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Glomerulonephritis 1 Flashcards

1
Q

Hematuria

A

Hematuria = PRESENCE OF ABNORMAL
RBS in the urine

Under physiological conditions, a healthy person eliminates
the urine about 1-2 erythrocytes per field
microscopic.

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2
Q

Hematuria classification

A

Macroscopic, microscopic

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3
Q

Macrohematoruia, origin, what is not

A

Macrohematuria = emission of red urine

The color of the urine
-does not depend on the extent of haematuria
 may be indicative of origin:
dark red -> kidney 
bright red-> lower urinary tract
Macrohematuria is not equal to: Hemoglobinuria, Myoglobinuria, Pseudoematuria
(Bile pigments, urate, porphyrins, drugs)

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4
Q

Methods to asses the presence of microscopic hematuria

A

Methods to assess the presence
of microscopic hematuria:
 TEST STRIPS
Very sensitive but not very specific

URINARY SEDIMENT
Very sensitive and very specific

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5
Q

types of hematuria by time

A

transitory and persitent

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6
Q

Transitional hematuria

A

Hematuria TRANSITIONAL
is quite frequent
 causes:

  • fever
  •  exercise
  •  trauma

 normally has little clinical significance, especially
if it is associated with other signs or symptoms

 may be the only manifestation of a
cancer of the urinary tract

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7
Q

Persistent hematuria origin types

A
  • glomerular
  • non glomerular origin.
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8
Q

first tree parameters of glomerular/not glomerular diagnostic comparison

A

Color
glomerular: Dark red (Coca Cola)
non-glomerular: Bright red (Washing meat)
Appearance of red blood cells
glomerular: Dysmorphic
non-glomerular: Not dysmorphic

Cylinders
glomerular: Present
_non-glomerular: _Absent

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9
Q

other two parameters of glomerular/not glomerular diagnostic comparison

A

Proteinuria
glomerular:> 500 mg / day
non-glomerular:<500 mg / day
Symptomatology
associated
_glomerular:_Hypertension, decreased GFR,
edema
_non-glomerular:_Pain, leucocyturia,
disorders
urination

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10
Q

Causes of hematuria of glomerular origin

A

• Glomerulonephritis primitive
GN mesangial deposits of IgA
GN acute post-infectious
GN membrane-proliferative
• Glomerulonephritis secondary
GN lupus
Cryoglobulinemia
Vasculitis
•** Syndrome diAlport
• Illness of thin membranes
• cystic kidney diseases
• persistent isolated microscopic hematuria**

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11
Q

Causes of hematuria of non-glomerular origin

A
  • KIDNEY (pyelonephritis)
  • ureteral (trauma)
  • urethral (stenosis)
  • bladder (cystitis)
  • prostate (neoplasm)
  • systemic (bleeding disorders)
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12
Q

physiological conditions concerning the release of protein

A

In physiological conditions:

 the glomerular ultrafiltrate contains a high
amount of protein, predominantly low MW.

 these proteins are almost completely
reabsorbed tubularly

WITH URINE are excreted
About 150 mg / 24 hours PROTEIN

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13
Q

Proteinuria definition, conditions for non pathological proteinuria

A

PROTEINURIA = EXCRETION of urinary protein > 150 mg / 24HH.

In the case of:  fever
 exercise
 orthostatic

it is possible to observe an increase in proteinuria
transient and modest, NON PATHOLOGICAL

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14
Q

Methods to determine proteinuria

A

• REACTIVE Stick
Dosage semi-quantitative
Sensitive for albumin
Not very sensitive to other proteins

Measuring quantity of proteins

ON TIMED COLLECTIONS ON SAMPLE OFFHAND

(Report Proteinuria / creatinine)
Turbidimetric or colorimetric methods
Very sensitive

Measuring dose of every protein

  • *Microalbuminuria (RIA)**
  • *IgG, Transferrina, alfa2microglobulina, ecc. (Nefelometrico) **
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15
Q

MICROALBUMINURIA

A

MICROALBUMINURIA
Urinary excretion of albumine

Measured by radioimmunoassay

VN = 30-300 mg / 24h
20-30 microg / min
NB: these values ​​are below the threshold
sensitivity of quantitative methods

The microalbuminuria is a marker of cardiovascular risk, renal, endothelial damage

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16
Q

cause of glomerular, tubular, hyperflow proteinuria

A

Cause

Glomerular:Alteration of
glomerular barrier

Tubular: Damage tubulo-
interstitial

Hyperflow:High concentration
plasma of a
pathological protein

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17
Q

Pahogenesis of glomerular, tubular, hyperflow proteinuria

A

Pathogenesis
glomerular:
Increased
permeability
the glomerular
protein

tubular:
Inability to
reabsorb proteins
normally filtered

hyperflow:
Glomerular filtration
beyond the capacity of
reabsorption
tubule

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18
Q

Proteins excreted of glomerular, tubular and hyperflow proteinuria

A

Proteins
excreted
Glomerular
Albumin
High protein PM
(IgG, transferrin)

Tubular
Low protein PM
(alfa-2
microglobulin,
lysozyme)

hyperflow
Pathological protein
(Chains K or lambda)

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19
Q

Patology of glomerular, tubular and hyperflow proteinuria

A

Pathology
Glomerular:Glomerulopathies
Tubular:
Nephritis tubulo-
interstitial

Hyperflow:

Paraproteinemie

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20
Q

Glomerular proteinuria
when?

