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CRRAB II > Renal Pathology Lecture III > Flashcards

Renal Pathology Lecture III Flashcards

1
Q

What happens in diseases of tubules and interstitium?

A
  • -Ischemic or toxic injury to tubules (Leads to acute tubular necrosis, acute tubular injury and ARF)
  • -Inflammatory reactions of the tubules and interstitium leading to tubulointerstitial nephritis
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2
Q

Acute tubular necrosis/acute tubular injury (ATN/ATI)

A
  • -Destruction of tubular epithelial cells
  • -Most common cause of ARF
  • -Reversible renal lesion
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3
Q

ATN patterns (2 types)

A
  1. Ischemic

2. Nephrotoxic

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4
Q

Ischemic ATN pattern of ATN

A
  • -Period of inadequate blood flow to kidneys, usually related to marked hypotension and shock.
  • -Hemolysis, mismatched blood transfusions, skeletal muscle destruction also cause this pattern
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5
Q

Nephrotoxic pattern of ATN

A

Drugs, heavy metals, organic solvents, contrast dye

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6
Q

Pathogenesis of ATN

A
  • -Same in nephrotoxic and ischemic patterns

- -Tubular injury, changes in blood flow

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7
Q

Tubular epithelial cell injury types

A
  • -Reversible: cell swelling, loss of polarity

- -Lethal: necrosis and apoptosis

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8
Q

Disturbances in blood flow leads to what?

A

Intrarenal vascoconstriction (Decreased glom plasma flow and oxygen to thick ascending limb and straight segment of proximal tubule

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9
Q

Tubular cell injury mechanism

A
  • -Depletion of ATP, increased intracellular Ca+++, redistribution of proteins, abnormal ion transport
  • -Injured cells recruit WBCs
  • -Luminal tubule obstruction by detached cells (increased intratubular P and decreased GFR)
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10
Q

Vasoconstrictor pathways

A
  1. Renin-angiotensin

2. Endothelin release by damaged endothelial cells with decreased NO

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11
Q

Recovery of ATN

A
  • -Patchiness of tubular necrosis and intact BM allow for repair
  • -Reversibly injured epithelial cells proliferate and differentiate
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12
Q

Pathology of ATN

A
  • -Epithelial necrosis
  • -Sloughing of tubular cells into lumen
  • -Hyaline and granular casts
  • -Interstitial edema and increased lymphocytes
  • -Toxic ATN may show specific changes
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13
Q

Ethylene glycol changes in tubular lumen

A

Ca++ oxalate crystals

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14
Q

3 clinical phases of ATN

A
  1. Initiation
  2. Maintenance
  3. Recovery
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15
Q

Initiation of ATN

A
  • -Slight decline in urine output
  • -Increased BUN
  • -Lasts about 36 hrs
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16
Q

Maintenance of ATN

A
  • -Oliguria
  • -Salt and water overload
  • -Increased BUN
  • -Hyperkalemia
  • -Metabolic acidosis
  • -Often need dialysis
17
Q

Recovery of ATN

A
  • -Steady increase in urine vol.
  • -Can cause HYPOkalemia
  • -Prognosis: 95% recovery if survives initial event
  • -Related to shock/multi-organ failure has 50% mortality
18
Q

Tubulointerstitial Nephritis

A
  • -Acute and chronic forms
  • -Acute: PMNs/Eos, edema
  • -Chronic: fibrosis and tubular atrophy
  • -Clinical: polyuria, nocturia, metabolic acidosis
  • -No or mild glomerular and vascular changes (until advanced disease)
19
Q

Vesicoureteral reflux

A
  • -Incompetence of vesicoureteral valve that allows bacteria to enter ureter and renal pelvis
  • -Usually due to congenital shortening of intravesicle portion of ureter
  • -Bladder infection, spinal cord injury increases reflux
20
Q

Morphology of acute pyelonephritis

A
  • -Interstitial supperative inflammation (PMNs)
  • -Intratubular aggregates of neutrophils
  • -Tubular necrosis
  • -Heals by scarring (tubular atrophy and interstitial fibrosis with lymphocytes)
  • -If due to reflux, upper and lower poles of kidneys most commonly affected
21
Q

Complications of acute pyelonephritis

A
  • -Papillary necrosis (seen in diabetics and patients w/obstruction.
  • -Pyonephrosis
  • -Perinephric abscess
22
Q

Papillary necrosis gross and micro features

A

Gross–yellow necrosis of papillary tips

–Micro: coagulative necrosis

23
Q

Chronic pyelonephritis

A
  • -Pelvocalyceal damage present
  • -Important cause of end stage renal disease
  • -Due to chronic reflux or chronic obstruction (don’t have to have bacterial infection)
24
Q

Morphology of chronic pyelonephritis

A
  • -Gross: irreg. scarred surface, discrete corticomedullary scar overlying blunted/deformed calyx
  • -Micro: focal tubular atrophy w/other areas of dilated tubules (chronic interstitial inflammation and fibrosis)
25
Q

Clinical course of chronic pyelonephritis

A

–Some patients develop focal segmental glomerulosclerosis and proteinuria

26
Q

3 ways drugs can induce tubulointerstitial nephritis

A
  1. Trigger interstitial immunologic reaction
  2. Cause acute tubular injury/acute renal failure
  3. Slow injury to tubules over many years w/resulting chronic renal insufficiency
27
Q

Acute drug-induced interstitial nephritis

A
  • -Onset: About 15 days after drug exposure
  • -Symptoms: fever, rash, eosinophilia, renal abnormalities
  • -About 50% develop ARF (esp. in older patients)
  • -Stop offending drug and majority of pts fully recover
28
Q

Micro findings of acute interstitial nephritis

A
  • -Interstitial edema and lymphocytes and macrophages
  • -Variable numbers of eosinophils and PMNs
  • -Granulomas and giant cells w/some drugs
  • -Lymphocytes infiltrate tubular epithelium and cause variable tubular necrosis
  • -Glomeruli typically normal on H and E
29
Q

Pathogenesis of acute drug-induced interstitial nephritis

A
  • -Immune response not dose related
  • -Mix of type 1 (IgE related) and type 4 (delayed) hypersensitivity reactions
  • -Drugs seem to act as haptens (covalently bind to cytoplasmic or extracellular component of tubular cells…elicits immune response
30
Q

NSAID associated nephropathy

A
  • -Can cause ARF, hemodynamically induced (inhibition of vasodilatory PG synthesis leads to decreased blood volume)
  • -Acute hypersensitivity interstitial nephritis leading to ARF
  • -Membranous GN
  • -AIN and MCD
31
Q

Urate nephropathy

A
  • -Acute uric acid nephropathy due to precipitation of uric acid crystals in renal tubules leading to obstruction and ARF (classic in patients undergoing chemo)
  • -Chronic urate nephropathy (associated w/gout)
  • -Hypercalcemia and nephrocalcinosis

CRRAB II (13 decks)

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