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patho II > Renal I(a) > Flashcards

Renal I(a) Flashcards

1
Q

Causes of Nephritic Syndrome

A
  • Children: IgA Nephropathy, Post-streptococcal GN, etc.
  • Adults: Membrano-Proliferative GN-I and -II, Rapidly
    Progressive (Crescentic) GN, SLE or Lupus Nephritis, etc.
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2
Q

Clinical Manifestations of Nephritic vs Nephrotic Syndrome.

A

Note : there is proteinuria and oedema in Nephritic however it’s mild

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3
Q

Primary Causes of Nephrotic Syndrome

A
  • Minimal Change Nephropathy (children)
  • Focal segmental Glomerulosclerosis
  • Membranous Nephropathy, etc.
  • Membrano-proliferative Glomerulonephritis
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4
Q

secondary causes of Nephrotic Syndrome

A
  • Diabetes Mellitus
  • Lupus Erythematosus
  • Viral infections, etc.
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5
Q

Clinical manifestations of Rapidly Progressive Glomerulonephritis

* Type of Nephritic Syndrome

A

1) Microscopic haematuria &
2) dysmorphic (spiked shape) RBC and RBC casts
3) Mild to moderate proteinuria

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6
Q

Causes of Acute Kidney disease

A
  • Glomerular injury (Rapidly Progressive GN)
  • Vascular injury (Thrombotic Micro-Angiopathy)
  • Interstitial injury
  • Acute tubular injury

Thrmobotic micro-angio –> injury to the small vessles

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7
Q

CM of Acute Kidney disease

A

1) Oliguria (low urine) or anuria (no urine)
2) Recent onset of azotaemia

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8
Q

Causes of Chronic Kidney Disease (Chronic Renal Failure)

A

1) Diabetes Mellitus
2) Hypertension
3) Glomerulonephritis

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9
Q

CM of Chronic Kidney Disease (Chronic Renal Failure)

A
  • High blood pressure –> CHF
  • Prolonged symptoms and signs of uraemia (lethargy, pericarditis, encephalopathy)
  • Hyperkalaemia –> Fatal cardiac arrhythmias
  • Fluid volume overload –> Pulmonary oedema

chronic –> affects the heart

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10
Q

CM of Urinary Tract Infection

A
  • Bacteriuria
  • Pyuria (puss in urine)
  • Pyelonephritis (kidney inflammation)
  • Cystitis (inflammation of the bladder)
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11
Q

*

CM of Nephrolithiasis

A
  • Renal colic (obstruction of urine flow –>pain in the kidney area)
  • Haematuria, without RBC casts
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12
Q

Causes of Podocyte injury

A
  • Abs against podocyte Ags
  • Toxins and Circulating factors
  • Mutations in structural components of slit diaphragm
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13
Q

Morphologic changes:
* Effacement (thinning) of foot processes
* Vacuolisation
* Retraction and detachment of cells from the GBM

of?

* Vacuolisation –> normally indicates exposure to pathogens

A

Podocyte Injury

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14
Q

CF of Podocyte Injury

A

Proteinuria

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15
Q

Compensatory mechanism of Nephron Loss?

* Nephron loss –> work overload on the remaining nephrons

A

Hypertrophy of the remaining glomeruli (not destroyed by the initial renal disease)

* cause? podocyte injury/ capillary obliteration

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16
Q

————- : thickening and sclerosis of arterial
walls and the renal changes associated with benign hypertension

A

Arterionephrosclerosis

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17
Q

patho of Arterionephrosclerosis

A

Two processes participate in the arterial lesions:
1) Medial and intimal thickening, as a response to haemodynamic changes, aging and genetic defects
2) Hyaline deposition in arterioles, caused by:
a. Extravasation of plasma proteins
b. Increased deposition of basement membrane matrix

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18
Q

Macroscopic Features:
* Symmetrical atrophy of the kidneys
* Diffuse fine granularity of the renal surface

Microscopic Findings:
* Hyaline Arteriolosclerosis
* Lumen narrowing of the affected vessels
* Ischaemic atrophy of all renal structures

Severe cases: tubular atrophy, scleroting glomerulus

Features of?

