RENAL Flashcards
Describe how the kidneys respond to an acidosis
- Secretes H+ and resorbs all the plasma bicarb
- Secretes more H+ and adds new bicarb to blood via bicarb generated by phosphate buffer
- Upragulates ammonia buffer - which metabolises glutamine in cells to produce ammonia (excreted) and bicarb moved into blood
Describe how the kidneys respond to an alkalosis
- Rate of H+ secretion from tubular cells not enough to match bicarb so excess bicarb excreted
- Down regulation of phosphate buffer
- Down regulation of ammonia buffer
What is normal urine output
around 1 ml/minute (this equates for 1.4 litres a day)
normal range is 800ml - 2L a day
AKI when less than half of BW per hour
What happens to creatinine during pregnancy
Falls because plasma clearance increases (the volume of blood that the kidney filters)
GFR increases by 50%
What 3 things grade/ affect AKI
rise in creatinine
fall in urine output
duration of fall in urine output
What 3 things grade/ affect AKI
rise in creatinine
fall in urine output
duration of fall in urine output
No urine output
What factors can cause a raised / low creatinine
Muscle mass Diet - High protein diet Surgery - ischemia Dilution - low (i think) Pregnancy - low
What amount of kidney injury produces a rise in urea and cr
50-60%
Why is creatinine used over egfr for AKI
Creatine more dynamic physiology, eg will increase in response to sudden injury. More of a moment to moment picture.
GFR better indicator for overall kidney function. Can have a low GFR and normal creatine (as the kidney has a lot of reserve to compensate for a low gfr)
What are the stages of AKI
- 1.5-1.9 x BL cr; <0.5 ml/kg/hr for 6-12 hrs
- 2.0-2.9 x BL cr; <0.5 ml/kg/hr for >12 hrs
- > 3.0 x BL cr; <0.3 ml/kg/hr for >24 hrs OR anuria for 12 hours
What clinical picture is typical of acute tubular necrosis
Raised Cr following hypovolaemia or nephrotoxic drug
Raised Urine
Raised K
Metabolic acidosis
What value indicates a moderate, significant, and severe hyperkalaemia
5-6
>6
>6.5
Is hyperkalaemia symptomatic
Usually not
But common manifestations can be muscle weakness and ECG changes, with the latter having the potential to progress to a life-threatening arrhythmia
What is the management of hyperkalaemia
- Cardio protection - calcium gluconate IV
- Move K+ into cells - insulin + glucose (to avoid hypo)
- Salbutamol neb
- If can’t control need renal replacement (haemodialysis or haemofiltration)
What drug groups are renotoxic and should be stopped in AKI
ACE - inhibitors
ARB (think antihypertensives)
NSAIDs
Aminoglycosides - gentamicin, neomycin, streptomycin
What antibiotic can cause a temporary rise in creatinine
Trimethoprim
When should you suspect acute tubular necrosis
Anybody with a severe and prolonged pre renal cause of AKI
Anybody with AKI that has started a new nephrotoxic drug
With a bad AKI - eg met acidosis and high potassium
Muddy brown casts
What are the risk factors for ATN
Poor renal function
Severe and prolonged hypovolaemia / under perfusion to kidneys
New nephrotoxic drug
Underlying renal disease
what is azotaemia
High levels of nitrogen compounds/ products in blood, eg urea, cr, other body waste products with N in
What chronic condition causes small kidneys, what are the exceptions to this rule
CKD
Exceptions - diabetes, HIV
What causes enlarged kidneys
Hydronephrosis
Pyenephrosis
How can USS be used to elicit causes of AKI
mainly to rule out/ in obstructive cause that would cause large kidneys asymmetry - eg renal artery cause small - CKD large - infection, obstruction normal - ATN, intrinsic renal causes
What investigations should be done to confirm acute tubular necrosis
Urea-creatinine ratio (10-1 in ATN because issue is in tubule not glomerulus, unless overlap with pre-renal)
Urinary sediment analysis - muddy brown casts
Urinary sodium - high because na-k pump stops working
Urine osmolality - high because tubules dont resorb
What are the life threatening complications of AKI
Pulmonary oedema
Metabolic acidosis
Hyperkalaemia
