Urinary Module 1 Flashcards
What if GFR?
This is the volume of fluid filtered from the renal glomerular capillaries in to the Bowmans capsule per unit in time
What tests can be used assess renal function?
Blood - urea, creatinine, SDMA
Urine - USG, sediment
Excretion tests to quantify GFR
Renal biopsy
Imaging
Culture and sens
What is creatinine to renal function
It is a late marker of renal function, need to see a reduction of 39-68% GFR to see changes, 75% changes relates to renal mass reduction
Released in muscle catabolism in a predictable way - mainly filtered through kidneys
What is urea to renal function
Made in the liver and produced by protein catabolism
It is decreased in animals with a negative energy balance/poor BCS, increased with high protein meal, GI haemorrhage increases
Not predictably released
AKI creatinine score
1-5, 3-5 will impact outcome
What is SDMA to renal function
released into circulation during protein degradation and is excreted by the kidneys
Almost exclusively renally excreted
Increased in about 40% loss of renal function - earlier than creatinine
dehydration, AKI, hypovolaemia and urinary obstruction will affect results
Imaging options for the kidneys/bladder
- radiography: pneumocystogram
- Urethrogram
- Excretory Iv urography - renal pelvis
- Ultrasound
- CT/MRI/Scintigraphy
3 things to know about kidneys and neonates?
- Renal function maturing till 8 weeks - hyposthenuria
- Physiological proteinuria present for a few days due to MDA
- Normoglycaemic glucosuria present
AKI pathophysiology
- Renal function impairment results from cell damage and or death most likely after diminished renal blood flow or O2 delivery
- Molecular changes activate destruction enzyme cascades and Na/K pump is influenced which results in changes electrolytes and cellular function - triggers inflammatory cascade (neutrophil activation and cytokine release activating vascular permeability)
- Cell edema contributes to tubular obstruction and formation of O2 free radicals and further toxic substance formation leading to progressive cell injury
7 Causes of AKI?
- Ischaemia
- Sepsis
- Toxins - ethylene glycol, lily tox, grape raisin, haemoglobinuria
- Drugs - NSAIDs, contrast agents, aminoglycosides
- Infections - pyelonephritis, lepto, babesia, lymes, leish
- Hypercalcaemia
- Hyperviscosity
What are clinical signs of renal impairment?
- Uraemia
- Isosthenuric urine
- Hyperkalaemia
- Hypertension
- GI haem - abonormal bun/crea ratio
- Increased phosphate
- Acidosis
- Changes to Na
Phases of AKI
- Initiation phase - initial insult resulting in tissue damage 0-36hrs
- Extension phase - damage from the insult extends - inflamm phase 48-72hrs
- Maintenance phase - stage where AKI is detected 7-21days
- Recovery phase - active repair 1-2 mths
Treatment of AKI
- Address/Treat cause: discontinue nephrotoxic drugs/treat infections/tx toxin
- Supportive care: Fluid therapy
- Uraemic signs tx: omeprazole, anti-emetic (maropitant, ondansetron, metaclop), pro-kinetics (metaclop/cisapride/low dose erythromycin)
- manage BP
How to manage oliguria
- Frusemide - acts diuretically on tubules - doesnt increase blood flow
- Mannitol - diuretic - can contribute to AKI at high doses
- Fenoldopam - renopreotective but not in AKI
- Diltiazem
How to manage hyperkalaemia
- Calcium gluconate - only works heart effects
- Glucose
- Glucose/insulin
- Terbutaline
- Bicarb