A

Arterionephroscleoris

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19
Q

CF of Arterionephrosclerosis

A
  • Loss of concentrating ability or diminished GFR
  • Mild degree of proteinuria
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20
Q

causes of MALIGNANT HYPERTENSION?

A

Appearance either de novo or with a sudden onset in patients with pre-existing mild hypertension

* de novo –> ‘from the beginning’

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21
Q

patho of MALIGNANT HYPERTENSION:
* Long-standing hypertension –> Injury to the arteriolar walls –> i. ——-,———-,———–> Fibrinoid necrosis of vessels —> (————) -> Increased narrowing of the arteriolar lumen –> Marked —— changes of the kidneys
* Renal ischaemia –> Further, Renin secretion (“———-”) -> Elevated ——— levels –> Salt retention -> Aggravation of blood pressure

A
  • Long-standing hypertension –> Injury to the arteriolar walls –> i. increased permeabilty, endothelial injury and platelet deposition–> Fibrinoid necrosis of vessels —> (Hyperplastic Arteriolosclerosis) -> Increased narrowing of the arteriolar lumen –> Marked ischaemic changes of the kidneys
  • Renal ischaemia –> Further, Renin secretion (“vicious cycle”) -> Elevated Aldosterone levels –> Salt retention -> Aggravation of blood pressure
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22
Q

Macroscopic features:
- Multiple small, pin-point petechial haemorrhages (on the kidneys)
- Flea-bitten Kidney

Microscopic features:
- Hyperplastic Arteriolosclerosis (Onion skin lesions)
- Fibrinoid Necrosis of Afferent Arteriole

A

Malignant HTN

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23
Q

————– : Disorders characterised by fibrin thrombi in glomeruli and small vessels, resulting in acute renal injury

A

Thrombotic Microangiopathies

24
Q

causes of Thrombotic Microangiopathies

A
  • Childhood Haemolytic Uraemic Syndrome: Intestinal infection with Shiga toxin-producing E. coli; 75% of cases
  • Adult Haemolytic Uraemic Syndrome:
  • Typical form (epidemic with diarrhoea) -> Shiga-like toxin
  • Atypical forms <> Excessive, inappropriate activation of complement by the alternative pathway
  • Thrombotic Thrombocytopenic Purpura: Defects in vWF <> Pathogenic auto-Abs directed against ADAMTS 13 (acquired) or mutations in the ADAMTS 13 gene (inherited)

* vWF (von Willebrand factor) -> clotting protein

25
Q

Light Microscopy:
* Fibrin thrombi in the glomeruli, arterioles and larger arteries
* Possible, presence of cortical necrosis

Electron Microscopy:
* Widening of the sub-endothelial space, in glomerular capillaries
* Duplication or splitting of GBMs
* Lysis of mesangial cells -> Mesangial break-down

Features of?

A

Thrombotic Microangiopathies

26
Q

CF of Thrombotic Microangiopathies

A

Sudden onset, after a GI or Flu-like prodromal episode, of:
* Haematemesis
* Melena
* Severe Oliguria
* Haematuria
* Micro-Angiopathic Haemolytic Anaemia

27
Q

Thrombotic Microangiopathies progresses into ———— , in children

A

Acute Kidney Injury

28
Q

prognosis of thrombotic Microangiopathies

A

25% of children –> Development of renal
insufficiency, as a consequence of the secondary scarring

29
Q

Macroscopic Features:
* Symmetrical contraction of the kidneys
* Red-brown and diffusely granular surfaces

Microscopic Findings:
* Advanced scarring and sclerosis of the glomeruli
* Marked interstitial fibrosis
* Atrophy and loss of renal tubules
* Thick-walled and stenosed small- and medium-sized arteries
* Lymphocytic infiltrates

Features of?