A

one of the main clinical manifestations of the damage of the glomerular barrier which is realized in the case of:

  • Glomerulonephritis
  • Diabetic nephropathy
  • Arterial hypertension
  • AMYLOIDOSIS
  • Gestosis
  • Acute rejection
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21
Q

GLomerular syndromes

A

Glomerular syndromes

 PERSISTENT urinary anomalies
Nephritic syndrome
GN RAPIDLY PROGRESSIVE
SYNDROME NEPHROTIC

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22
Q

Persistent urinary faults

A

Persistent urinary faults

  • Proteinuria <1.0-1.5 g / 24h isolated or associated with microhematuria
  • Normal renal function
  • Absence of symptoms
  • Sometimes hypertension
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23
Q

Nephritic syndrome

A

Acute onset of:

  • Gross hematuria
  • Proteinuria <3g / 24h
  • Reduction of glomerular filtration rate
  • Decreased excretion of urine (sometimes up all’oligo-anuria)
  • Hypertension
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24
Q

Nephrotic syndrome clinic, complications

A
  • Proteinuria> 3g / 24h
  • Hypoalbuminemia and dysproteinaemias
  • Dyslipidemia (hypertriglyceridemia, hypercholesterolemia)
  • Generalized edema
  • Dyslipidemia (hypertriglyceridemia, hypercholesterolemia)

COMPLICATIONS: Hypovolemia, thrombosis, infections

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25
Q

Glomerulonephritis (GN)
definition

A

group of inflammatory diseases,
heterogeneous pathogenesis, histology
clinical manifestations and prognosis, which
predominantly affecting or
only the renal glomeruli,
bilaterally

26
Q

Pathogenesis of glomerulonephritis

A

 Do not fully known

 Key role plays immunological mechanisms

MECHANISMS PRIMARY = trigger the inflammatory process

Humoral, cellular
Secondary mechanisms = responsible glomerular injury

27
Q

Diagnosis of glomerulonephritis

A

SUSPECT glomerular injury
• hematuria of glomerular origin
• Proteinuria isolated persistent
• S. Nephritic
• S. Nephrotic
• Iradi rapid onset and of unknown origin
**then do **

  • HISTORY, objective examination
  • LABORATORY TESTS: routine, IgG-AM, C3-C4, Autoantibodies
  • renal sonography
  • *then if needed**

biopsia renale

28
Q

RENAL BIOPSY
Purposes

A

 definition of DIAGNOSIS
 Assessment of PROGNOSIS
 choice of THERAPY

29
Q

Renal biopsy absolute contraindications

A

ABSOLUTE
Bleeding diathesis
Pz solitary
Reni “small”
Abnormalities of position
Severe obesity
Pz un cooperative

30
Q

Relative biopsy contraindications

A

RELATive
Arterial Hypertension
Hypotension
Cystic disease
Kidney tumors
Hydronephrosis
Pyelonephritis

31
Q

Complications of renal biopsy

A

Complications:
Hematuria, perirenal hematoma, A-V Fistule

32
Q

Classifications

A

… On the basis of the pathogenesis
 GN PRIMITIVE= Glomerular lesions isolated
 GN SECONDARY = Glomerular lesions due to
other pathology well defined

… Depending on the extent of damage
 FOCAL = Only some glomeruli
WIDESPREAD = All (or most) glomeruli
SEGMENTAL = Only a part of each glomerulus
 GLOBAL = Whole glomerulus

33
Q

Proliferative Primary glomerulonephritis

A

Primary GN are divided based on histopathological criteria to proliferative and non-proliferative

Proliferative
Proliferative GN exudative
widespread (post-infectious)
GN mesangial deposits of IgA
(Berger)
Proliferative GN extracapillary
(Rapidly progressive)
GN membrane-proliferative

34
Q

Not proliferative primary glomerulonephritis

A

NOT proliferative
GN to minimal lesions
Focal glomerulosclerosis and
segmental
Membranous GN

35
Q

Proliferative GN diffuse exudative (post-infectious)
Histology, microscopy, imunofluorescence, electron microscopy

A

Microscopy
increased Volume glomeruli;
X hypercellularity and mesangial proliferation endocapillar
x inflammatory cell infiltrates

imunofluorescence
Sub-epithelial and mesangial deposits of IgG and C3
Electron microscopy
Huge deposits sub-epithelial

