ChemPath: Assessment of Renal Function 2 Flashcards
Define AKI.
Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis.
What are the three stages of AKI?
Stage 1: increase in serum creatinine by 1.5-1.9 times baseline
Stage 2: increase in serum creatinine by 2-2.9 times baseline
Stage 3: increase in serum creatinine by >3 times baseline
What is pre-renal AKI?
AKI caused by reduced renal perfusion
Describe the normal response to reduced circulating volume.
- Activation of central baroreceptors and renin-angiotensin system
- Release of vasopressin
- Activation of sympathetic system
- Results in vasoconstriction, increased cardiac output and renal sodium retention
Name and describe the two mechanisms that maintain renal blood flow despite changes in systemic blood pressure.
- Myogenic stretch - if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that pressure to the glomerulus
- Tubuloglomerular Feedback - high chloride concentration in the early distal tubule (suggestive of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and, hence, chloride concentration
List some causes of pre-renal AKI.
- True volume depletion
- Hypotension
- Oedematous state
- Selective renal ischaemia (e.g. renal artery stenosis)
- Drugs affecting renal blood flow
List some drugs that affect renal blood flow.
- ACE inhibitors - reduce efferent arteriolar constriction
- NSAIDs - decreased afferent arteriolar constriction
- Calcineurin inhibitors - decrease afferent arteriolar constriction
- Diuretics - affect tubular funciton and decrease preload
What is a consequence of prolonged pre-renal insult?
Acute tubular necrosis (ATN)
What might be seen on urine microscopy in a patient with ATN?
Epithelial cell casts
What causes post-renal AKI?
Physical obstruction of urine flow
List some sites of urine obstruction.
- Intra-renal
- Ureteric
- Prostatic/urethral
- Blocked urinary catheter
Outline the pathophysiology of post-renal AKI.
- GFR is dependent on a hydraulic pressure gradient
- Obstruction results in increased tubular pressure
- This results in an immediated decline in GFR
What are some consequences of prolonged renal obstruction?
- Glomerular ischaemia
- Tubular damage
- Long-term interstitial scarring
List the possible sites of disease in intrinsic AKI.
- Vascular (e.g. vasculitis)
- Glomerular (e.g. glomerulonephritis)
- Tubular (e.g. ATN)
- Interstitial (e.g. AIN)
What can cause direct tubular injury?
- Ischaemia (MOST COMMON)
- Endoengous toxins (e.g. myoglobin, immunoglobulin)
- Exogenous toxins (e.g. aminoglycosides, amphotericin, aciclovir)