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Pathophysiology 4 > Renal: glomerular dzs, nephrotic, nephritic > Flashcards

Renal: glomerular dzs, nephrotic, nephritic Flashcards

1
Q

define glomerulopathies

A

significant cause of kidney disease

  • acute and chronic
  • group of diseases
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2
Q

Glomerulonephopathies can result from

A
  1. systemic inflammatory dz—>glomerulonephritis

2. non-inflammatory dzs–>metabolic dz–>DM, herediatary nephropathies like Alport’s

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3
Q

primary glomerulopathies occur where

A

kidney

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4
Q

secondary glomerulopathies occur

A

multisystem dz involving kidneys

–ex SLE

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5
Q

degree of proteinuria determisn?

A

if its nephrotic or nephritic

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6
Q

normal amt of protein in urine in 24 hrs?

A

100-200 mg/hr

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7
Q

how does protein get into the urine?

A
  • inflammation alters GBM (podocytes) permeability (normally resitricts things by size and charge…aka proteins)
  • incrs in GBM permeability= pore sizes enlarge and RBCs and protein can pass through
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8
Q

types of PU

A
  1. orthostatic or postural–>elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent posiiton
  2. overproduction
  3. tubular
  4. glomerular dysfunctino
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9
Q

nephritis versus nephrotic

  • define each
  • basic CM for each one
A

Nephritic=caused by systemic inflammation/ immune complex dz (SLE, vasculitis) or an infection
*inflammation in glomerulus=BLEEDING
*renal vascular changes that cause HTN
*Proteinuria <3,000
TYPES=post infectious glomerulonephropathy (post strep), IGA nephropathy, Memabnoproliferative

Nephrotic= damange to filterting mechanism–leading to protein wasting in urine—>protein waisitng causes decr serum protein (hypoproteinemia.MC seen as hypoalbuminemia),
*decr serum protein= causes HYPOTONIC surroundings–>so fluid flows OUT of HYPOtonic–>

  • EDEMA**
  • *liver tries to compensate by producing more proteins…. and in doing so makes more lipids too
  • Proteinuria >3,000
  • hypoproteinuria
  • hyperlipidemia

TYPES=minimal change dz, focal segmental glomerulura sclerosis, membranous nephropathy, DM nephropathy

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10
Q

greater degree of proteinuria=?

A

nephrotic

>3,000

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11
Q

injury to podocytes

A

nephrotic

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12
Q

inflammation causing enalrged pores and “leaky” glomeruluar BM

A

nephritic

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13
Q

describe the sediment for nephrotic

A

urine bands

urine >3,000 PU in 24/hrs

+lipidemia
+hyperlipidemia—>seen as oval fat bodies and maltese cross
+/- microscopic hematuria

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14
Q

describe urine sed for nephritic

A

“acitve”

  • hematuria
  • RBC casts
  • WBC casts
  • Proteinuria variable… <3,000 BUT over >1 gram
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15
Q

MC causes for transient PU

A

stessful conditions–>fever, exercise, CHF,

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16
Q

major causes of nephritic syndrome

A

auto-immune or allergic interstitial inflammation

heavy metal intoxications

drug-induced intersitial injury

17
Q

major causes of nephrotic syndrome

A

primary and secondary glomerular dzs
dm
htn

18
Q

typical clinical findings in a pt with nephrotic syndrome

A
  • **EDEMA (bc major loss of protein.. mainly albumin)
  • hyperlipidemia
  • hypoproteinemia-hypoalbuminemia
19
Q

define abnormal amt of PU

A

over 200 about

20
Q

Glomerulonephritis

-define

A

Inflammation/proliferation of glomerular tissue, scaring and fibrosis
-immune complexes (antigen/AB) form in ciruclation–>activation of compliment–>recruit and activate immune cells–>deposite in glomerulus–>cause damage to GBM, mesanial or capillary endothelium

ANTIGEN CAN BE TO:

  • ->glomerular antigens
  • ->glomerular BM
  • ->trapped as circulating immune complexes
  • ->cell mediated

**basically antigens/AB can be made directly against the GBM or there was an infection (strep) and those antigens/AB get trapped in glomerulus=inflammation

21
Q

mechanisms contributing to decline in GFR for glomerulonephritis

A
  • ***decr glomerular perfusion secondary to
    1. inflammation
    2. scarring/sclerosis
    3. thickening of glomerular basememt membrane with increased permeability to proteins and RBC
22
Q

causes of glomerulonephritis

A
  1. post infectious GN
  2. IgA nephropathy
  3. membranoproliferative glomerlunonephropathies (MPGN)
  4. Rapidly progresive crescentic GNs
23
Q

MCC of nephritic syndrome

A

IGA nephropathy

24
Q

Post-infectious Glomerulonephritis

  • mcc
  • other causes
A

MC etiologies= STREP 2nd to nephritic strain of B-hemolytic GAS
other causes= SKIN or respiratory sources, Hep B, Hep C, Malaria, Syphilis, HIV

