5/6 Chronic Glomerulonephritis Flashcards Preview

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Flashcards in 5/6 Chronic Glomerulonephritis Deck (28)
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what are the classification of chornic glomerulonephrtis ?

minimal change disease = mostly in children

measngioproliefartive glomerulonephritis IgM

focal and segmnetal sclerosis and hyalinosis

mebranous glomerulonephrtis

idiopathic IgA berger = NEPHRITIC


what is the diagnosis of minimal change disease ?

nephrotic syndrome =SELECTIVE ALBUMINUREA WITHOUT evidence of hypertension and hematuria - the only one with selective


renal function is preserved

no changes when viewing kidney biopsy specimens under light microscopy,

Under immunofluorescence, there are no immunoglobulins or complement deposits

= hence minimal change disease

electron microscopy =
hallmarks of the disease were discovered.
diffuse loss of visceral epithelial cells foot processes podocyte effacement,
vacuolation, and growth of microvilli on the visceral epithelial cells, allowing for excess protein loss in the urine


etiology of minimal change disease ?

unknown - idiopathic


clinical presentation of minimal change disease ?

nephrotic syndrome

swellings that often occur suddenly, most prominent in the morning, initially covering the eyelids and the face, and later on spreading across the limbs, in the sacral region and can generalize to anasarca with leak in the body cavities.

abdominal discomfort due to ascitis , diarrhea

edema of scrotum

increased tendency for infection and thrombotic events


what is the treatment for minimal change disease

everything for nephrotic syndrome

albumin infusion


high dose methyl prednisolone replaced by by oral prednisolone
= good reposes then we taper it

if not effective add
cyclophosphamide/ cyclosporin - monitoring of bone marrow and gonadal toxicity

high dose of immunovenin if still not responsive


ACE inhibitors to reduce protein



direct and indirect anticoagulants

iv heparin , the end of the month switched to indirect anticoagulant (dabigartan)


mesangioproliferative glomerulonephritis is classified as a ?

type 2 lupus nephritis


what is the pathophysiology of mesangioproliferative GN?

Mesangial use endocytosis degrade circulating immunoglobulin.

This normal process stimulates mesangial cell proliferation and matrix deposition.

Therefore, during times of elevated circulating immunoglobulin (i.e. lupus / IgA nephropathy) increased number of mesangial cells and matrix

we can also find but not necessary to find IgM and C3 deposits in the mesangium which is why the disease is also called igm nephorpathy


what is the diagnosis of mesangioproliferatve glomerulonephritis ?

immunoflorecence - igm and c3 deposits in mesangium

LM - varied mesangial proliferation affecting ALL glomeruli to the same extent


what is the clinical presentation of mesangioporliferative glomerulonephritis

nephrotic syndrome
hematuria is established for majority of patients
igm positive have more nephrotic syndrome
HOWEVER igM negative have macroscopic hematourea


what is the treatmnet of MSGN ?

pulse treatmnet with methylprednisolone

add cyclosphosphamide monthly pulses
if iGm positive - cytosporin a

immunovenin if still not responsive


then oral prednisone

anticoagulants such as IV heparin


focal segmental glomeruloscelrosis is the most common what ?

most common cause of nephrotic syndrome in adults
esp african american and hispanic


what is the characteristics of FSGS

it has subacute lesions , segmental sclerotic changes , poor prognosis and resistance to corticosteroid therapy


what is the classification of FSGS?

primary = when no underlying cause is found =
role of circulating permeability factor
because FSCG rapidly occurs in graft of renal transplant , however if plasmaphoresis is done before transplant the disease is limited


secondary = underlying cause is identified

presents with kidney failure

toxins = such as heroin , pamidronate

familial = mutatation in nephron and podocin

HIV infection

hypertension , DM and obesity causing glomerular hyper filtration = mechanical stress on podocytes


what are the pathological variants of FSGS?

collapsing variant = higher risk for ESRD = heavy proteinurea
one glomerulus segmnetal or global obliteration of the glomerular capillary by wrinkling and collapse of the glomerular basement membrane because of podocyte hypertrophy and hyperplasia


glomerular tip lesions variant = low risk

at least 1 segmental lesion involving the tip domain (ie, the outer 25% of the tuft next to the origin of the proximal tubule


cellular variant =
intermediate isk

1 glomerulus with endocapillary hypercellularity involving at least 25% of the tuft and causing occlusion of the capillary lumen/lumina

perihilar variant :
of at least one glomerulus with perihilar hyalinosis with or without sclerotic lesions

not otherwise specified variant


how do we diagnose focal segmental glomerulosclerosis ?

massive non selective porteinurea

microscopic hematurea in pronounced mesangial proliferation

progressive decrease in GFR

increase in serum urea and creatinine

LM : segmental sclerosis and hyalinosis

IM : most commonly negative
maybe I'm , C1 and C3 inside the sclerotic regions

EM : effacement of podocyte foot process


what is the clinical presentation of FSGS?

hypertension and deterioration of renal function - oligourea - usual find
nephrotic syndrome


management of FSGS?

