renal vol 2 Flashcards
definition of AKI
spectrum of disease.
an abrupt (1-7/7) and sustained (more than 24 hours) decreace in kidney function.
mortality is high (50-60%)
many do not return to baseline kidney function.
distinct stages: initiation
oligo-anurea- unabe to filter the blood
polyurea- unable to concentrate the urine
restitution.
risk factors for AKI
sepsis
race (black)
pre existing kidney disease
admission to non-ICU ward
surgical patients
cardiovascular disease
emergency surgery.
Causes of AKI
Pre-renal: volume responsive, sepsis induced, hypotension, renovascular disorders.
renal: nephrotoxins, glomerular disease, rhabdomyolysis
Post-renal: obstruction, abdo compartment syndrom.
what is the rifle + AKIN criteria for AKI
AKI IX:
FBC inc U+E. potassium eGFR.
CXr to see if pulm odema.
ECG for hyperkalaemia signs.
urineanalysis: for protein, blood, leucocytes, nitrites and glucose.
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
AKI Rx:
hypovolaemic- fluid resus, medication review + halt nephrotoxins. identify and Rx cause of AKI.
if K= 5.5-5.9 Rx cause
k= 6-6.4 with no ecg signs- insulin + glucose.
if 6 + ecg or 6.5 add calcium also.
hypervolaemic: loop diuretic, GTN if pulm odema. Rx K as above.
consider dialysis in significant met alcidosis, uraemia, hyperk
additions of AKI in post surgical scenarios.
often surgery results in AKI, generally low grade.
can also be masked by reduction in serum creatine due to muscle metabolism and content in the post operative period.
higher rates of AKI seen in aortic bypass surg, vasc surgery (because of the non-pulsatile flow) due to the neurohormonal changes and disruption due to the operated area.
what is urethral syndrome, signs and symptoms and epidaemiology
LUTS without physiologic cause- no urine pathogen caused, no structural abnormalities.
suprapubic discomfort, dysuria, urinary frequency.
common in young white women, multiparous, 2 or more abortions, delivery without episiotomy.
differential diagnosis, Ix, Rx of urethral syndrome
stress incontinence, vag atrophy, sterile pyuria, urethral stenosis + spasm, sexual trauma, anxiety
Ix: urine dipstick, culture, cystoscopy
Mx: underlying psych problems should be treated
behavioural therapy
highly acidic food should be avoided
chronic kidney disease overview
slow irreversable attrition of nephron number resulting in end stage renal faliure
self reinforcing- more nephrons fail the faster the rest go
Risk Factors: Age, HTN, DM, smoking, nephrooxic medications.
S+S: usually asymptomatic until more severe stages,
puritis, patelet dynfunction, anorexia, nausea, oedema, cramps, periph neuropathy, pallor, HTN, bone disease, hyprk
investigations, stages of CKD
Ix:
urine- haematuria (painless is renal cancer)
albumin: creatinine ratio - 1st line proteinurea screening test (common in DM- initially microalbumin present- then as kidneys worsen more creatinine)
urine electrolites
urien microscopy (look for red cell casts- blood + protein stuck together- glomerular-nephritis)
Bloods- (anemia), bone profiles, ANCA (vasculitis tests), rule out SLE,
Imaging: USS (small/ large)
Renal biopsy- rare + last line
stages based on eGFR
1: 90 + proteinurea/ haematuria
2: 60 + haem/proteinurea
3a: 45-59
3b: 30-59
4: 15-30
5: less than 15.
treatment of CKD
Several classes of agents have been shown to slow CKD progression. Renin-angiotensin system blockade and sodium-glucose co-transporter 2 (SGLT2) inhibitors (e.g., empagliflozin, canagliflozin, dapagliflozin) can preserve kidney function by reducing intra-glomerular pressure independently of blood pressure (BP) and glucose control
BP less than 140.
ACEi Or angiotensin blocker
2nd line dapagliflozin
if stage 5 or uraemic = dialysis. +/- transplant.
mechanism of microablinuria in diabetes
loss of negative charge in the basement membrane - as albumin is also negatively charged so repulsion is lost.
more will sneak through now.
can also happen in acidosis/ intense exercise (H+ binds to albumin, causing less nagtivity)
renal replacement therapy (HD, PD, etc)
HD- 3x weekly. machine is semipermeable membrane (small holes in it) pulls toxins out via diffusion. - uses dialysis fluid.
PD- peritoneal membrane is the semi permeable membrane- peritoneal fluid is pumped in- this is ‘clean’ and ‘dirt’ is pulled across.
PD can be ambulatory or intermittent.
haemoinfiltration- same as HD but water not fluid
complications:
fistula issues
amylodosis
cerebral oedema
causes of nephrotic
causes of nephritis
minimal change + membranous
goodpasture disease, vasculitis, iga nephropathy
diff between acute and chronic renal faliure
acute is reversable
chronic is no
where is epo produced
juxtaglomerular cortex
progression of renal disease
blood and protein for a glomerulonephritis
fresh urine - red cell casts- also a sign of glomerularnephritis
vasculitis or iga disease common causes.
factors that accelerate CKD progressions
HTN
proteinurea
CCF and prev cardiovascular risk
anaemia
long history of diabetes
ethnicity (afro carribean, native americans, asians)
episodes of AKI
smoker
male
things that reduce proteinurea
SGLT2 inhibitors - reduce proteinurea well
to remember consultant said so
3 drugs to help ckd decline
ARB
ACEi
sglt2 inhibits
other things to help
limit salt
reduce potassium if struggling.
limit phosphate
stop cmoking, inc phys activity
reduce bp, glycaemia, proteinurea
reduce aki episodes
stop offending drugs.(nsaids)
