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PATHOLOGY 2 > Kidney and Collecting system > Flashcards

Kidney and Collecting system Flashcards

1
Q
  1. End-stage kidney and renal failure:

KIDNEY FUNCTIONS

A
  • excretion of waste products of metabolism
  • regulate salt + H2O
  • maintain acid balance
  • secrete hormones + autacoids
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2
Q
  1. End-stage kidney and renal failure:

RENAL SYNDROMES

A
  1. Nephritic syndrome⇒ glomerular injury
  2. Nephrotic syndrome ⇒ glomerular disease
  3. Asymptomatic hematuria ⇒ mild glomerular abnormalities
  4. Rapidly progressive glomerulonepthiris ⇒ severe glomerular injury
  5. Acute kidney injury ⇒ glomerular, vascular, intestinal or acute tubular injury
  6. Chronic kidney injury ⇒ progressive scarring of the kidney
  7. UTI ⇒ bacteremia and pyuria
  8. Nephrolithiasis
  9. Urinary tract obstruction
  10. Renal tumors
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3
Q
  1. End-stage kidney and renal failure:

END STAGE KIDNEY

A

= complete failure of kidneys to function
- kidney function <20% of normal, GFR <15ml/min
- no longer removes waste products, concentrate urine, regulate endocrine functions
- CAUSES: DM, HT
MORPHOLOGY:
- kidneys skrink, red-brown color, granular
- sclerosis
- interstitial fibrosis
- lymphatic infiltration in interstitium
TREATMENT:
- dialysis
- transplant

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4
Q
  1. End-stage kidney and renal failure:

AZOTEMIA

A

= elevation of BUN (blood urea nitrogen) and serum creatinine due to renal failure

  • BUN >9mM, Creatinine >120 microM
    1. PRERENAL AZOTEMIA:
    • decreases GFR in absence of parenchymal damage ⇒ hypo perfusion ⇒ hemorrhage
      2. RENAL AZOTEMIA:
    • renal parenchymal damage
      1. POSTRENAL AZOTEMIA:
    • urine flow obstructed
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5
Q
  1. End-stage kidney and renal failure:

UREMIA

A

= azotemia + biochemical abnormalities + clinical manifestations

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6
Q
  1. End-stage kidney and renal failure:

UREMIA clinical features

A
  1. weakness, dyspnea, lethargy, edema, confusion
  2. Electrolyte imbalance + Ca2+/PO4 imbalance
    ⇒ hyperkalemia, hyperphosphatemia, hypocalcemia
  3. Cardio-pulmonary symptoms
    ⇒ HF, pulmonary edema, uremic fibrinous pericarditis, anemia, HT, arrhythmias
  4. Hematopoietic symptoms
    ⇒ anemia (no EPO or tissue factor)
  5. Neural
    ⇒ muscle twitch, weakness, headache, coma
  6. Retinal
    ⇒ AS or HT retinopathy
  7. Dermal
    ⇒ eyelid swelling, pruritus, purpura
  8. Respiratory
    ⇒ Kussmaul breathing, urine smell, pleuritis, pneumonitis
  9. GI
    ⇒ bleeding, anorexia, nausea, vomiting
  10. Metabolic acidosis
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7
Q
  1. End-stage kidney and renal failure:

ACUTE RENAL FAILURE types

A
  1. PRERENAL FAILURE:
    - reversible, function reduced by external factors
    - e.g. HT, salt depletion, dehydration
  2. RENAL FAILURE;
    - malfunction of nephrons
    - e.g. acute GN, pyelonephritis
  3. POSTRENAL FAILURE:
    - urinary tract obstruction
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8
Q
  1. End-stage kidney and renal failure:

ACUTE RENAL FAILURE morphology + clinical features

A

MORPHOLOGY:
- decreased cortical blood flow ⇒ ischemia
- large, pale pink kidney
- thick, pale cortex + dark, hyperemic pyramids
- Histo: glomeruli normal, distal tubules dilated with flattened epithelia
CLINICAL FEATURES:
- decreased urine output
- inquired azotemia, metabolic acidosis + serum potassium

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9
Q
  1. End-stage kidney and renal failure:

CHRONIC RENAL FAILURE

A

CAUSE:
- primary glomerular disease (acute GN)
- primary tubular disease (chronic hypercalcemia)
- vascular disease (nephrosclerosis)
- infections (tuberculosis)
- obstructive disease
- collagen disease (scleroderma)
- metabolic renal disease (amyloidosis)
- congenital anomalies of kidneys (polycystic kidney disease)
CLINICAL FEATURES:
- secondary hyperparathyroidism
- metabolic bone disease

