Renal - AKI and CKD Flashcards
Role of renal corpuscle
Produces glomerular filtrate
Role of Proximal convoluted tubule
Isotonically reabsorbs 2/3 Na+ + H2O
Also absorbs HCO3- + glucose
Role of LH - descending limb
Passive transport of H2O by increased medularly osmolarity
Tubular fluid concentrated
Role of LH - ascending limb
Reabsorbs 20% Na
Dilutes tubular fl b/c H2O impermeable
Role of DCT
Reabsorbs remaining H2O, Na+, HCO3-
Secretes K+
Synthesises HCO3-
Role cortical collecting duct
Fine adjustments to [ ]
Principle cells secrete K+
Intercalated cells secrete H+ into lumen + synthesise HCO3- for blood
Role medullary collectign duct
Draws H2O + urea out b/c hypertonic interstitium
2’ functions of kidney (3)
Secretes EPO (stim erythropoeisis)
Secetes renin to incr BP
Hydroxylation/activation vit D
Anatomical position of kidneys
L1-3
Retroperitoneally
What is an AKI
Acute decline in GFR over 48hrs
= a sudden reversible deterioration in kidney fct
What are NICE’s req for an AKI to be present (3)
UO <0.5ml/kg/hr 6hrs
>50% rise creatinine over 7 days
>26micromol rise creatinine over 48hrs
AKI stage 1
Se Creatinine: 150-200% incr
or
25 umol/l incr in 48hr
UO <0.5ml/kg/h 6hr
AKI stage 2
Se creatinine 200-300% incr
Or <0.5ml/kg/h 12 hr
AKI stage 3
Se creatinine >300% incr
UO <0.3ml/kg/hr 24hr or anuria 12hr
Who is AKI more common in
Elderly pt w/ pre-existing CKD, DM, HTN, sepsis or hypovolaemia
What Sx does AKI usually PS with
ASYMP
or oliguria
2’ Sx AKI (3)
Uraemia –> Vom, pruritis, encephalopathy
Hyperkalaemia
Pulm oedema
How are the causes of AKI split up?
Into :
pre renal
renal
post renal causes
What is pre-renal AKI to do with
Perfusion
What type of AKI is most common in hospital pt
Pre-renal
What are the 2 main causes of pre-renal AKI
SHock
Renovascular obstruction
E.g.s of conditions –> shock + pre-renal AKI
Hypovolaemic shock - haemorrhage/fl loss
Cardiogenic: CCF, valve disease
Distributive
Sepsis
E.g.s of conditions –> renovsacular obstruction + pre-renal AKI
Embolus
Aortic dissection
RAS
Thrombosis
If interuption to blood supply of kidneys is prolonged, what occurs
ATN
= Acute tubular necrosis
Urine osm, urine Na + concentrating powers - initial pre-renal AKI
Urine osm = high (>500)
Urine Na = low (<25)
Concentrating powers = retained
Urine osm, urine Na + concentrating powers - ATN
Urine osm = isotonic w/ plasma (<400)
Urine Na = high (>40)
Concentrating powers = lost
What are post-renal AKI’s due to ?
Obstruction to outflow urinary tract
Where is the blockage often in post-renal AKI?
Ureters
E.g.s of conditions –> bladder outflow obstruction + post-renal AKI (4)
Prostatic enlargement
Urethral strictures
Phimosis / paraphimosis
What is the cause of 85% renal AKI?
Acute tubular necrosis (post ischaemic or Dx)
Other causes of renal AKI
Interstitial nephritis
Glomerular disease
Intratubular obstruction
Vascular disease