Renal Flashcards
what are the pre-renal causes of AKI?
Volume Depletion: Such as from haemorrhage, gastrointestinal losses (vomiting, diarrhoea), and excessive diuresis.
Reduced Cardiac Output: Conditions like heart failure, shock (septic, hypovolaemic, cardiogenic), or large vessel occlusion can lead to reduced renal perfusion.
Systemic Vasodilation: Septic shock and anaphylaxis can lead to systemic vasodilation and relative renal hypoperfusion.
Drugs: Non-steroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors can interfere with renal autoregulation.
what are the intrinsic causes of AKI?
Acute Tubular Necrosis (ATN): Caused by ischaemia (sustained prerenal factors) or toxins (drugs, contrast, rhabdomyolysis).
Acute Interstitial Nephritis (AIN): Typically drug-induced, but can also be caused by infections or autoimmune diseases.
Vascular: Includes conditions like renal artery or vein thrombosis, malignant hypertension, and vasculitides.
Glomerular: Rapidly progressive glomerulonephritis or other glomerulopathies.
What are the post renal causes of AKI?
Obstruction: Obstruction can occur at any level from the renal pelvis to the urethra due to stones, tumours, strictures, or prostatic hypertrophy.
pathophysiology of pre renal AKI?
Reduction in renal perfusion without primary damage to kidney tissue.
This diminished perfusion leads to decreased glomerular filtration, triggering the release of renin, aldosterone, and antidiuretic hormone to conserve fluid and maintain perfusion pressure.
Prolonged prerenal states, if not rectified, can progress to ATN, causing intrinsic renal damage.
What is the pathophysiology of intrinsic AKI?
Acute Tubular Necrosis:
Ischaemic ATN occurs due to prolonged prerenal states, leading to tubular epithelial cell death. Cells slough off and can form casts, obstructing tubules.
Toxic ATN results from direct toxin exposure, leading to necrosis and apoptosis of tubular cells.
Glomerulopathies: Immune-mediated injury to the glomeruli results in inflammation and often crescent formation, diminishing the filtering capacity of the glomerulus.
Interstitial Diseases: Inflammatory infiltration of the interstitium disrupts tubular function and can cause tubular atrophy.
Vascular Causes: Compromise of the renal vasculature leads to ischaemic injury or inflammation, damaging the renal parenchyma.
what is the pathophysiology of post renal AKI?
Obstruction results in increased intratubular pressure. Initially, this increases tubular reabsorption, but if prolonged, it can diminish glomerular filtration rate (GFR).
Backflow of urine can cause tubular damage and expose the kidney to infection.
Investigations for AKI?
Urine analysis - dipstick, MC&S, Protein: creatinine ration if glomerulonephritis is suspected
Bloods
U&E’s, FBC, CRP
consider doing creatinine kinase
ANA, ANCA, anti GBM, complement levels, immunoglobulin levels, antistreptolysin O tire, HIV
USS KUB
Pre-renal uraemia
The kidneys hold on to sodium to preserve volume
How is AKI diagnosed?
A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
How is AKI staged?
1 -
1.5-1.9 * baseline creatine or
> 26 umol/L within 24 hours
< 0.5ml/kg/hour urine output for 6 hours
2-
2.0-2.9 * baseline creatine
< 0.5 mL/kg/hour for 12 hours
3
> 3.0 * baseline creatine or
> 353.6 umol/L or
initiation of renal replacement therapy or
decrease of eGFR to < 35 mL/min
< 0.3 mL/kg/hour for 24 hours or
anuria for 12 hours
How is AKI managed?
supportive
careful fluid balance
stop nephrotoxics - NSAIDs, Aminoglycosides, ACEi, angiotensin II receptor antagonists, diuretics
may have to stop - metformin, lithium, digoxin - don’t worsen AKI but there is an increased risk of toxicity
