003 - renal pathology iii
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7/30/2019 003 - Renal Pathology III
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Vijesh Pate
Renal Pathology III
Diseases affecting the tubules and interstitium usually both are affected together not individually, hence tubule-interstitial disorders
- No nephritic or nephrotic syndrome present- InsteadProblem w/ tubular function
o Concentration ability leading to polyuria, nocturia, salt wasting, disturbance acid secretion (metabolic acidosis)o ARF: abrupt suppression of renal function leading to s/s ofazotemia & uremia w/in weeks
Oliguria: less than 400 ml / day of urine Anuria: less than 100 ml / day of urine
Classifications: 1) Pre-renal: starts before the kidney (thrombosis of renal artery)o 2) Intra-renal: disease starts at the kidney (RPGN, other renal disease)o 3) Post-renal: starts after the kidney (obstruction, stone, etc.)
**Most common cause = Acute tubular necrosis (ATN) / Acute kidney injury (AKI)Epi Pathogenesis / Antibodies S/S *
ATN Death of the tubular epithelium
cells = loss of function
Reversible
Loss of polarity = Na/K ATPase @
apical instead of the basolateral
side = Na lossMacula densa
osmotically swell afferent
arteriole constriction GFR
Detachment of epithelial cells =
formation of casts in the urine =
GFR
Irreversible Ischemia b/c of loss of blood =
adrenergic response, leading to
afferent arteriole constriction =
flow to efferent arteriole =
necrosis and apoptosis of the cells
= tubular flow
ALL result in OLIGURIA
Early management can be
reversed
- Initiation phase: swollen kidneys
urine output + BUN
- Maintenance phase: urine
output at lowest point, electrolyte
imbalance, K, uremia
Need dialysis to survive
- Recovery phase: regenerationoccurs, maturation of the tubular
cells, polyuria (b/c immature cells
leak), K
- Better prognosis w/ toxic
Ischemia blood supply (Hypotension,
shock, hypovolemia [diarrhea,
bleeding])
Multiple points w/ SKIPS
History: recent hemorrhage,
hypotension, surgery
Urinalysis: muddy (dirty) brown
urine b/c of many cytochrome
pigments
Coagulative necrosis: cells
appear eosinophillic (pink) w/ no
nuclei
o Regeneration = flattened cellsbut not truly functional (ie. leaky
edema)
Toxins Exogenous: nephrotoxins
Antibiotics (aminoglycosides,
amphotericin B)
Radiographic agents, heavy
metals, organic solvents
(ethyelene glycol @ brake fluids /
anti-freeze)
Endogenous: proteins
Myoglobulins: massive trauma
(crush) = enter blood
Hemoglobulins: excessive
hemolysis (wrong blood type =
HSR) = overload of hemoglobins
Mostly PT w/ NO SKIPS
spares the distal tubule and BM
Mercury: damaged cells have
acidophilic inclusions
CCl4: accumulation of lipids with
necrosis
Ethylene glycol (antifreeze /
brake fluid): metabolized in the
liver by ADH = Oxalic acid + Ca =
Calcium oxylate crystals
Ballooning degeneration +
vacuolization
Tubulo-interstitial nephritis
Acute PN More in young women (15-40)
- 1) Shorter ureter
- 2) No anti-bacterial protection
(ie. Prostatic fluid)
- 3) Progesterone :. Common
during child bearing age
Mostly gram negative bacilli
(E.coli, proteus, klebsiella)
Affects tubules, interstitium &
renal pelvis
2 routes:
- Hematogenous route (staph)
- Ascending infection
From lower urinay tract
Vesico-ureteral reflux
- PROGESTERONE = flaccid, loss of
oblique course b/c of congenital or
many infections
Intra-renal reflux
- Upper + lower poles have
indentations (round papillae) that
allow for stagnationallow
bacterial growth
N infiltrate of interstitium &
tubules
- Abscesses: @ upper/ lower poles
Costovertebral angle tenderness
Fever, chills, N&V, dysuria,
freq.