A

Chronic kidney disease

30
Q

progression of Chronic Kidney disease

A

End-stage Kidney Disease (sclerosing of all renal structures)

31
Q

Prognosis of Chronic kidney disease:
If not treated, either with dialysis or transplantation –>

A

Death from Uraemia (accumulation of toxins in the blood)

32
Q

Patho of Nephrotic Syndrome
* physicochemical alterations in capillary walls of the glomeruli –> ———-
* Long-standing proteinuria –>———- -> Sever ———
* Hypo-Albuminaemia –> Increased synthesis of lipoproteins and Impairment of peripheral break-down of lipoproteins. -> —–
* Increased permeability of GBM to lipoproteins –> ———

A
  • physicochemical alterations in capillary walls of the glomeruli –> Proteinurea (Severe)
  • Long-standing proteinuria –>Hypoalbunaemia -> Sever Oedema
  • Hypo-Albuminaemia –> Increased synthesis of lipoproteins and Impairment of peripheral break-down of lipoproteins. -> Hyperlipidaemia
  • Increased permeability of GBM to lipoproteins –> Lipiduria
33
Q

Epi of Minimal-Change disease

* Type of Nephrotic Syndrome

A

Most common cause of Nephrotic
Syndrome in children (1-7 years)

34
Q

Light microscopy
* Normal appearance of the glomeruli
* Protein droplets and lipids within the PCT -proximal convoluted tubules

Electron microscopy (Masson’s trichrome dye)
* Flattening of podocytes’ cytoplasm -> effacement (d.t cytokine damage)
* Epithelial cell vacuolisation
* Microvillus formation
* Focal detachments

Features of?

A

Minimal change disease

35
Q

CF of Minimal change disease

* Type of Nephrotic syndrome

A

1) Insidious (slow) onset of Nephrotic Syndrome
2) Albumin selective proteinuria

36
Q

Macroscopic Features:
* Involvement of some of the glomeruli (focal); initially only the juxta-medullary glomeruli -> With disease progress, all cortical levels

Microscopic Findings:
* segmental glomerular lesions
* Increased mesangial matrix
* Obliterated capillary lumina
* Deposition of hyaline (hyalinosis)
* Foamy (lipid-laden) macrophages
* IF: Non-specific trapping of IgM and complement (C1,C3)
* EM: Effacement of podocytes’ foot processes; similar to Minimal Change Disease

Features of?

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)

* ass. w/ HIV and sickle cell disease

37
Q

Association of FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)

A
  • In association with HIV, sickle cell disease
  • Secondary event in other forms of GN (e.g. IgA Nephropathy)
  • Inherited or congenital forms; Association of
    autosomal dominant forms with mutations in
    cytoskeletal proteins and podocin
38
Q

CF of focal segmental Glomerulosclerosis

A
  • Hypertension and haematuria (FSGS>MCD)
  • Non-selective proteinuria
39
Q

progression/ prognosis of Focal Segmental Glomerulosclerosis

A

 Development in 50% of patients –> End-Stage Renal Disease
 Children better prognosis than adults

40
Q

Primary/ secondary Causes of Mebranous Nephropathy

*Type of Nephrotic syndrome

A

Primary: Auto-Abs that cross-react with
Ags on podocytes (80% of cases)

Secondary to other disorders, such as:
- Infections (Chronic Hepatitis B and C, Syphilis, etc.)
- Malignancies (e.g. Carcinoma of the Lung and Colon, Melanoma, etc.)
- SLE and other Autoimmune Diseases (e.g.Thyroiditis)

41
Q

Patho of Membranous Nephropathy:

diffuse thickening of the —– and —- caused by subepithelial immune deposits -> Activation of the Complement –> ———— –> Damage of the mesangial cells and ——- –> Loss of slit filter integrity -> ——-

A

diffuse thickening of the glomerular capillary wall and GBM caused by subepithelial immune deposits -> Activation of the Complement –> C5b-C9 Membrane Attack Complex (MAC) –> Damage of the mesangial cells and podocytes –> Loss of slit filter integrity -> Proteinuria

42
Q

**

Microscopic Findings:
Light microscopy: Uniform, diffuse thickening of the glomerular capillary wall and BM
IF: Granular deposits of IgG and complement (C5b-C9 -MAC) along the GBM

