Intrinsic Kidney Disease Flashcards
OVERVIEW
i) which two areas of the kidney may be damaged but urine dip may be normal?
ii) what will be seen on dipstick in glomerular damage?
iii) which cell type regulates what is filtered through?
i) tubules aand interstitium
ii) blood and protein on dippstick
iii) podocyte
IGA NEPHROPATHY
i) in what age group does it typically present? what % of glomerular disease does it constitute?
ii) what symptom do most patients have? what usually follows this?
iii) what is the pathophys? (first and second hit) what ultimately happens?
iv) what can it become?
i) typically presents in young - 20-30s
- makes up 15-20% of glom disease
ii) most patients have haematuria then upper resp tract infection (pt with haemturia + SOB/cough > do a dip)
iii) 1st hit is genetic and second hit is infection > results in immune dysregulation
- IgA immune compleex depos in kidney is final common pathwaay
iv) can becomes IgA vasculitis (widespread rash)
IGA VASCULITIS
i) give four presentations?
ii) when does it most commonly present?
iii) does it have a worse or better prognosis than IgA nephropathy?
iv) how is it treated
i) rash, arthralgia, haematuria, abdo pain
ii) most commonly present in children in first decade
iii) better prognosis
iv) treat with steroids
GLOMERULAR DISEASE
i) what is the most prominent feature of nephritic syndrome in the urine? what is it due to?
ii) what is the most prominent feature of nephrotic syndrome in the urine? what is this due to?
iii) which one doesn’t really have haematuria and presents with peripheral oedema?
iv) name two causes of nephritic syndrome? name two causes of nephrotic syndrome? what condition can cause both
i) nephritic > haematuria
- due to inflammation and breaks in the glomerular basement membrane
ii) nephrotic > proteinuria due to podocyte injury
iii) nephrotic doesnt really have haematuria and present with peripheral oedema
iv) nephritic > goodpastures (anti GBM), ANCA vasculitis, IgA
nephrotic > minimal change disease, FSGS
- SLE can cause both
NEPHROTIC SYNDROME
i) what is the triad of presentations?
ii) name three things this can lead to
iii) name four causes of nephrotic syndrome
iv) what are the three main treatments? what must also be considered?
i) triad of px > proteinuria (>3.5g/24hrs), hypoalbuminaemia (<30g/l) and oedema
ii) can lead to
- increased infections (due to loss of protein inc Ig)
- pro thrombotic state (loss of protein C and S)
- hypercholesterolaemia (loss of HDL > VLDL prod in liver)
iii) minimal change disease, focal segment glomerulosclerosis (FSGS), SLE, diabetes
iv) fluid and salt restrict (loss of albumin > fluid collects in vasc space)
ACEi are mainstay > relax efferent arteriole > decrease glom pressure and less protein leaked into urine (also get inc RAAS activ so ACEi to dampen this)
Diuretics - get rid of fluid from extravascular space
- also consider VTE (hep, warfarin, DOAC) as pro thombotic state
- treat the underlying cause
MINIMAL CHANGE DISEASE
i) what is it?
ii) when does it present? what is the pathophysiol?
iii) how does it usually present?
iv) how is it treated?
i) damage to glom that can only be seen under EM
ii) presents usually in childhood (can be seen in adults) > slit diaphraghm defect
iii) usually present with facial oedema
iv) treat with steroids
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
i) who does it present in?
ii) what is seen on histology?
iii) what does it present with?
iv) how is it treated?
i) presents in adults
ii) see segmental sclerosis on histol
iii) present with nephrotic syndrome
iv) tx for nephrotic syn - fluid/salt restric, ACEi, diuretics
- also give steroids
MEMBRANOUS NEPHROPATHY
i) when does it present? does it affect M or F more?
ii) what do 70% of patients present with?
iii) what is deposited in the glomeruli?
iv) what may it be associated with?
i) presents in 4th and 5th decade - M>F
ii) 70% patients present with nephrotic syndrome
iii) IgG depos in glom
iv) may be associated with cancer