extremely important to differentiate the primary from the secondary because the secondary leads to more cases in ESRD , and to treate the underlying disease



in primary forms
corticosteroids - prendisole
cyclosporin a


renal transplant has not been success due to frequent reoccurrence



what is the pathopsyiology of membranous glomerulonephritis ?
and clinical presentation?

immune complex in subeipthelium! - between podicytes and gbm

the antigens may be part of the basement membrane - which are M type phospholipase A2 receptor
or neutral endopeptidase -expressed in the podocyte surface lining the basement membrane

or deposited there from systemic circulation

immune complex forms the MAC

inflammation of the basement membrane , PODOCYTES

initially, proteinuria may be mild, and nephrotic syndrome may develop at a later stage.
nephrotic syndrome

The swelling could appear without any other symptoms and later disappear spontaneously

Arterial hypertension and worsing of the renal function


what re the causes for membranous glomerulonephritis ?

idiopathic - antigen targets

immune complex deposition by cationic bovine serum albumin seen in cows milk and beef protein

autoimmun - sle
infection such as - hep c , hep b , HIV , syphilus

drugs - captopril and nsaids
organic gold

lung carcinoma, colon carcinoma, lymphoma, leukemia


diagnosis of membranous glomerulonephritis ?

High-grade non-selective proteinuria,
in a small percentage of patients there is a microscopic haematuria

Hypoproteinaemia with hypoalbuminemia and hyperlipidemia is observed.
Coagulation status shows a tendency to hypercoagulability

serum c3 are usually low esp in case of viral hep c

LM :
1) diffuse thickening of basement membrane
GBM appears to be spiked and holey appearance appearance - Swiss cheese).

em : spike and dome pattern of basement membrane
podocyte effacement
subepitheila deposits - as it progresses these deposits cleared and leave cavities - can then become sclerosed and hylainsed

IMF= granular deposition of immunoglobulin and complement along basement membrane


what is the treatment of membranous glomerulonephritis ?

ACE inhibitors or ARB’s


ponticelli regiment :

Starts with a 3-day pulse of methylprednisolone cyclophsopamide alternating with corticosteroid (mixed results) such as prednisolone

On the second month, the corticosteroid treatment stops and the oral intake of cyclophosphamide or chlorambucil iniciated for one month.

Corticosteroids and cytostatics alternate for a total of 6 months

corticosteroid must always be combined with one of the mentioned above or these :





Besides the Pontichelli regiment there is the pulse treatment with corticosteroids and cyclophosphamide that we treate of idiopathic nephrotic syndrome.

A very good effect in patients is the tacrolimus

spontaneous remission common and higher remission rates with anti proteinuria therapy

progression - dialysis


complication of membranous glomerulonephritis

more prone to thromboembolism than other nephrotic syndrome diseases


what is the etiology berger disease ?

most likely upper respiratory tract infection or go infection triggered - isa antibodies form immune complex that are deposited in kidney (TYPE 3 HYPERSENTITIVTY)

secondary :
systemic disease - henoch
chrons ,
sjoren syndrome

neoplasma 0 giga monoclonal gammopathy , lung carcinoma
infectious toxoplasmosis


what is the clinical features of berger disease ?

asymptomatic - microscopic hematurea
recurring epodes of gross hematurea may have flank pain

hypertension is initially absent but may develop

it may progress into rpgn or nephrotic syndrome


what is the diagnosis of iga nephropathy ?

- perisitant microhematurea
Dysmorphic erythrocytes with erythrocyte cylinders are found in the sediment

in flare ups or intercurrent infections - gross hematurea

low to moderate proteinurea mostly less than 2g/24

or nephrotic syndrome findings

GFR usually remains unchanged


serum iga elevated

C3 levels are generally normal so is the rest of the complement panel

renal biopsy - usually indicated only when severe progression f disease such as hypertension increases , creating levels increase

lm - mesangial proliferation

IMF : mesangial iga deposits
with C3
maybe also igG and ism

EM - mesangial immune complex deposits


what is the treatmnet for berger disease ?

patients with just isolated hematurea
- monitor kidney function and start treatmnet if progresses

symptoms usually resolve spontaneously for these patients

persistence of proteinurea above 1g/24hr and hypertension -
acei and arb
polyunsaturated fatty acids
corticosteroids at a conventional dose for two years

pronounced nephrotic syndrome in histological variation, appropriate to administer corticosteroid pulse then conventional corticosteroid

for proteinuria below 1 g/24h, the arterial pressure should be maintained below 130/80 mmHg

With proteinuria above 1 g/24h it should not exceed 125/75 mmHg.


patients with recurrent macroscopic haematuria, recommendations include aggressive hydration.
severe or rapidly progressive = glucocorticoids plus ,cyclophosphamide / azathioprine

selective plasma plasmapheresis synchronized with cytostatic therapy.

high chance of reoccurrence with renal transplant


what is the pathopshyiology of isa nephropathy ?

iga depostion in mesangium

thought to produce mac

b lymphocytes also produce glycan specific antibody of the egg class directed at the abdonamlly gluycsilated igA1


about 20 percent of isa can develop kidney failure and what is a good prognostic indicator of that ?

These 20% were usually with expressed high arterial pressure and proteinuria above 2 g/24 h or with nephrotic syndrome.