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10
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    COMPLETE OR BILATERAL RENAL AGENESIS
A

= failure to develop kidneys
CAUSE:
- Potter sequence: no kidneys ⇒ oligohydramnios
⇒ clubbed feet, flat nose, low-set ears, recessed chin

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11
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    UNILATERAL RENAL AGENESIS
A

= 1 kidney missing due to failure of development

  • no major health consequences
  • prone to HT
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12
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    RENAL ECTOPIA
A

= abnormal localization of kidneys

- found in pelvis

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13
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    HORSESHOE KIDNEY
A 
= fusion of kidneys during development
- 1/400
CONSEQUENCES:
  - obstruction
  - infection
  - stones
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14
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    DUPLICATED URETER
A

= 2 ureters due to ureteric bud arises twice

- may present as UTI- due to vesicouteral reflux

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15
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    SIMPLE CYST
A
  • single cyst lined by membrane and filled with fluid
  • usually on cortical area/surface
  • can cause hemorrhage + pain
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16
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    DIALYSIS AQUIRED CYSTIC DISEASE
A
  • in patients with end-stage renal disease on dialysis
  • fibrosis ⇒ distal area becomes dilated
  • both cortex and medulla
  • may cause bleeding, hematuria
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17
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE
A 
- 1/500-1000
= multiple expanding cysts on both kidneys that destroy the intervening parenchyma ⇒ chronic renal failure
PATHOGENESIS:
  - deletion in PKD1 gene ⇒ polycystin 1⇒ dysfunctional tubules ⇒ cyst formation
  - PKD2 gene ⇒ no dimerization of PKD1
CLINICAL FEATURES:
  - symptoms in 40s-50s⇒ huge kidneys
  - renal failure
  - pain (Hemorrhage, obstruction)
  - UTIs
  - hematuria
TREATMENT:
  - dialysis + transplantation
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18
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE
A
  • perinatal, neonatal, infantile and juvenile subgroups
    PATHOGENESIS:
    • mutation in PKHD1 gene ⇒ fibrocystin ⇒ dysgenesis of collecting tubules ⇒ cysts
      CLINICAL FEATURES:
    • liver, lung, spleen and pancreas affected
    • early RF + hepatic failure
      MORPHOLOGY:
    • small cysts in cortex + medulla (sponge kidney)
    • epithelium lined cysts in liver
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19
Q
  1. Developmental abnormalities and cystic diseases of the kidney:
    MEDULLARY CYSTIC DISEASE OF KIDNEY
A 
- infantile, juvenile, adolescent and adult types
PATHOGENESIS:
  - AD or AR
  - mutation in NPHP1-NPHP5
MORPHOLOGY:
  - numerous small cysts in cortico-medullary junction
  - kidneys small + contracted
  - intestinal fibrosis + inflammation
  - tubular atrophy
CLINICAL FEATURES:
  - polyuria + polydipsia
  - end-stage kidney in 5-10 years
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20
Q
  1. Pathogenesis of glomerular diseases:

GLOMERULAR DISEASES groups

A
  1. Groups based on clinical features:
    - acute nephritic syndrome
    - RPGN
    - nephrotic syndrome
    - asymptomatic hematuria
    - CGN
  2. Groups based on morphology:
    - glomerular hypercellularity
    - basement membrane thickening
    - sclerosis + hyalinization
  3. Groups based on immunological manifestations:
    - circularoty immune complex GN
    - in-situ immune complex GN
    - heymans GN
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21
Q
  1. Pathogenesis of glomerular diseases:

ACUTE NEPHRITIC SYNDROME/NEPHRITIS

A
  • accompany immune-mediated GN
  • symptoms develop suddenly
    CLINICAL FEATURES:
    • hematuria
    • proteinuria
    • HT
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22
Q
  1. Pathogenesis of glomerular diseases:

RAPID PROGRESSIVE GLOMERULOSNEPHRITIS

A 
- characterized by rapid loss of renal function ⇒ acute RF + death
CLINICAL FEATURES:
  - oliguria/anuria
  - hematuria + proteinuria
  - HT
TYPES:
  1. Anti-glomerular BM nephritis
    - AB against BM  ⇒ fibrosis
    - eg. Goodpasture syndrome
    - plasmaphoresis may help
  2. Immune-complex mediated crescentic GN
    - hereditary, homogenous
    - prolif. of Bowmans capsule, subepithelial deposit in EM + necrosis of capillary ducts
  3. Pauci-Immune type 3 crescentic GN
     - ANCA
     - necrosis of segments
     - endothelia preserved, BM fragmented
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23
Q
  1. Pathogenesis of glomerular diseases:

NEPHROTIC SYNDROME

A 
= glomeruli of kidney damaged ⇒ leak of large amounts of protein into urine
CLINCAL FEATURES:
  - proteinuria
  - edema + lipiduria
  - hyperlipoproteinemia
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24
Q
  1. Pathogenesis of glomerular diseases:

ASYMPTOMATIC HEMATURIA

A
  • no clinical symptoms
  • some protein/blood in urine
  • mild disease
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25
Q
  1. Pathogenesis of glomerular diseases:

CHRONIC GLOMERULONEPHRITIS

A
  • end-stage kidney + decreased renal function
  • barrier defect ⇒ leakage of proteins ⇒ mesangial cell prolif. ⇒ obliterates glomeruli ⇒ hyaline glomeruli ⇒ kidneys shrink + have irregular surface
    CLINICAL FEATURES:
    • HT
    • oliguria/ anuria
    • anemia
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26
Q
  1. Pathogenesis of glomerular diseases:

GLOMERULAR HYPERCELLULARITY

A
  1. Cellular proliferation ⇒ endothelial, epithelial and mesangial cells
  2. Infiltration ⇒ cells not part of glomeruli infiltrate capsule (leukocytes)
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27
Q
  1. Pathogenesis of glomerular diseases:

BASEMENT MEMBRANE THICKENING

A
  • whole fibrinogenesis

- linear or granular

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28
Q
  1. Pathogenesis of glomerular diseases:

SCLEROSIS AND HYALINIZATION

A
  • precipitation of proteins in an onion-skin-like fashion ⇒ sclerosis ⇒ hyaline like secretion
  • end-stage kidney
  • diffuse or focal
  • segmental or global
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29
Q
  1. Pathogenesis of glomerular diseases:

CIRCULATORY IMMUNE COMPLEX GN

A
  • HR type 3
  • endogenous or exogenous AG
  • AG-AB complex formed in circulation ⇒ deposited in glomeruli ⇒ activation of complement system + recruitment of leukocytes ⇒ GN
    LOCATIONS:
    • mesangium
    • sub endothelial area
    • sub epithelial area
  • demonstrated by immunofluorescence ⇒ granular deposit
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30
Q
  1. Pathogenesis of glomerular diseases:

IN-SITU IMMUNE COMPLEX GN

A
  • Type 2 HR
    1. Anti-BM AB GN
    • AB directed against fixed AG in GBM
    • immunofluorescence ⇒ linear deposit
    • sometimes cross react with BM in lung alveoli ⇒ Goodpasture syndrome
      2. AB against GBM fixed AG
    • AB act with previously planted non-glomerular AG
    • e.g. DNA, bacterial product. large aggregated proteins
    • immunofluorescence ⇒ linera/granular deposit
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31
Q
  1. Pathogenesis of glomerular diseases:

HEYMANS GN

A
  • experimental model of membranous GN
  • brush-border antigen of rabbit injected into rat ⇒ anti-brush border AB ⇒ reinfected into rabbit ⇒ cross react with podocyte antigens ⇒ membranous GN
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32
Q
  1. Nephritic syndrome:

NEPHRITIC SYNDROME general

A 
= set of clinical signs and symptoms that accompany immune-mediated GN
- acute onset
- glomeruli cells proliferate accompanied by leukocytic infiltrate
SYMPTOMS:
  - hematuria with dysmorphic RBCs
  - oliguria
  - azotemia
  - mild hypertension
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33
Q
  1. Nephritic syndrome:

NEPHRITIC SYNDROME causes

A 
1. Primary GN
 ⇒ IgA nephritis
2. Postinfectious GN
 ⇒ poststreptococcal GN
 ⇒ bacterial endocarditis associated GN
3. Secondary GN associated with systemic diseases
 ⇒ SLE
 ⇒ Wegener's granulomatosis
 ⇒ Goodpasture's syndrome
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34
Q 
71. Nephritic syndrome:
IGA NEPHROPATHY (BERGER DISEASE)
A
  • affects children and young adults
    PATHOGENESIS:
    • abnormality in IgA production and clearance
    • IgA is high in serum due to increased production in marrow
    • abnormality of IgA glycosylation
    • in mesangium trapped IgA activates alternative complement pathway ⇒ acute nephritic syndrome
      CLINICAL FEATURES:
    • slow progression to chronic renal failure⇒ 20 years
35
Q
  1. Nephritic syndrome:

ACUTE POSTSTREPTOCOCCAL GN pathogenesis

A
  • immune complexes between bacterial AG and AB deposit in glomeruli ⇒ activate complement system ⇒ GN + proliferation of mesangial cells
  • Tonsillitis (s.pyogenes) ⇒ rheumatic fever ⇒ humps deposits
  • also pneumococcus, s.aureus, common cold viruses
36
Q
  1. Nephritic syndrome:

ACUTE POSTSTREPTOCOCCAL GN clinical features + diagnosis

A 
CLINICAL FEATURES:
  - malaise, fever, nausea and nephritic syndrome
  - hematuria
  - oliguria
  - periorbital edema
DIAGNOSIS:
  - microscope: light, electron, immunofluorescence
  - blood test
37
Q
  1. The nephrotic syndrome:

NEPHROTIC SYNDROME

A

= diseases that cause increased permeability of the glomerular capillaries
SYMPTOMS:
- massive proteinuria
- hypoalbuminemia
- generalized edema
- hyperlipidemia and lipiduria
PATHOGENESIS:
- derangement in capillary walls of glomeruli⇒ increased permeability ⇒ proteinuria
⇒ hypoalbuminemia ⇒ edema + increased synthesis of lipoproteins
- in children ⇒ lesion primary to kidney
- in adult ⇒ systemic disease

38
Q
  1. The nephrotic syndrome:

MINIMAL- CHANGE DISEASE (LIPID NEPHROSIS)

A
  • primary lesion of kidney ⇒ nephrotic syndrome in children
  • age: 1-7yrs (any ages)
    MORPHOLOGY:
    • glomeruli show diffuse thinning/ detachment of podocyte foot processes
      PATHOGENESIS:
    • T-cell derived factor ⇒ podocyte damage + thinning of foot processes ⇒ proteinuria
      CLINICAL FEATURES:
    • no HT + renal function preserved
    • slow development of nephrotic syndrome
      TREATMENT:
    • corticosteroid therapy
39
Q
  1. The nephrotic syndrome:

FOCAL AND SEGMENTAL GLOMERULOSCLEROSIS general + pathogenesis

A

CAN OCCUR:
- in association with other known conditions
- secondary to GN
- maladaptation after nephron loss
- inherited or congenital forms
- primary disease
UNLIKE MCD:
- more hematuria + HT
- hematuria is non-selective
- poor response to corticosteroid therapy
- 50% develop end-stage kidney within 10yrs
PATHOGENESIS:
- deposition of hyaline masses ⇒ entrapment of plasma proteins and lipids in foci of injury where sclerosis develops

40
Q
  1. The nephrotic syndrome:

FOCAL AND SEGMENTAL GLOMERULOSCLEROSIS morphology + clinical features

A

MORPHOLOGY:

  • focal: affects initially juxtamedullary glomeruli but progresses
  • segmental: only segments undergo sclerosis
  • increased mesangial matrix, obliterated capillary lumens + deposition of hyaline masses and lipid droplets
  • thinning + detachment of foot processes of podocytes
41
Q
  1. The nephrotic syndrome:

MEMBRANOUS GN cause

A
  • idiopathic in 85%
  • infections (hepatitis B, syphilis, malaria)
  • malignant tumors
  • exposure to inorganic salts
  • SLE or other autoimmune diseases
  • Drugs
42
Q
  1. The nephrotic syndrome:

MEMBRANOUS GN pathogenesis

A
  • slowly progressive
  • age: 30-50yrs
  • circulating immune complex ⇒ trigger MAC complex on podocytes ⇒ release of proteases and oxidants ⇒ damage capillary walls ⇒ leakage
43
Q
  1. The nephrotic syndrome:

MEMBRANOUS GN morphology

A
  • Spike and dome:
    • subepithelial IC deposits in BM
    • podocyte foot process flat
  • thick BM with holes
  • sclerotic glomeruli with hyaline
44
Q
  1. The nephrotic syndrome:

MEMBRANOUS GN clinical features

A
  • non-selective proteinuria
  • no response to corticoid therapy
  • renal failure after 2-20yrs
45
Q
  1. The nephrotic syndrome:

MEMBRANOPROLIFERATIVE GN pathogenesis

A

MPGN-1 (sub endothelial deposit disease):
- circulating immune complexes ⇒ complement activation
- association with hepatitis B and C antigens, SLE, infected AV shunts, extrarenal infections
MPGN-2 (dense-deposit disease):
- Autoantibodies against C3-convertase ⇒ uncontrolled cleavage of C3⇒ excessive complement activation
- mutation in gene encoding Factor H ⇒ deficiency ⇒ excessive activation

