sign and symptoms
-hematuria(nephritic syndrome)
-protienuria(nephrotic syndrome)
type
-non-proliferative
-proliferative types
-primary(intrinsic)
-secondary(extrinsic)
what is the diff btwn non-proliferative and proliferative?
non-proliferative
Minimal change GN (also known as Minimal Change Disease)
Focal Segmental Glomerulosclerosis (FSGS)
Membranous glomerulonephritis
Thin BM nephropathy
etio-genetic causes
symptom-hematuria(rarely proteinuria)
diagnosis-biopsy electrom microscope(thinning of BM)
prognosis-benign(small risk to CRF) but can preceed to INC BP and proteinuria
Proliferative
IgA nephropathy (Berger's disease)
Post-infectious
Membranoproliferative/mesangiocapillary GN
Rapidly progressive glomerulonephritis
Minimal change GN (also known as Minimal Change Disease)
ages:children 80% while adult 20%
Etio-T-Lymphocytes mediated
Symptom-main-nephrotic syndrom,may also present with hematuria.
dignosis? selective proteinuria(albumin)
change: no change seen in light microscope only seen in electron microscope(accumulation of podocyte)
treatment:
1.supportive treatment- to decrease edema
2. steroid to halt the disease.(to those who are steroid resistance,use cyclophosphamide, cyclosporin(cytoxic theraphy)
*children more respond to theraphy
*3 months of treatment-deasea will cured
Focal Segmental Glomerulosclerosis (FSGS)
Syndrome : nephritic syndrome(nephotic syndrom according to oxford)
few focus of gemorules been fibrosis(sclerosis) with hyalinization of arterioles(IgM deposition0
maybe primary or secondary( reflux nephopathy,alport syndrome,heroin abuse)
treatment -corticosteroidand cyclosporine and cyclophosphamide (if streroid not effective)
Progressive until renal failure(30-50%)
Membranous glomerulonephritis
more frequent in adult(maybe heridetary,but only 9 cases in world)
what is it? thickening of glomerular basement membrane without hypercelular(diffuse granulat uptake of igG)
symptomes due to : hypersensitivity type 3-lead endothelial accumulation
symptoms? nephrotic(main) and nephritic symptoms
-high risk of vein thrombosis)
etiology : unknown ,maybe( cancer of lung or bowel,hepatitis or malaria drugs(penicillamine),autoimune dx(SLE)
how to diagnose? imunoflurescense
prognosis? Rule of third -one-third remain with MGN indefinitely, one-third remit, and one-third progress to end-stage renal failure
progress to? atrophy and hyalinisation(kidney keep to shrink)
treatment? corticosteroid
spike and dome explaination
These are due to membrane formation around the deposits, creating "spikes", followed by membrane formation over the deposits, creating the “domes”.
proliferative type
Berger's disease( igA nephropathy)
age-young men have URTI (few attack)-overproduction of IgA
what is is?
deposition of IgA in mesingium lead to mesingium cell proliferation with increase matrix
what is IgA ?
antibody ussuakky present in mucus
have 2 type IgA and IgA1(ussually cause nephropatogenicity)
causes?
primary
secondary
-URTI
-Liver disease
-GI infection
-henoch-schonlien purpura(what is it?vasculitis)
disease of the skin and other organs that most commonly affects children,causes palpable purpura (small hemorrhages); often with joint and abdominal pain.Withkidney involvement,
sign and symptomes
1.nephriti symptoms
-primaryly hematuria(see even gross)
-mild proteinuria (
2.occasinally nephrotic syndrom
pathogenesis?