Electron microscopy:
* Characteristic “spike and dome” appearnace of sub-epithelial deposits
* Irregular dense deposits of immune complexes , deposition between the BM and the overlying epithelial cells
* Effacement of podocytes’ foot processes

A

MEMBRANOUS NEPHROPATHY

43
Q

CF of Membranous Nephropathy

A
  • Insidious onset of Nephrotic Syndrome (most cases)
  • Non-selective proteinuria
  • Haematuria and mild hypertension (15-35% of cases)
44
Q

Progression and Prognosis of Membranous Nephropathy

A
  • Persistent proteinuria (>60% of cases)
  • Progressive disease leading to Renal Failure, after 2 to 20 years (40% of cases)
  • Partial or complete remission (disappearnace) of proteinuria (10-30% of cases)
45
Q

**

MPGN-1 vs Dense Deposit disease

A
46
Q

Microscopic features:
Light microscopy:
* “Double-contour” or “Tram-track” appearance of the glomerular capillary wall.
* “Splitting” of GBM

IF: IgG and early complement components.
EM: Discrete sub-endothelial electron-dense deposits.

features of?

A

Membrano-Proliferative GN type 1

47
Q

Microscopic Findings (Electron & Fluorescence Microscopy):
* Deposition of dense material of unknown composition (EM)
* Presence of C3 in irregular granular or linear foci in the BM and as mesangial rings in the mesangium (IF)
* Absence of IgG and early complement components (IF)

Features of?

A

Dense Deposit disease

48
Q

Common Histopathological Findings among disorders associated with the development of Nephritic syndrome

A
  1. Cellular Proliferation within the glomeruli
  2. Leukocytic inflammatory cell infiltrates –> Damage of the capillary walls–> Passage of blood into the urine (Haematurea) –> Haemo-dynamic changes –> Reduction in the GFR -> Oliguria and Azotaemia, as well as fluid retention (mild oedema) –> increased BP (HTN)
49
Q

Cause Post-Streptococcal GN

* type of Nephritic Syndrome

A

~ 2-4 weeks after infection w/ certain “Nephritogeninc” strains of group Α,β-heam. Streptoc.
(infection of pharynx or skin)

* most common in children

50
Q

**

Microscopic Findings:

  • LM:Glomeruli enlarged and Hypercellular
    (in a diffuse pattern : Leukocytic infiltration [neutrophils and monocytes, Proliferation of endothelial and mesangial cells, Crescent formation (severe cases)]
  • EM: Subepithelial IC “humps”
  • IF: Scattered granular appearance “lumpy hump” due to IgG, IgM, and C3 deposits within GBM walls and mesangium

Features of?

A

Acute Post-streptococal Glomerulonephritis

51
Q

CF of Acute Post-Infectious Streptococcal GN

A

Abrupt onset of:
* Malaise
* Slight Fever
* Nausea
* Oliguria and Haematuria (smoky or cola-coloured urine)
* HTN
* Peripheral and periorbital oedema
* Mild Proteinuria

52
Q

Lab findings of ACUTE POST-INFECTIOUS
(POST-STREPTOCOCCAL) GN

A
  • +ve strep titers (Elevated anti-Streptolysin O Ab-titers)
  • ↓ complement levels (C3) due to consumption (during the active phase)
53
Q

prognosis and progression of Acute post-strep GN

A
  • >95% of children –> Total recovery, with
    conservative treatment
  • <1% of children –> Development of Rapidly
    Progressive Glomerulonephritis
  • 15-50% of adults –> Development of End-Stage
    Renal Disease     in the next years
54
Q

The localisation of Ag, Ab or immune complexes
determines the glomerular injury response:
* Deposits in endothelium or sub-endothelium –> [Inflammatory/ non-inflammatory reaction]?

A

Inflammatory rxn in the glomerulus with leukocyte infiltrates and proliferation of glomerular resident cells

55
Q

The localisation of Ag, Ab or immune complexes
determines the glomerular injury response:
* Abs directed to sub-epithelial region of glomerular capillaries [Inflammatory/Non-inflammatory reaction]

A

Non-inflammatory rxn

patho II (29 decks)

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