
Acute deterioration of renal function (improves on cessation of drug use)
Treatment is supportive
Stop drug --> usually fully reversible
Chronic Interstitial Nephritis
CRF with mixed infiltrate in interstitium
Tubular atrophy and fibrosis
Mechanism is Physical/Chemical or Ischemic
Main causes: drugs (NSAIDs, lithium), UTO, stones, PCKD
Asymmetrically scarred, shrunken kidneys
Remove inciting agent
Support renal failure
Acute Pyelonephritis
Usually due to bacterial infection
Ascending infections affect pelvis
Hematogenous infections affect cortex
Presents as fever, chills, flank pain
Predisposed: pregnant women, diabetics, catheters
Ascending --> E. Coli; Hematogenous --> Staph Aureus
Acute inflammatory infiltrate of tubules
Treatment is anti-biotics
Chronic Pyelonephritis
Infections secondary to vesicuretereal reflux
Small kidneys with coarse scars, dilated papillae, atrophy
Non-specific interstitial infiltrate
Tubular atrophy with "THYROIDIZATION"
Fibrosis, Glomerulosclerosis
Treatment is support and treatment of hypertension
Prophylactic anti-biotics to prevent UTIs
Acute Tubular Necrosis
Most common cause of ARF
ARF secondary to tubular damage
Causes: ischemic, POST-TRANSPLANT, toxic, obstructive
Phases: oliguric, diuretic, regenerative
Histo -- Prox. tubular epithelial cell degeneration, interstitial edema
Mitotic activity in regenerative phase
Treatment is supportive
30% return to normal renal function
Poor prognostic factors: severe oliguria
Papillary Necrosis
Predisposed: analgesic use (PHENACETIN), diabetics, sickle cell pts.
Histo -- acute inflammation in papillae, with necrosis
5% of women; 10% of men
40 - 70% recur
50% symptomatic within 5 yrs.

Etiology: idiopathic (75%), Infection (15%), Hypercalciuria
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
Very large cystic kidneys
NO dysplasia
ALL portions of neprhon involved (bilateral)
Declining renal function --> 50% ESRD
Cysts also in liver, spleen, and pancreas (do NOT affect function)
MV prolapse (25%), Cerebral aneurysms (10-20% [15% of deaths])
PKD 1, 2, 3 encode polycystins (85%, 15%, <1%)
Effect cell-cell and cell-matrix interactions
Dialysis Related Cysts
75% after 5 yrs on dialysis
Form stones --> hematuria
RCC in 5-10%
BOTH cortical and medullary
Benign Simple Cystic Disease
Translucent cysts on surface of cortex
NO clinical significance
50% once older than 50
Multicystic Renal Dysplasia
Multiple cysts of variable size
Misshapen kidney
Most common cause of abdominal mass in newborns
Acute Cellular Rejection
Most common form
Usually within first 3 months (can occur any time)
Presents with rising creatinine and fever
Histo -- tubulitis, interstitial inflammation
Treat wih increased immunosuppression
Can have a vascular component
Acute Humoral Rejection
Affects capillaries
Can use fluorescent Abs to C4d to diagnose
Also, increased donor-specific Abs
Rarely, severe with necrotizing arteritis
Chronic Allograft Nephropathy
Most frequent cause of graft loss today
Creatinine SLOWLY rises
Non-specific tubular atrophy, interstitial inflammation, glomerular sclerosis
Calcineurin-Inhibitor Toxicity
Causes NODULAR HYALINIZATION of arterioles
Also, causes changes identical to chronic rejection
Recurrent disease in grafts
Type II MPGN (100%)
Diabetic GN (>90%)
IgA Nephropathy (40-60%)
FSGN (35%)

Loss of graft is rare in all of them EXCEPT for FSGN (10-30%)

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