25
Q

IgA Nephropathy

  • another name
  • explain
  • MC population and gender
  • etiology
A

Berger Dz

abnormal IgA immune complexes binds to glomerular mesangial cells–>cause injury
*IGA is first line defense in respiratory and GI secretions—so infections cause an OVERPRODUCTION which then damage kidneys

MC affects young males
**24-48 HOURS after URI or GI infection

26
Q

Membranoproliferative GN

  • mcc
  • typical lab finding and what it means
A

immune complex mediated

  • involves mesanigal cell proliferation and complement deposition
  • gives glomurli a lobular apperance due to mesangial proliferation
  • the GBM splits–> causing Tram tracking or double counter apperance on histology

ASSOC WITH HEP C—tx the hep c— MPGN goes away

27
Q

HUS Vasculitis

  • often asoc with
  • explina patho
A

HEMOLYTIC UREMIC SYNDROME

  • *e. coli diarrhea shiga-toxin
  • MCC of ARF in kids
  • complement dysregulation via gene mutations
  • antibodies to complement factor H

SECONDARY CAUSES
-infection: shiga toxin producing E. coli or strep pneumoniae or HIV

28
Q

Lupus GN

  • mc type
  • pu levels
A 
diffuse lupus nephritis class IV 
**alllllll over leads to progressive kidney dz

six types

PU mostly nephritic— but sometimes cna show nephrotic range

29
Q

rapidly progressive GN (RPGN)

  • characterized by?
  • types
A
  • crescent lesions–acute chronic or mixed
  • cresents form from fibrin and plasma potein despotiion collapsing the cresecent shape of bowmans capsule
  • crescents may be secondary to severe injury to glomerular capillary wall
  • severity of dz correlates to degree of crescents
  • ***ANY CAUSE OF AGN CAN PRESENT WITH RPGN–the following ONLY PRESENT WITH RPGN

TYPES

  1. anti-GBM–>goodpastures
  2. Pacui-immune–ANCA assoc vasculitis—> Wegners (granulomatosis polyangiitis and Microscopic polyangiitis
30
Q

Wegners aka Granulomatosis Polyangiitis

  • whart is it
  • (+) ???
  • classically involves what part of body
A

systemic vasculitis of MEDIUM AND LARGE size arteries
90% are ANCA (+)
—-> C-ANCA= 80%–> ANTI-PROTEINASE 3 ****
—-> P-ANCA=15%

involves–>upper and lower resps, kidneys

31
Q

microscopic polyangiitis

A

renal small vessel vasculitis
-usually renal limited
*abesence of granulmatosis inflammation—how to tell the difference on biopy b.w this and wegners
70%= P-ANCA

32
Q

Goodpastures

  • type of rxn
  • explain age distribution
A

Type 2 hypersensitivity—AB mediated

  • ***ANTIBODIES TO: type IV collagen in lungs and kidney
    1. anti-GBM—->GN (renal)
    2. anti-alveolar BM—>alveolar hemorrhage (pulm) —>hemoptysis

BIOMODAL age distribution—> 3rd and 6th decade of life (can presnt in 30s,,, and then again in 60s)

M»>F

33
Q

Nephrotic

  • cause thought to be secondary to?
  • primary etiologies
  • secondary etiologies
A

podocyte malfunction or injury

PRIMARY ETIOLOGIES

  1. membranous
  2. Focal Segmental Glomerular Sclerosis
  3. Minimal Change dz

SECONDARY ETIOLOGY:
4. Diabetic Nephropathy

34
Q

reason for hyperlipidemia in nephrotic syndrome

A

increased synthesis from liver and decreased catabolism

  • hepatic lipoprotein synthsis is stimulated by decreased oncotic pressure–>hypercholesterolemia
  • also acquired defect in LDL receptor that causes diminished clearance
  • incrs trigs due to decreased catabolism NOT overproduction
35
Q

why are PT at risk for thrombosis in nephrotic syndrome

A

-DVT, PE, renal vein thrombosis

-multifactorial etiology
*increase urinary loss of anti-thrombin III, protein C and S
*increased platelet aggregation
BUT BOTH CAN LEAD TO ANASARCA—– total body swelling

36
Q

minimal change dz

A

-loss of negative charge of basement membrane promotes proteinuria

KIDS*

T-lymphocyte abnormalities that lead to increased glom. permeability—> effacement of visceral epithelial foot processes

37
Q

membranous nephropathy

A

increased glomerular permeability and glomerulosclerosis
-idiopatic
or
-secondary forms

*circulating IGG against antigen PLA2R on GBM

38
Q

Focal Segmental glomerulosclerosis (FSGS)

-

A
  • idiopathic
  • primary
  • secondary
  • genetic

2nd to circulating factor toxic to the podocyte–can be adaptive
“FOCAL” bc involves some glomeruli but not others
“SEGMENTAL” bc involves a segment of glomerulus
NOT THE WHOLE GLOMERULUS THO

Pathophysiology 4 (8 decks)

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