36
Q

Proliferative GN diffuse exudative (post-infectious)
clinic

A

S. nephritic that occurs after 7-10 days after infection of the respiratory aerial or elsewhere.

37
Q

Proliferative GN diffuse exudative (post-infectious)
lab exams and prognosis

A

**Lab. exam. **

highly decreased C3 (for 3-8 wk.)
Prognosis
Good in childhood; in adults in 50% of cases evolves
to Chronic renal injury

38
Q

GN mesangial deposits of IgA (GN Berger)
histology. microscopy, imunofluorescnece

A

GN mesangial deposits of IgA (GN Berger)
**Microscopy **
And focal segmental mesangial proliferation with increased of the matrix. In more severe forms: areas of sclerosis, fibrinoid necrosis or crescents
Imunofluorescence
Diffuse mesangial deposits (also in the glomeruli
apparently unharmed) of IGAE C3 and, sometimes, IgG and IgM.

39
Q

GN mesangial deposits of IgA (GN Berger)
Clinic

A

Recurrent episodes of gross hematuria (usually after 1-2 days by an infectious episode); persistent hematuria; proteinuria of variable entity. Sometimes, hypertension arterial.

40
Q

GN mesangial deposits of IgA (GN Berger)
lab. exams, prognosis

A

**Lab. exams. **
increased serum IgA (in 50% of cases), C3 and C4 in the standard

Prognosis
20-50% of cases: Chronic renal injury after 20 years.

41
Q

GN proliferative extra-capillary

Histology MO, IF

(Rapidly progressive GN)

A

Histology MO
Epithelial proliferation with crescents> 50% of glomeruli
In Type II endotelial proliferation

IF
Type I: linear deposits of IgG (in cigarette smoke) along MB
Type II: deposits sub-endothelial and mesangial IgG and C3
Type III: negative

42
Q

GN proliferative extra-capillary
(Rapidly progressive GN)
Clinic

A

Rapid deterioration of renal function with oligo-anuria.
Proteinuria variable, sometimes hematuria.

43
Q

GN proliferative extra-capillary
(Rapidly progressive GN)

lab. exams, prognosis

A

Exams lab.
high decrease of C3 in Type II, ANCA+ in Type III

Rapid progression to uremia in case of poor response to therapy

44
Q

GN membrane-proliferative

Histology MO, IF

A

MO
Type I: mesangial proliferation with wall thickening
capillary aspect “track”.

Type II: mesangial proliferation; Diffuse thickening MB with aspect “scalloped”.
IF
Type I: sub-endothelial deposits of C3, IgG, IgM, C4 and C1q
Type II: C3 linear long-MB and granular in the mesangium

45
Q

Membranoproliferative GN Clinic

A

Variable: S. Nephrotic or nephritic (+ freq. Type II)

46
Q

Membranoproliferative GN lab. exams, prognosis

A

Lab exams.
In both decreased C3 persistent. In Type I decreased C4

Prognosis
Progression to uremia especially in Type II

47
Q

Minimal change GN
Histology MO, IF, EM

A

MO. Normal. Sometimes, mild mesangial proliferation

IF.
Negative

ME
Fusion of pedicels????

48
Q

Minimal change GN Clinic

A

S. Nephrotic

49
Q

Minimal change GN lab. exams.

A

C3 and C4 in the standard

50
Q

Minimal change GN. prognosis.

A 
Good if the response to immunosuppressive therapy
is good (90% of cases)
51
Q

Focal glomerulosclerosis

Histology MO, IF

A

Histology MO

Segmental sclerosis
Mesangial proliferation, Adhesions floc-capsular, <20-50% of glomeruli
IF
Deposits of IgM and C3 in the areas of sclerosis

52
Q

Focal glomerulosclerosis. clinic.

A

Clinic
S. Nephrotic. Sometimes, microscopic hematuria and arterial hypertension

53
Q

Focal glomerulosclerosis. lab. exams.

A

C3 and C4 in the standard

54
Q

Focal glomerulosclerosis. prognosis.

A

**Focal glomerulosclerosis. prognosis. **
Slow progression to uremia; possible remissions
Spontaneous more or less long-lasting

55
Q

focal glomerulosclerosis MO, IF

A

Histology MO
Segmental sclerosis
Mesangial proliferation
Adhesions floc-capsular

<20-50% of glomeruli

IF
Deposits of IgM and C3 in the areas of sclerosis

56
Q

Focal glomerulosclerosis. clinic.

A

S. Nephrotic. Sometimes, microscopic hematuria and hypertension arterial

57
Q

Focal glomerulosclerosis
Laboratory examinations.

A

**Laboratory examinations. **
C3 and C4 in the standard

58
Q

Focal glomerulosclerosis. prognosis.

A

Slow progression to uremia; possible remissions
Spontaneous more or less long-lasting

59
Q

Membraneous GN Prognosis.

A

**Prognosis. **
Frequent spontaneous remissions with possible consequences.
Progression to uremia or persistence of
proteinuria

60
Q
A

nefrologia (6 decks)

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