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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
Glomerulonephritis (GN) definition
group of inflammatory diseases, heterogeneous pathogenesis, histology clinical manifestations and prognosis, which predominantly affecting or only the renal glomeruli, bilaterally
26
Pathogenesis of glomerulonephritis
 Do not fully known  Key role plays immunological mechanisms MECHANISMS PRIMARY = trigger the inflammatory process Humoral, cellular Secondary mechanisms = responsible glomerular injury
27
Diagnosis of glomerulonephritis
**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
RENAL BIOPSY Purposes
 definition of DIAGNOSIS  Assessment of PROGNOSIS  choice of THERAPY
29
Renal biopsy absolute contraindications
ABSOLUTE Bleeding diathesis Pz solitary Reni "small" Abnormalities of position Severe obesity Pz un cooperative
30
Relative biopsy contraindications
RELATive Arterial Hypertension Hypotension Cystic disease Kidney tumors Hydronephrosis Pyelonephritis
31
Complications of renal biopsy
Complications: Hematuria, perirenal hematoma, A-V Fistule
32
Classifications
**... 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
Proliferative Primary glomerulonephritis
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
Not proliferative primary glomerulonephritis
NOT proliferative GN to minimal lesions Focal glomerulosclerosis and segmental Membranous GN
35
Proliferative GN diffuse exudative (post-infectious) Histology, microscopy, imunofluorescence, electron microscopy
**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
Proliferative GN diffuse exudative (post-infectious) clinic
S. nephritic that occurs after 7-10 days after infection of the respiratory aerial or elsewhere.
37
Proliferative GN diffuse exudative (post-infectious) lab exams and prognosis
**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
GN mesangial deposits of IgA (GN Berger) **histology. microscopy, imunofluorescnece**
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
GN mesangial deposits of IgA (GN Berger) Clinic
Recurrent episodes of gross hematuria (usually after 1-2 days by an infectious episode); persistent hematuria; proteinuria of variable entity. Sometimes, hypertension arterial.
40
GN mesangial deposits of IgA (GN Berger) lab. exams, prognosis
**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
GN proliferative extra-capillary Histology MO, IF | (Rapidly progressive GN)
**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
GN proliferative extra-capillary (Rapidly progressive GN) Clinic
Rapid deterioration of renal function with oligo-anuria. Proteinuria variable, sometimes hematuria.
43
GN proliferative extra-capillary (Rapidly progressive GN) lab. exams, prognosis
**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
GN membrane-proliferative Histology MO, IF
**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
Membranoproliferative GN Clinic
Variable: S. Nephrotic or nephritic (+ freq. Type II)
46
Membranoproliferative GN lab. exams, prognosis
Lab exams. In both decreased C3 persistent. In Type I decreased C4 Prognosis Progression to uremia especially in Type II
47
Minimal change GN Histology MO, IF, EM
MO. Normal. Sometimes, mild mesangial proliferation IF. Negative ME Fusion of pedicels????
48
Minimal change GN Clinic
S. Nephrotic
49
Minimal change GN lab. exams.
C3 and C4 in the standard
50
Minimal change GN. prognosis.
``` Good if the response to immunosuppressive therapy is good (90% of cases) ```
51
Focal glomerulosclerosis Histology MO, IF
**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
Focal glomerulosclerosis. clinic.
**Clinic** S. Nephrotic. Sometimes, microscopic hematuria and arterial hypertension
53
Focal glomerulosclerosis. lab. exams.
C3 and C4 in the standard
54
Focal glomerulosclerosis. prognosis.
**Focal glomerulosclerosis. prognosis. ** Slow progression to uremia; possible remissions Spontaneous more or less long-lasting
55
focal glomerulosclerosis **MO, IF**
**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
Focal glomerulosclerosis. clinic.
S. Nephrotic. Sometimes, microscopic hematuria and hypertension arterial
57
Focal glomerulosclerosis Laboratory examinations.
**Laboratory examinations. ** C3 and C4 in the standard
58
Focal glomerulosclerosis. prognosis.
Slow progression to uremia; possible remissions Spontaneous more or less long-lasting
59
Membraneous GN Prognosis.
**Prognosis. ** Frequent spontaneous remissions with possible consequences. Progression to uremia or persistence of proteinuria
60

nefrologia (6 decks)

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