Bacteriuria, WBC (pyuria), WBC
casts
Complications:
- Pyonephritis: pus in renal pelvis
- Papillary necrosis: destroy small
tubular capillaries in medulla
(Also w/ sickle cell, renal TB,
diabetes)
Chronic PN Scarring + flattening of calyces Corticomedullary scar over a
blunted, dilated, deformed calyx
Lymphocytes + plasma cell
infiltrate
Thyroidization colloid casts in
tubules
Reflux type Most common VU reflux beginning in childhood * Only pole calycies affected
Obstructive type Progress from acute PN Obstruction of lower urinary tract
- Cause:
Large scarred areas + distortion
of pyramids (Papillary necrosis)
Gradual onset renal insufficiency
HTN
Proteinuria b/c of FSGS + end
stage renal failure
* All calycies affected
DDX: CGN
- this is asymmetric
Xanthogranulomatous PN Ass w/ proteus infections Accumulation of foamy M and
giant cells
Large yellow nodules DDX: NOT renal carcinoma
- Yellow nodules occur here too
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7/30/2019 003 - Renal Pathology III
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Vijesh PateEpi Pathogenesis / Antibodies S/S *
Acute drug induced
tubulointerstitial nephritis
(Hypersensitivity nephritis)
15 days after drug exposure
(Methicillin, Ampicillin,
sulphonamides, NSAIDS)
Drugs act as hapten
Type 1 HSR = Eosinophillia
Type 4 HSR = Granulomas
Azotemia, oliguria, fever,
eosinophilia, rash, proteinuria
(mild), hematuria
Papillary necrosis
Renal failure in 50% of pxns
Analgesic abuse nephropathy Analgesic mixtures = chronic TI
nephritis + renal papillary necrosis
Analgesic abuse
- Phenacetin Acetaminophen
(free radical damage)
- Aspirin inhibits prostaglandinleading to vasoC of afferent art. =
Papillary necrosis followed by TI
nephritis
All papillae are affected
- Different stages of necrosis
- DDX: Diabetes = same stage
Dystrophic calcification, sloughing
Long term complication
- Transitional cell carcinoma of
renal pelvis / ureter / bladder
**Papillary Necrosis**
1) Acute tubulo-interstitial nephritis, 2) Analgesic nephropathy, 3) Diabetes, 4) Sickle cell anemia or trait, 5) Renal TB, 6) Urinary tract obstr uction
**NSAID associated nephropathy**
1) Acute hypersensitivity Tubulo-interstitial nephritis, 2) Lipoid nephrosis (MCD), 3) Membranous GN
Urate nephropathy Uric acid crystals
w/ adjacent fibrosis + atrophy of
renal parenchyma
Acute uric acid nephropathy Chemotherapy leading to tumor
lysis syndrome
- ARF b/c of uric acid
Chronic uric acid nephropathy Gout tophi
- Moonshine for gouty attack
precipitating in tubules
- Tophi present causes a fibrosing
reaction (via fibroblasts)
Nephrolithiasis Uric acid stones
Multiple myeloma Plasma cell cancer = light chains
- Bence jones + Tamm horsfall
proteins Complexes
- Obstruct tubular lumen =
granulomatous inflammation
- Multinucleate giant cells present
Amyloidosis
Hypercalcemia & Hyperuricemia
**Urinalysis in ARF**
ATN = dirty brown casts + epithelial cells
AGN = RBC casts + proteinuria
Acute TI nephritis = WBC casts + pyuria (pus)
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Vijesh PateEpi Pathogenesis / Antibodies S/S *
Kidney complications that can result as a complication to HTN
Benign nephrosclerosis
(Hyaline arteriosclerosis)
HTN (moderate) - Medial + intimal thickening
- Hyaline deposition b/c proteins
are pushed out
Sclerosis of renal arterioles + small
arteries
GFR + mild proteinuria
Shrunken kidney
- Surface is fine granular
Malignant nephrosclerosis Malignant HTN
History of MI, stroke, papilledema
- permeability to proteins
- Endothelial injury
- Platelet deposition GF release
leads to hyperplastic arteriolitis
Onion skin appearance
- Fibrinoid necrosis + thrombosis
NECROTIZING ARTERIOLITIS
Flea bitten kidney
- Rupture of capillaries = petechial
hemorrhages
mortality
Renal artery stenosis (RAS) HTN caused by RAS activity in
the ischemic kidney
- renin
** Important b/c this can be
surgically cured
DDX: Hyperaldosteronism (Cohns
syndrome) renin
1. Occlusion by atheromatous
plaque
Older males
2. Fibromuscular hyperplasia Younger females Smooth muscle hyperplasia
(media)
- blood flow to kidney
Angiogram = beading effect
- Multiple constrictions
Trichrome stain = thickening of
media
Thrombotic microangiopathies
HUS / TTP Syndrome
Thrombosis of capillaries and
arterioles throughout the body
MAHA
Thrombocytopenia
Renal failure
1. Hemolytic uremic syndrome E.coli infectin (Type O157:H7)
- Infected meat
Renal symptoms mostly
- Diarrhea, MAHA- Oliguria, hematuria, HTN, ARF
Blood smear schistocytes
Kidney cortical necrosisArterioles fibrinoid necrosis +
subENDOthelial fibrin deposits
2. Thrombotic thrombocytopenic
purpura
CNS symptoms mostly
Diffuse cortical necrosis **Occurs in conditions w/ DIC
- Abruptio placentae, HUS, septic
shock
Bilateral + symmetrical cortical
necrosis
- columns of berteni are affected
- medulla is unaffected
- smallest vessels are in the cortex
Pale changes to cortex
Renal infarctions **Develops b/c ofthromboemboli
or vegetations on the left heart
- Results of atrial fib
- Flank pain, fever, leukocytosis
- Proteinuria, hematuria
Pale wedged shaped lesions
- Coagulative necrosis (no nuclei)
Obstructive uropathy
(Hydronephrosis)
Male
BPH
Female
pregnancy (ureter pressed)
uterine prolapse (cystocele)
Both stones (urinary calculi)
Obstruction of the urine outflow
- Leads to dilation of renal pelvis &
calyces
- Atrophy of the kidney
Stagnation of urine = risk ofinfection & stone formation
Permanent damage if:
- Partial obstruction for 3 mths
- Complete obstruction for 3 wks
Intravenous pyelogram shows:
- dilation of renal pelvis + calyces
Cortical thinning
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