Renal 2 Flashcards
damage to the podocytes
non prolif
proteinuria
damage to the endothelial cells or meningeal cells
prolif
haematuria
franc haematuria 1-2 days after URTI
Ig A neph
nephrotic syndrome occurring 1-3w after a strep infection
post infective GN
haemoptysis with rapidly porgressing GN
good pastures
obesity linked to which nephropathy
FS
nephrotic syndrome
proteinuria, hypoalbuminuria, oedema, increased cholesterol
nephritic syndrome
AKI, oliguria, hypertenion, urine has RBCs and RBC and casts
minimal change neuropathy commones cause for what ix cx causes treatment
commonest cause ofr nephrotic syndrome in children
children with atopy. follows URTI
EM - podocyte foot fusion
doesn’t cause progressive RF
idiopathic, IL-13, NSAIDs
steroids. relapse cyclophosphamde
focal segmental commonest cause of what causes ix cx rx
nephrotic syndrome in adults
idiopathic. HIV
50% go onto end stage renal failure over 10y
steroids, relapse - cyclophosphamide
membranous nephropathy commonest cause for what causes ix rf rx
second commonest cause of nephrotic syndrome in adults (esp elderly)
thickened BM on silver stain
30% progress tp ESRF in 10y
steroids/alkylating agents/B monoclonal ABs
IgA nephropathy commonest wha symp causes ix cx rx
commonest GN in the world
young men frank haematuria 1-2 days after URTI
idiopathic. HSP
meningeal cells prolif. IGA deposits in mesangium
25% progress to ESRF in 10-30y
BP control ACEI/ARBs
Rapidly progressing GN causes
crescents on biopsy
ANCA pos - wegners, microscopic polyangitis
ANCA neg - SLE, HSP, good pastures
TBW male and female
male 60% of body weight
females 50%
TBW = what
ICF (67%) and ECF (33%)
ECF
20% plasma
80% interstitial fluid
lymph and transcellular fluid
ADH and vasopressin type 2 receptor causes what
ATP -> cAMP
which increases H2O permeability
which leads to a concentrated urine output
aldosterone
sodium reabsorption and potassium secretion
ANP is stored in what
how is it released
what does it lead to
atrial cells
cells stretching due to increased plasma volume causes it to be released
leads to increased BP
leads to increased excretion of sodium and diuresis leading to a decrease in plasma volume
renal transplantation HLAs
HLA A
HLA B
HLA DR
rejections hyper acute
acute
chronic
hyper acute - within mins
acute <6m - B/T cell mediated. treat with immunosuppression
chronic >6m - immunological and vascular - deterioration of transplant
anti rejection therapy cyclosporin and tacrolimus
renal dysfunction
tremor
hypertension
DM
anti rejection therapy azathioprine and myelophenate
leucopenia, anaemia, GI S/E
anti rejection therapy steroids
osteoporosis, weight gain, infection, DM
ADPKD chromosomes
signs and symp
cx
type 1 chromosome 16 - develop ESRF faster
type 2 - chromosome 4
hypertension. big kidneys with cysts
intracranial aneurysms
ARPKD chromosome
who
6
young children
Alports genetics
symp/signs
X linked recessive
sensineural hearing loss - bilateral
proteinuria, haematuria
anderson fabric disease is what
genetics
ix
rx
inborn error of glycosphingolipid metabolism. lysosomal storage disease
plasma/leucoyte alpha GAL activity on renal/skin biopsy
fabryz - enzyme replacement