46
Q
  1. The nephrotic syndrome:

MEMBRANOPROLIFERATIVE GN morphology + clinical features

A

MORPHOLOGY:
- glomeruli are large
- proliferation of mesangial cells + endothelial cells + infiltrating leukocytes
- GBM thickened ⇒splitting of GBM⇒ tram track appearance
- MPGN1: sub endothelial electron-dense deposits
- MPGN2: intramembranous deposits
CLINICAL FEATURES:
- progress to renal failure
- nephrotic syndrome
- poor prognosis

47
Q
  1. Systemic diseases associated glomerular damage:

DIABETIC GLOMERULAR SCLEROSIS/ NEPHROPATHY

A

= BM thickening due to non-enzymatic glycosylation of proteins

  • diffuse GS ⇒ all glomeruli ⇒ hyaline deposit
  • nodular focal GS ⇒ Kimmelstiel Wilson
  • proteinuria ⇒ sclerosis ⇒ renal failure
48
Q
  1. Systemic diseases associated glomerular damage:

AMYLOIDOSIS

A

= deposition of amyloids in sub endothelium of glomeruli
⇒ severe proteinuria ⇒ renal failure
- corticosteroids make it worse

49
Q
  1. Systemic diseases associated glomerular damage:

GOODPASTURE SYNDROME

A
  • genetic autoimmune disease: GN + hemorrhage of lungs

- immune system attacks Goodpasture antigen in GBM (component of non-collagenous domain of alpha-3 chain of collagen 4)

50
Q
  1. Systemic diseases associated glomerular damage:

POLYARTHRITIS NODOSA/ WEGENER GRANULOMATOSIS

A
  • autoimmune vascular diseases
    • PN: granular deposits
    • WG: ANCA
      WG:
      ⇒ acute necrotizing granulomas of upper respiratory tract
      ⇒ necrotizing granulomastous vasculitis
      ⇒ necrotizing GN
51
Q
  1. Systemic diseases associated glomerular damage:

SYSTEMIC LUPUS ERYTHEMATOSUS SLE

A
  • deposition of DNA/anti-DNA complexes within glomeruli ⇒ inflam. ⇒ proliferations ⇒ necrosis
    CLASS 1:
    • <5%, normal by LM, EM, IF
      CLASS 2: (mesangial lupus GN)
    • 10-25%, mild clinical symptoms
      CLASS 3: (focal proliferative GN)
    • 25-30%, a few foci show swelling + prolif. + infiltrate
    • hematuria, proteinuria
      CLASS 4: (diffuse proliferative GN)
    • 35-60%, endothelial + mesangial prolif. ⇒ diffuse hypercellularity
    • glomerulosclerosis, hematuria, proteinuria, HT, renal insufficiency
      CLASS 5: (membranous GN)
    • 10-15%
    • widespread thickening of capillary wall
    • severe proteinuria
52
Q
  1. Vascular diseases of the kidney:

BENIGN NEPHROSCLEROSIS

A

= renal changes in benign HT
⇒ hyaline arteriolosclerosis
- causes: HT + DM
MORPHOLOGY:
- atrophic kidneys, granularity on surface
- hyaline thickening of walls of small arteries + arterioles
- narrow lumen ⇒ ischemia
- severe: glomerular tufts globally sclerosed

53
Q
  1. Vascular diseases of the kidney:

MALIGNANT NEPHROSCLEROSIS pathogenesis

A
  • initial event: vascular damage
    ⇒ increased permeability to fibrinogen and plasma proteins + endothelial injury + platelet deposition ⇒ fibrinoid necrosis + intravascular thrombosis
  • PDGF + plasma ⇒ intimal smooth muscle hyperplasia ⇒ hyperplastic arteriolosclerosis ⇒ narrowing ⇒ ischemia
  • affected afferent arterioles ⇒ RAAS ⇒ HT
54
Q
  1. Vascular diseases of the kidney:

MALIGNANT NEPHROSCLEROSIS morphology + clinical features

A 
MORPHOLOGY:
  - normal/shrunken size
  - pinpoint petechial hemorrhages on cortical surface
  - fibrinoid necrosis
  - hyperplastic arteriolosclerosis
CLINICAL FEATURES:
  - increased BP ⇒ proteinuria + hematuria ⇒ renal failure
  - prognosis: 50% survive at least 5yrs
55
Q
  1. Vascular diseases of the kidney:

