Renal

Question 1

what diagnoses AKI

Answer 1

serum Cr rise >26 in 48hr
or serum Cr rise >1.5x in 7 days

oliguria 0.5ml/hr/kg for 6hr

Question 2

what are the stages of AKI according to KDIGO

Answer 2

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+

Question 3

what are 3 types of AKI

Answer 3

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

Question 4

when is ACEi harmful

Answer 4

in AKI = nephrotoxic
in CKD = protective

Question 5

what are RF for AKI

Answer 5

age 65yr+
CKD, HTN, liver disease, diabetes
drugs - NSAID, ACEi
contrast agents for CT

Question 6

how is AKI managed

Answer 6

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

Question 7

when is dialysis given for AKI

Answer 7

if complications:
hyperK
fluid overload, leading to pulmonary oedema + HF
metabolic acidosis
uraemia, leading to encephalitis + pericarditis

Question 8

is RRT given for AKI

Answer 8

no only for CKD

AKI = dialysis, CKD = dialysis -> RRT

Question 9

how do AKI + CKD differ

Answer 9

CKD is progressive irreversible decline in kidney function

while AKI is reversible

Question 10

what are diagnostic criteria for CKD

Answer 10

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

Question 11

how is CKD classified

Answer 11

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)

Question 12

from what age does renal function decline

Answer 12

30yr onwards
progressive loss in renal mass + structural changes (glomerulosclerosis), causing decline in renal function

Question 13

how does CKD affect bones

Answer 13

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)

Question 14

how is eGFR measurement taken for CKD

Answer 14

twice 3 months apart

Question 15

when to refer to specialist for CKD

Answer 15

if eGFR <30ml/min OR ACR>70

15-25% or 15ml/min decrease in eGFR in 1 year
drug resistant HTN on 4+ antihypertensives

Question 16

how is CKD managed + what are target BP

Answer 16

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

Question 17

how to treat CKD complications

Answer 17

metabolic acidosis = sodium bicarb
anaemia = Fe supplements, EPO
renal bone disease = VitD supplements
ESRD = dialysis ->RRT

Question 18

how do nephritic + nephrotic syndrome present

Answer 18

nephritic = HTN + haematuria
hallmark feature : glomerular inflammation

nephrotic = oedema (peripheral, periorbital) + proteinuria >3.5g/day + hypoalbuminaemia <35g/l

Question 19

how do post-strep + IgA glomerulonephritis differ

Answer 19

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

Question 20

what is pathophysiology of good pasture syndrome

Answer 20

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

Question 21

what nephritic disease presents with pulmonary haemorrhage

Answer 21

goodpasture syndrome
as anti-GBM attack type 4 collagen in pulmonary basement membrane

Question 22

why does nephrotic syndrome also cause hyperlipidaemia

Answer 22

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

Question 23

when is biopsy not done

Answer 23

only for minimal change disease

every other nephritic + nephrotic syndrome is confirmed with biopsy