plasma IgA increase ,IgA circulating contain imune complex.deposition of imune complex lead nephropathy
TX immunosuppresion drug(cyclophosphamide and mycophenolate)
20% of cases lead to ESRF worse if the is INC BP,male and have proteinuria
Post-Infectious
etiology- any infections espcially streptococus pyogenous
time to occur- 10-14 days after infection(pharyngitis or skinn lesion)
sign n symptome _glomerularnephritis(nephritic(main) and nephrotic symptoms)
diagnosis
1.history of disease(anamnesis)
2.streptococus titer(antistreptolysin O titers)
microscopic changes
-hypercellurarity of messingial cell and endothelial in capaliry
lead to influx of neutrophil and monocytes in urine
(in some situation hypercelularity of mesingial and endocapaliry lead to cpmpression of capsule bowman(cresentic formation)
progression?
ussually 2-4 weks resolve without complication
membranoproliferative?mesinggiocapalliry GN
most severe,why?
rapid progression to ESRF over weeks(steroid maybe help to halt the progression)
main presentaion -nephrotic syndrome
causes?
2 main disease lead to RPGN
1.Goodpasture syndrome?
-autoimune dx against BM of kidney and lungs.
-s n s-hemoptysis
-histologically -we can see deposition of IgG
-tx-imunosupressive therapy( steroid-methylprednisolone) and plasmapheresis(extraction of plasma remain the RBC)
2. vasculitic dx
-wegener dx(vaslulitis in organ like kidney and lung)
-blood test-ANCA not imune complex deposition
histologically(general)
-cresent(why? fibrin in capsule bowman-increase permeability-stimulate proliferation of parietal cell and influx of monocytes)
rapid growth of fibrosis lead to compression of capallary loops and decrease capsule bowman space
how to examine the patient?
1.dx history
-diabetes m
-hypertension
-sore throat(post infectious GN)
-medication (nsaid)
-family hx(sickel cell dx)
-neoplasm
2.general examination
-edema(face,pitting edema of the leg or hand)
-ridge of the nail(sign of hypoproteinimia)
-pallor(?)
ridge of the nail
what to check?
1.ascitis
2.protein n sugar in urine
3.24 hours urine protein ,creatinine clearence and albumin
4.FBC(full blood count) , ESR and crp
5.serum cholesterole
6.DNA antibody,ANCA,ANA,anti-GBM
7.renal ultrasound andrenal biopsy
how to manage?
1.refer t nephrologist
-by keep the BP less than 130/80 or less125/75 if proteinuria more than 1g/d
what is nephtrotic syndrome?
-albuminuria
-hypoalbuminimia
-edema
-lipiduria
-hyperlipidemia(hyperfunction of liver) why?
complication?
1.thoboembolic event(loss of antitrombin 3 factor..which produce in liver and has bee loss trough kidney)
2.protein malnutrition
3.athereosclerosis(hihg lipid production)
4. infection
What is pitting edema?
Pitting edema can be demonstrated by applying pressure to the swollen area by depressing the skin with a finger. If the pressing causes an indentation that persists for some time after the release of the pressure
CAuses of non pitting edema..
Non-pitting edema can occur in certain disorders of the lymphatic system such as lymphedema, which is a disturbance of the lymphatic circulation that may occur after a mastectomy, lymph node surgery, or congenitally.
What is nEPHROTIC SYNDRME ACTUALLY?
1.proteinuria more than 3g/24h
2.hypoalbumininia (less 30g/L)
3.edema
what will happen?
loss protein-decrese albumin-decrease oncotic pressure in blood vessel-fluid go to extracellular space-plasma oncotic pressure remain the same-lead to sodium retention-edema
diff diagnose?
cardic failure(pulmonary edema,mild proteinuria)
liver dx (decrease in albumin level)
complication?
1.inc susceptibility to infection-Ig leak to urine
2.thromboembolismm-inc clotting factor(hyperfx of liver)
3.hyperlipidemia-(the same reason-in respond to dec oncotic pressure)
what we have to do?
1.if the is ni family history or other previous dx-we gave them steroid (why? most of the case due to minimally change GN whic can be cure by steroid therapy)
2.but if the protenuria is not regress in 1 months ..we have to do renal biopsy)
Tx
1.restrict salt intake
2.diuretic (furasemid
3.infection?(give vaccination)
4.prophylactic (heparin)
5.hypertension(ace i and A2A)