Renal Pathology Lecture III Flashcards
(31 cards)
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
2
Q
Acute tubular necrosis/acute tubular injury (ATN/ATI)
A
- -Destruction of tubular epithelial cells
- -Most common cause of ARF
- -Reversible renal lesion
3
Q
ATN patterns (2 types)
A
- Ischemic
2. Nephrotoxic
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
5
Q
Nephrotoxic pattern of ATN
A
Drugs, heavy metals, organic solvents, contrast dye
6
Q
Pathogenesis of ATN
A
- -Same in nephrotoxic and ischemic patterns
- -Tubular injury, changes in blood flow
7
Q
Tubular epithelial cell injury types
A
- -Reversible: cell swelling, loss of polarity
- -Lethal: necrosis and apoptosis
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
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)
10
Q
Vasoconstrictor pathways
A
- Renin-angiotensin
2. Endothelin release by damaged endothelial cells with decreased NO
11
Q
Recovery of ATN
A
- -Patchiness of tubular necrosis and intact BM allow for repair
- -Reversibly injured epithelial cells proliferate and differentiate
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
13
Q
Ethylene glycol changes in tubular lumen
A
Ca++ oxalate crystals
14
Q
3 clinical phases of ATN
A
- Initiation
- Maintenance
- Recovery
15
Q
Initiation of ATN
A
- -Slight decline in urine output
- -Increased BUN
- -Lasts about 36 hrs
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
Clinical course of chronic pyelonephritis
--Some patients develop focal segmental glomerulosclerosis and proteinuria
26
3 ways drugs can induce tubulointerstitial nephritis
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
Acute drug-induced interstitial nephritis
- -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
Micro findings of acute interstitial nephritis
- -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
Pathogenesis of acute drug-induced interstitial nephritis
- -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
NSAID associated nephropathy
- -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
Urate nephropathy
- -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