THROMBOTIC MICROANGIOPATHIES pathogenesis

A

PATHOGENESIS OF HUS:
- endothelial injury + activation ⇒ intravascular thrombosis + vasoconstriction ⇒ microangiopathy
- E.coli O156:H7 ⇒ shiga toxin ⇒ carried by neutrophils ⇒ renal glomerular epithelial cells
⇒ increased adhesion of leukocytes
⇒ increased endothelia production
⇒ loss of endothelial NO
⇒ endothelial damage
- toxin gains entry into cells ⇒ cell death
PATHOGENESIS OF TTP ( thrombotic thrombocytopenic purpura):
- aquired defect in proteolytic cleavage of vWF multimers (ADAMTS13)

56
Q
  1. Vascular diseases of the kidney:

THROMBOTIC MICROANGIOPATHIES morphology + clinical features

A

MORPHOLOGY:
- widespread thrombosis in microcirculation
- microangiopathic hemolytic anemia + thromocytopenia
CLINICAL FEATURES:
- HUS: sudden onset, bleeding manifestations, oliguria, hematuria, hemolytic anemia, neurological changes

57
Q
  1. Diabetic nephropathy:

DIABETIC NEPHROPATHY causes

A

= progressive kidney disease caused by angiopathy of capillaries + glomeruli
- nephrotic syndrome + diffuse GN
- result of DM
CAUSES:
- Non-enzymatic glycosylation: glucose ⇒ AAs ⇒ AGEs⇒ cross-links between polypeptides ⇒ net ⇒ entrap proteins ⇒ thick BM
- Hypercalcemia: ⇒ hyperosmolarity ⇒ overload of filtration ⇒ destroy filtration capacity
- increased synthesis of collagen 4 ⇒ increased BM

58
Q
  1. Diabetic nephropathy:

GLOMERULAR LESIONS

A
  1. Glomerular BM thickening:
    - thickened thought entire length, more porous ⇒ nephrotic syndrome
  2. Diffuse mesengial sclerosis:
    - increased mesangial matrix + proliferation + GBM thickening ⇒ nephrotic syndrome
    - age: >10yrs
  3. Nodular glomerulosclerosis:
    - ball like deposits in mesangium ⇒ Kimmelstriel-Wilson lesion
    - induce ischemia ⇒ granular cortical surface
59
Q
  1. Diabetic nephropathy:

RENAL VASCULAR LESIONS

A
  • renal atherosclerosis + arteriolosclerosis ⇒ macrovascular disease in diabetics
  • both afferent + efferent arterioles affected
60
Q
  1. Diabetic nephropathy:

PYELONEPHRITIS

A

= aute/chronic inflammation of kidneys, begins in interstitial tissue ⇒ affected tubules

  • acute: necrotizing papillitis (more in diabetics)
  • symptoms: micro- and macroalbuminemia + HT
  • may progress to end-stage renal disease
61
Q
  1. Acute tubular necrosis ATN:

CAUSES OF ACUTE RENAL FAILURE

A
  1. ATN
  2. glomerular disease + RPGN
  3. diffuse renal vascular disease
  4. acute drug induced interstitial nephritis
  5. diffuse cortical necrosis
62
Q
  1. Acute tubular necrosis ATN:

PATHOGENESIS

A

= damaged epithelial cells + acute suppression of kidney function

  • reversible renal lesion
  • causes: tubular injury or disturbance in blood flow
  • ischemia ⇒ structural change in epithelial cells ⇒ detach

⇒ loss of cell polarity ⇒ redistribution of membrane proteins ⇒ decreased Na+ reabsorption in proximal tubule ⇒ vasoconstriction through RAAS

⇒ further damage to tubules + debris ⇒ block urine outflow ⇒ increase pressure ⇒ decreased GFR

⇒ fluid can leak to interstitium ⇒ edema ⇒ compression ⇒ collapse of tubules ⇒ ATN

63
Q
  1. Acute tubular necrosis ATN:

TYPES

A
  1. Ischemic ATN:
    - shock ⇒ decreased O2 + substrate delivery to tubular cells
  2. Nephrotoxic ATN:
    - poisons (heavy metals, drugs, organic solvents) ⇒ necrosis of tubular cells
  3. Pigment ATN (crush syndrome):
    - pigment stuck in lumen ⇒ obstruction ⇒ increased pressure ⇒ leakage ⇒ collapse
    - pigments: hemoglobin and myoglobin
64
Q
  1. Acute tubular necrosis ATN:

MORPHOLOGY

A
  1. Ischemic + pigment:
    - segmental influence
    - damaged cells ⇒ fragmentation of BM
  2. Nephrotoxic:
    - proximal tubule
    - prognosis good (preserve BM)
65
Q
  1. Acute tubular necrosis ATN:

