RENAL 1 Flashcards
proliferative GN vs
non prolif
heamaturia - proliferation of mesangial/endothelial cells
proteinuria - fusion of podocyte foot processes
RBC and casts
granular casts indicate active granular injury causing glomerual bleeding
crescentic GN
epithelial cell extra capillary proliferation
minimal change nephropathy prolif? commonest cause of what who causes ix rx progressive renal failure?
non proliferation nephrotic syndrome in children children with atopy 0- follows URTI idiopathic, NSAIDs, hodgkins EM shows podocyte foot fusion steroids if relapse cyclophosphamide no
FCS prolif? commonest cause of what who causes ix rx progressive renal failure?
non prolif
nephrotic syndrome in adults
obese
genetics. idiopathic, HIV, heroin, sickle cell, alports
focal segmental scaring - contain ig and complement. podocyte foot fusion
steroids. relapse - cyclophosphamide/cyclosporin
50% -> ESRF in 10y
membranous prolif? commonest cause of what who causes ix rx progressive renal failure?
non
2nd commonest cause of nephrotic syndrome in adults
esp older px
idiopathic, malignancy, hep B, SLE, gold/penicillamine
thickened BM and sub epithelial immune complex deposits in BM seen on silver stain. diffuse IgG uptake on IF
steroids. alkylating agents. B cell monoclonal ABs - rituximab
1/3 to ESRF in 10y. 1/3 chronic. 1/3 remission
IgA prolif? commonest cause of what who causes ix rx progressive renal failure?
prolif
commonest GN worldwide
young man who develops macroscopic haematuria 1-2 days after URTI, proteinuria and progressive renal failure
idiopathic. HSP
mesangial cell proliferation. increase in mesangial matrix, IgA deposits in mesangium
BP control ACEI/ARB. steroids/cyclophosphamide
25% in 10-30y
post strep prolif? who causes ix rx progressive renal failure?
prolif and non - heamaturia and proteinuria
young kids after viral infection usually strep progenies (tonsillitis) - 2w after infection - proteinuria, haematuria, htn, decreased c3, headache, malaise
proliferation of mesangial cells, neutrophils and monocytes. bowmen space is compressed. IF - granular.starry sky appearance
supportive - resolves in 2-4w
good prognosis
RPGN prolif? causes ix rx progressive renal failure?
prolif ANCA pos: wegners, MPA ANCE neg: GP, HSP, SLE glomerular crescents seen on biopsy steroids, cytotoxic, monoclonal ABs, plasmapheresis poor prognosis
nephritic syndrome
proliferation? non proliferation?
PROLIF
AKI, oliguria, htn, urine - RBC and casts, oedema
nephrotic syndrome
proteinuria >3g/24h
hypoalbuminaemia <30
oedema, increased cholesterol, normal renal function
what can nephrotic syndrome cause
infections, renal vein thrombosis, volume depletion, PE, vit D déficit, subclinical hypothyroidism
treatment of nephrotic syndrome
underlying, steroids (membranous, FCS, minimal), ACEI/ARB, anti coag, IV albumin (if volume depleted)
chronic kidney disease stages
GFR >90 and kidney damage >60-90 and kidney damage 3A 45-60 3B 30-44 15-30 <15 OR on RRT
what can affect CK
muscle mass, pregnancy, eating red meat
what does CKD do to the cardiovascular risk
increases it
causes of chronic kidney disease
DM, htn, vascular disease, chronic GN, reflux nephropathy, PKD, chronic pyelonephritis, idiopathic
what increases the progression of chronic kidney disease
proteinuria
symptoms of CKD and when do they occur
what occurs early
<20 GFR
itch, tired, poor appetite, sleep problems
impaired urine concentrating ability - nocturia
how can progression be slowed
decrease proteinuria and BP - ACEI/ARB
good glycemic control
stop smoking
how can the CVD risk be decreased
BP and proteinuria, smoking, simvastatin
anaemia in CKD why does it occur
when does it become apparent
treatment first line and second line
what is the target Hb
decreased erythropoietin
when GFR <35
IV iron. 2 -> erythropoietin stimulating agents like erythropoietin, darbepoetin
10.5-12.5
bone disease in CKD why
symptoms/signs
treatment
impaired vit D hydroxylation - decreases calcium absorption. secondary hyperparathyroidism
osteomalacia, osteoporosis, vascular calcification, heart vessels calcify
ergocebeferon, alfocolcadol, phosphate, cal citron (vit D)
when should dialysis be started
resistant hyperkalaemia
urea <45
unresponsive acidosis
GFR <15
restrictions of dialysis
fluid if anuric 1L/day
decreased salt/potassium
decrease phosphate - phosphate binders
arteriovenous fistula
how long does it take to heal
good points
bad points
6 weeks
good blood flow. infection unlikely.
requires surgery, can limit blood flow distally - steal syndrome, can block
tunneled venous catheter goes where
good points
bad points
large vein - femoral, subclavian, jugular
easy to insert and can be used immediately
damage to vein, can block, high risk of infection
TVC infections of unrx
ix
rx
if infection is untreated it can lead to endocarditis
FBC, CRP, blood cultures, exit site swab
vancomycin, like removal/exchange
starting haemodiaylysis
gradual build up if too quick can lead to cerebral disequilibrium syndrome
4 hours 3 times a week
problems with haemodialysis
fluid overload, blood leaks, loss of vascular access, hypokalaemia and cardiac arrest, intradialytic hypotension
peritoneal dialysis types
CAPD - 4 bad exchanges throughout the day 30m/exchange
APD - 1 bag stays in all day - overnight machine drains, fluid in and out over 9-10 hours or overnight
starting PD
training - smaller fill volumes to begin with
problems with PD - infection what
causes
ix
rx
peritonitis/exit site infection
contamination: SA, strep, diphtheroid. gut bacteria translocation: Coli, klebsiella
culture PD fluid
intraperitoneal ABs, catheter may have to be removed
PD problems membrane failure
inability to remove enough water - fluid overload
may have to switch to HD
PD problems hernia
due to increased abdominal pressure
smaller fill volumes and treat hernia
metabolic complications of dialysis
bone mineral metabolism
anaemia
water and sodium retention
increased CDV disease
what can long term dialysis lead to in the kidneys
simple cysts - no functional disturbance
