Renal function, AKI and CKD Flashcards
What is clearance?
Volume of plasma that can be completely cleared of a marker substance per unit time
What are the 3 criteria that need to be fulfilled for a marker to be used to measure GFR?
Marker is NOT bound to serum proteins
Freely filtered by the glomerulus
NOT secreted or reabsorbed by tubular cells
What factors affect creatinine
- Muscularity (proportional to mass)
- Age
- Sex (higher in men)
- Ethnicity (higher in Afro-Caribbean)
What is an alternative endogenous marker used to measure GFR
CYSTACIN C
What is PCR and how is it collected
• Urine protein: creatinine ratio (PCR):
o This is a quantitative assessment of the amount of proteinuria
o Measurement of creatinine corrects for urinary concentration- since creatinine is released at constant rate into urine
o Two methods to do PCR:
24hr urine collection (cumbersome and messy; highly inaccurate without patient education)
Spot urine measurement
What is investigated in a urine dipstick
o pH = 4.5 to 8.0
o Specific gravity (density of urine)
o Protein = sensitive to albumin, not BJPs (Bence-Jones Proteins); Zero Trace 1+ to 4+
o Blood (neg excludes haematuria)
o Leucocyte esterase (negative result is significant – reliably excludes bacteria)
o Nitrite (detects bacteria, esp. Gm negatives – cannot reliably excludes bacteria if -ve)
What to look for in urine microscopy
Crystals calcium oxalate crystals RBCs ‘little doughnuts’ WBCs ‘multi-nucleate cells’ Casts ‘fuzzy burritos’ Bacteria ‘wannabe RBCs’
Difference between AKI and CKD
AKI- abrupt, reversible decline in GFR, with treatment targeted to precise cause of AKI
CKD- long, irreversible decline of GFR, with treatment targeted to prevent complications of CKD
Stages of AKi
1- 1.5-1.9x serum creatinine 0r <0.5ml/kg/hr 6-12hrs
2- 2-2.9x or >12hrs
3- >3x or <3 >24hrs
Why ACEi are contraindicated in RAS or AKI
Angiotensin II causes increased constriction of the efferent compared to other vessels to maintain GFR
However since ACEi and ARB inhibit this- it will reduce efferent constriction reducing GFR
Causes of Pre renal AKI
o True volume depletion (e.g. haemorrhage) Hypotension
o Oedematous state Selective renal ischaemia (e.g. renal artery stenosis)
o Drugs affecting renal blood flow
ACE inhibitors or ARBs – reduce efferent constriction
• ACEi are very contraindicated in RAS
NSAIDs or Calcineurin inhibitors – decrease afferent dilatation
Diuretics – affect tubular function, decrease preload
Pre renal AKI va ATN
o Pre-Renal AKI is NOT associated with structural renal damage
o ATN does NOT respond to restoration of circulating volume
o Epithelial cell casts would be seen in the urine on microscopy
Cause of post renal AKI
o (Intra-renal obstruction) Ureteric obstruction (bilateral)
o Prostatic / urethral obstruction Blocked urinary catheter
o Retroperitoneal fibrosis / Ormond’s disease
Cause of intrinsic AKI
o Vascular disease (e.g. vasculitis)
o Glomerular disease (e.g. glomerulonephritis)
o Tubular disease (e.g. ATN) = MOST COMMON, myoglobin- DTI
o Interstitial disease (e.g. analgesic nephropathy – long-term excessive use of analgesics)
Stages of CKD
1- damage with normal GFR
2- GFR 60-89
3- 30-59
4- 15-29
5- <15 or dialysis