CLINICAL FEATURES

A
  1. Initiation (36h):
    - drop of urine output
    - increase urine creatine
  2. Maintenance (3-6d):
    - anuria
    - uremia + fluid overload
  3. Recovery:
    - increase in urine volume
    - electrolyte-balance disturbance (deranged tubular function)
    - urine volume normalizes
66
Q
  1. Tubulointerstitial nephritis:

TUBULOINTERSTITIAL NEPHRITIS

A

= group pf inflammatory diseases involving interstitium and tubules

  • usually caused bacterial infection ⇒ renal pelvis involved
  • non-bacterial TIN ⇒ interstitial nephritis
    • drugs
    • metabolic disorders
    • physical injury
    • viral infection
    • immune reaction
67
Q
  1. Tubulointerstitial nephritis:

ACUTE PYELONEPHRITIS pathogenesis + predisposing factors

A

= inflammation of lower and upper urinary tract due to bacterial infection
PATHOGENESIS:
- causative agents: E.coli, Klebsiella, Proteus, Enterobacter, Pseudomonas etc.
- hematogenous spread by septicemia or infective endocarditis embolism
- ascending infection from lower urinary tract
PREDISPOSING FACTORS:
- obstruction (e.g. stones, prostate hyperplasia)
- vesicouteral reflux
- catheters
- females more prone
- immunosuppression

68
Q
  1. Tubulointerstitial nephritis:

ACUTE PYELONEPHRITIS morphology + clinical features

A

MORPHOLOGY:
- yellow raised abscesses on renal surface ⇒ heals ⇒ fibrosis ⇒ flowerbed scar
- HISTO: suppurative necrosis/ abscess formation in parenchyma ⇒ rupture into tubules
CLINICAL FEATURES:
- sudden onset pain at costovertebral angle + infection symptoms
- pyuria, bacteruria
- bladder + urethral irritation
- benign + self-limiting ⇒ risk for chronic PN
DIAGNOSIS:
- leukocytes in urine by urine analysis + culture

69
Q
  1. Tubulointerstitial nephritis:

CHRONIC PYELONEPHRITIS

A

= end-stage kidney after several APN infections
TYPES:
1. Chronic obstructive PN
- obstruction ⇒ recurrent infection ⇒ scarring
2. Chronic reflux PN
- superimposition of UTI on congenital vesicoureteral reflux
- more in children
MORPHOLOGY:
- scar formation ⇒ contraction of parenchyma ⇒ flowerbed scar on surface

70
Q
  1. Tubulointerstitial nephritis:

ACUTE DRUG-INDUCED INTERSTITIAL NEPHRITIS

A 
= adverse reaction to drugs (e.g. diuretics, antibiotics, NSAIDS)
- HR type 1 or 4 
- infiltration of interstitium with eosinophils, lymphocytes, macrophages etc. ⇒ tubular necrosis
SYMPTOMS:
  - hematuria
  - leukouria
  - renal failure
  - increased size of kidneys
TREATMENT: withdraw drug
71
Q
  1. Tubulointerstitial nephritis:

ANALGESIC ABUSE NEPHRITIS

A
  • large amount of analgesics (painkillers) ⇒ chronic interstitial nephritis + renal papillary necrosis
    SYMPTOMS:
    • hematuria
    • chronic renal failure
72
Q
  1. Urinary outflow obstruction:

RENAL STONES consequenses + pathogenesis

A

= calculus formation at any level in urinary system
- familial predisposing factors
CONSEQUENCES:
- pyelonephritis due to stasis
- hydronephrosis
PATHOGENESIS:
- increased urine concentration ⇒ exceeds solubility in urine ⇒ precipitation
- lack of Tamm-Horsfall protein, nephrocalcin
- obstruction ⇒ intense pain, hematuria

73
Q
  1. Urinary outflow obstruction:

RENAL STONES types

A
  1. Calcium stone (Ca-oxalate, Ca-phosphate) 80%
    - hypercalcemia, hypercalcuria, hyperoxalemia
  2. Struvite stone (Mg-NH4-PO4) 10%
    ⇒ alkaline urine - UTIs
  3. Uric acid stone 6-7%
    ⇒ acidic urine
    - leukemia, gout
  4. Cysteine stone 1-2%
    ⇒ acidic urine
74
Q
  1. Urinary outflow obstruction:

HYDRONEPHROSIS general + pathogenesis

A

= dilation of renal pelvis and calyces + atrophy of parenchyma
- caused by obstruction to outflow of urine
* congenital
* aquired: foreign body, tumor, inflammation, neurogenic, pregnancy
PATHOGENESIS:
- obstruction ⇒ still filtration ⇒ renal interstitial ⇒ lymph + veins
- leads to dilation ⇒ increased pressure ⇒ compression of vasculature
- obstruction ⇒ inflammation ⇒ fibrosis

