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
Drugs causing ATN
Aminoglycosides
Cephalosporin
Radiological contrast mediums
NSAIDS
Toxins causing ATN
Heavy metal poisoning
Myoglobinuria
HUS
Appearance kidneys ATN
Enlarged
Pale
Markings are lost
Where does ischaemic damage start in ATN
In cortex
Which parts of the nephron are most commonly affected by ATN
PCT
Ascending LH
What does myoglobinuria follow
Rhabdomyolysis
Appearance urine myoglobinuria q
Dark urine
Cause HUS in children
Diarrhoeal illness b/c verotoxin prod by E.Coli 0157
Cause HUS adults
FOllowing URTI
Sx HUS
Thrombocytopenia –> purpura
Haemolyis
ATN
Prognosis - HUS in kids
Usually recover in a few weeks
Prognosis HUS in adults + Mx
Poor
Mx supportively w/ dialysis
What is interstitial nephritis caused by
Abx
Diuretics
Allopurinol
PPIs
How does interstitial nephritis differ from ATN
Damage bypassses BM to cause damage to interstitium
Mx interstitial nephritis
Withdraw Dx
Short course PO steroids
Ix AKI/CKD
Obs incl BP O/E - palpable bladder Bloods - FBC, U+E, HCO3- PO4-, CRP, clotting, CK Nephritic screen ABG Urine Dip + MCS ECG Renal USS
What is included in a nephritic screen? (6)
ANCA + antiGBM ANA + dsDNA + complement studies Immunoglobulins Se electrophosis RF Hep B/C - MCGN ASO (post streptococcal)
Common electrolyte abnormalities in AKI (5)
Uraemia Hyperkalaemia Hypernatraemia Met acidosis Hypokalaemic/hypophosphataemia (> in CKD)
Causes hyperkalaemia (5)
AKI/CKD
Drugs - K sparing diuretics, ACEi, NSAIDs
Acidosis
Addisons/tumour lysis syndrome/burns
Causes of pseudohyperkalaemia (3)
haemolysis
incorrect order blood draw
sample taken from drip aarm
Hyperkalaemia - changes on ECG (3)
Tall tented T waves
Widened QRS
Flattened P waves/prolonged PR interval
If hyperkalaemia is unTx, what cardiac condition can develop
VF/TachyC
Mx K+ >6.5
Continuous ECG
Stabilise heart: 10ml 10% Ca gluconate IV
50ml 50% glucose + 10U ACTRAPID insulin large vv 30 mins
+/- 10mg salbutamol nebs
If pH <7.2 - NaHCO3- IV
Tackle underlying cause
Stage 1 CKD
eGFR 90+
Normal kidney fct but urine findings/structural abnorm or genetic traits that point to kidney disease
Stage 2 CKD
60-89
Mildly reduced kidney fct
+ other findings pointing to kidney disease
Stage 3 CKD
30-59
Moderately reduced kidney function
Stage 4 CKD
15-29
Severely reduced kidney function
Stage 5 CKD
<15
V severe or established RF
Aetiology CKD (8)
DM HTN Chronic glomerulonephritis Chronic pyelonephritits Obstructive uropathy Renovascular disease Dx - l term NSAIDs PKD
Sx CKD (7)
Asymp till advanced Polyuria/nocturia Restless leg syndrome Fatigue/anorexia Sexual dysfunction Nausea + pruritis Pedal oedema + pulm oedema
Signs CKD (3)
Pallor
HTN/fl overload
Pericardial rub
Ix CKD (9)
Cockcroft Gault eq Bloods: FBC, U+E. LFT, Ca, PO4, PTH, glucose Urinalysis +MCS 24hr protein/creatinine clearance CXR Renal USS
Conditions who should be offered testing for CKD (7)
DM HTN CV disease Structural renal disease/stones/BPH FHx Haematuria Multisystem disease
Mx CKD (4)
ACEi = 1st line
Aim for BP <130/80
Start statin + low dose aspirin (CV prevention)
2nd line Mx CKD (3)
Recombinant EPO
Ca/Vit D
K+ restriction
How does renal anaemia occur
Kidney norm secretes EPO in response to hypoxia
CKD - loses ability to secrete EPO partially –> Anaemia
Mx renal anaemia
Recombinant EPO added to dialysis
How does renal bone disease occur
Kidneys norm prod 1-a-hydroxylase
Which activates Vit D
Which increases Ca
Hence if low –> osteomalacia –> osteopenia
Tx of renal bone disease (3)
Restrict dietary phosphase
Phosphate binders (calcichew)
AdCal (Ca + Vit D)
Haemodialysis - how often do pt have to have it
4hrs 3xw
Main issue w/ haemodialysis
Haemodynamic instability during dialysis
What is haemofiltration
Variant of dialysis
Blood = continuously filtered across highly permeable membrane
What is peritoneal dialysis
Pt instills 2L isotonic/hypertonic solution –> peritneal cavity
Equilibrates w/ blood in peritoneal capillaries
Fl = drained after 2hrs, 3-4times a day
Risk peritoneal dialysis
Infection
Peritonitis
Annual % mortality dialysis
20%
Common complications of dialysis (5)
Infection CVD Renal bone disease/anaemia Bleeding tendencies Incr risk renal malignancy
Complications - renal transplant (4)
Operative
Rejection
Ciclosporin/lacrolimus toxicity
Infection/malig b/c immunosuppression
Prognosis Renal transplant
80-95%