Renal Flashcards
what diagnoses AKI
serum Cr rise >26 in 48hr
or serum Cr rise >1.5x in 7 days
oliguria 0.5ml/hr/kg for 6hr
what are the stages of AKI according to KDIGO
3 stages total
S1: Cr rise >26umol in 48hr or >1.5x in 7 days, oliguria 0.5ml in 6hr
S2: Cr rise >2x in 7 days, oliguria 0.5ml in 12hr+
S3: Cr rise >3x in 7 days, oliguria 0.3ml in 24hr+ OR anuria for 12hr+
what are 3 types of AKI
usually pre-renal cause
pre-renal = renal hypo perfusion
shock (hypovolaemia)
drugs - ACEi, NSAID
dehydration
renal artery stenosis
intrinsic - ATN is most common cause, that results from renal hypo-perfusion (artery stenosis)
ATN, acute interstitial/glomerular nephritis
post-renal = obstructive uropathy
renal stone
ureter/urethral strictures
BPH, malignancy
when is ACEi harmful
in AKI = nephrotoxic
in CKD = protective
what are RF for AKI
age 65yr+
CKD, HTN, liver disease, diabetes
drugs - NSAID, ACEi
contrast agents for CT
how is AKI managed
STOP NEPHROTOXIC DRUGS (ACEi, NSAID)
if pre-renal, IV fluids to increase blood supply to kidney
if post-renal, catheter to relieve obstruction
dialysis if complications
when is dialysis given for AKI
if complications:
hyperK
fluid overload, leading to pulmonary oedema + HF
metabolic acidosis
uraemia, leading to encephalitis + pericarditis
is RRT given for AKI
no only for CKD
AKI = dialysis, CKD = dialysis -> RRT
how do AKI + CKD differ
CKD is progressive irreversible decline in kidney function
while AKI is reversible
what are diagnostic criteria for CKD
eGFR <60ml/min OR markers of kidney damage
measure eGFR twice 3 months apart
markers:
albuminuria, ACR >3mg/mmol or 30mg/g
white/red cell casts
radiological abnormalities - PCKD
histological abnormalities on biopsy
how is CKD classified
G + A score, based on eGFR + ACR (albuminuria)
G1 >90ml/min
G2 60-89ml/min
G3a 45-59ml/min
G3b 30-44ml/min
symptomatic - specialist referral
G4 15-30ml/min
G5 <15ml/min
A1 <3
A2 3-30 (evidence of proteinuria, so CKD diagnosis)
A3 >30 (if >70, specialist referral)
from what age does renal function decline
30yr onwards
progressive loss in renal mass + structural changes (glomerulosclerosis), causing decline in renal function
how does CKD affect bones
CKD causes high PO4 + low active VitD, leading to renal bone disease
leads to 2ndary hyperPTH as low Ca
low bone density (osteoporosis) + low bone mineralisation (osteomalacia)
so rugger jersey sign on spine x-ray (sclerosis of vertebral ends)
how is eGFR measurement taken for CKD
twice 3 months apart
when to refer to specialist for CKD
if eGFR <30ml/min OR ACR>70
15-25% or 15ml/min decrease in eGFR in 1 year
drug resistant HTN on 4+ antihypertensives
how is CKD managed + what are target BP
aim to optimise blood glucose + HTN
target BP <140/90
unless ACR>70, then aim for 130/80
before starting ACEi - check UE 2wks before starting to monitor K levels
how to treat CKD complications
metabolic acidosis = sodium bicarb
anaemia = Fe supplements, EPO
renal bone disease = VitD supplements
ESRD = dialysis ->RRT
how do nephritic + nephrotic syndrome present
nephritic = HTN + haematuria
hallmark feature : glomerular inflammation
nephrotic = oedema (peripheral, periorbital) + proteinuria >3.5g/day + hypoalbuminaemia <35g/l
how do post-strep + IgA glomerulonephritis differ
post-strep presents 2-3wks after strep infection (sore throat, skin infection)
involves IgG immunoglobulins - contain group A B-haemolytic strep antigens, cross-reactive
IgA presents few days after URTI infection
involves IgA immunoglobulins
what is pathophysiology of good pasture syndrome
anti-GBM antibodies target type 4 collagen in basement membrane
causes linear deposition of IgG in glomerular capillaries
seen histologically as crescent nephritis on immunofluorescence
sometimes reacts with pulmonary basement membrane causing pulmonary haemorrhage
what nephritic disease presents with pulmonary haemorrhage
goodpasture syndrome
as anti-GBM attack type 4 collagen in pulmonary basement membrane
why does nephrotic syndrome also cause hyperlipidaemia
cytokines damage podocytes, so they fuse together changing shape of GBM
this increases serum protein permeability, so protein lost in urine (proteinuria)
causes low oncotic pressure, resulting in oedema
to increase oncotic pressure, liver produces lipoproteins causing hyperlipidaemia
when is biopsy not done
only for minimal change disease
every other nephritic + nephrotic syndrome is confirmed with biopsy