75
Q
  1. Urinary outflow obstruction:

HYDRONEPHROSIS morphology + clinical features

A

MORPHOLOGY:
- obstruction below ureters: bilateral ⇒ renal failure
- obstruction above ureters: unilateral
* subtotal: enlarged kidney, atrophy of parenchyma
* complete: decreased renal function
- hydroureter
CLINICAL FEATURES:
- bilateral complete: anuria
- bilateral incomplete: polyuria
- unilateral: silent
- with time irreversible

76
Q
  1. Tumors of kidney:

RENAL CELL CARCINOMA

A 
- derived from renal tubular epithelium ⇒ located in cortex
RISK FACTORS:
  - age (60-70yrs)
  - sex (men)
  - smoking
  - HT + obesity
  - hypercholesterolemia
  - polycystic disease due to chronic dialysis
MORPHOLOGY:
  - yellowish color, necrosis, hemorrhage, cystic degeneration
CLINICAL FEATURES:
  - painless hematuria
  - palpable abdominal mass
  - dull flank pain
  - paraneoplastic syndromes
METASTASIS:
  - renal vein ⇒ IVC ⇒ right heart
  - vertebrae, lung, bone, liver, brain
77
Q
  1. Tumors of kidney:

CLEAR CELL RENAL CARCINOMA

A
  • most common type
  • histo: cells with clear or granular cytoplasm
  • sporadic or familial ⇒ von Hippel-Lindau disease
    VHL:
    • AD disease
    • hemangioblastomas of cerebellum + retina
    • mutation in VHL gene on chr. 3p25
78
Q
  1. Tumors of kidney:

PAPILLARY RENAL CELL CARCINOMA

A
  • papillary growth pattern ⇒ multifocal and bilateral
  • familial or sporadic forms
    ⇒ MET proto-oncogene on chromosome 7
79
Q
  1. Tumors of kidney:

CHROMOPHOBE RENAL CARCINOMA

A
  • arise from intercalated cells of collecting ducts
  • cancer cells stain dark ⇒ blue cytoplasm + clear halo around nuclei
  • have loss in entire chromosome ⇒ chr. 1, 2, 6, 10, 13, 17, 21 ⇒ extreme hypodiploidy
  • good prognosis
80
Q
  1. Tumors of kidney:

WILMS TUMOR

A
  • children 2-5yrs
  • derived from mesoderm
  • 2 forms:
    1. epithelial cell differentiation
    2. stromal cell differentiation
      PATHOGENESIS:
      1. WAGR syndrome ⇒ WT1
      2. Denys-Drash syndrome ⇒ WT1
      3. Backwith-Wiedemann syndrome ⇒ WT2
      MORPHOLOGY:
      - large, solitary, well-circumscribed mass
      - soft, homogenous, tan-grey color
      - foci of hemorrhage, cystic degeneration, necrosis
      CLINICAL FEATURES:
      - palpable abdominal mass
      - fever, abdominal pain, hematuria, intestinal obstruction
81
Q
  1. Tumors of the urinary bladder and collecting system:

PREDISPOSING FACTORS

A
  • sex (men 3:1)
  • age (50-70yrs)
  • exposure to beta-naphtylamine
  • cigarette smoking
  • chronic cystitis
  • drugs
  • genetics (p16, p53, FGFR3)
82
Q
  1. Tumors of the urinary bladder and collecting system:

TUMOR CLASSIFICATION

A
  • rare benign papilloma
  • urothelial carcinoma
  • a group of papillary urothelial neoplasms of low malignant potential
  • in-situ stage of bladder carcinoma
83
Q
  1. Tumors of the urinary bladder and collecting system:

MORPHOLOGY

A
  1. Benign papilloma:
    - 0,2-1cm frond-like structures with delicate fibrovascular core covered by multilayered well-differentiated transitional epithelium
  2. Urothelial carcinomas:
    - papillary to flat
    - noninvasive to invasive
    - lowgrade to high grade
  3. In-situ stage of bladder carcinoma
84
Q
  1. Tumors of the urinary bladder and collecting system:

CLINICAL FEATURES

A
  • painless hematuria
  • usually arise in urinary bladder
  • tend to recur after surgical removal
  • cause urinary tract obstruction
  • low-grade shallow lesion has good prognosis
  • deep penetration 5yr survival: <20%

PATHOLOGY 2 (11 decks)

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