Renal Flashcards
What is Stage 1 AKI
rise in serum creatinine > 26.5 micromol/L within 48hrs or 1.5 - 1.9 x the baseline
urine output less than 0.5ml/kg/hr for 6 - 12hrs
What is Stage 2 AKI
rise in serum creatinine 2.0 - 2.9 x the baseline
urine output less than 0.5ml/kg/hr for more than 12hrs
What is Stage 3 AKI
rise in serum creatinine > 353.6 micromol/L or 3 x the baseline
On RRT
urine output less than 0.3ml/kg/hr for more than 24hrs or anuric for more than 12
what is the most common type of AKI
pre-renal
What can cause decreased renal perfusion
reduced circulating volume: hypovolaemia
reduced cardiac output: cardiac failure
systemic vasodilation: sepsis
arteriolar changes: secondary to ACEi or NSAIDs
what can prolonged renal ischaemia cause
acute tubular necrosis
what is the most common intrinsic cause of AKI
ATN
what are the intrinsic causes of aki
vascular:
- large vessels e.g. atherosclerotic, thromboembolic, renal artery stenosis;
- small vessel disease: vasculitides, thromboembolic disease, microangiopathic haemolytic anaemias (DIC), malignant hypertension
Glomerular: can cause nephritic/nephrotic syndrome; major cause of CKD
Tubulointerstitial: damage to renal parenchyma eventually leading to scarring and fibrosis
- ATN
- Acute interstitial nephritis secondary to medications e.g. PPI, NSAIDs, penicillins and infections
Percentage of AKI that are post-renal
10%
Causes of post renal AKI
urinary stones (urolithiasis)
malignancy
strictures
bladder neck obstruction (e.g. BPH)
Risk factors for developing AKI
10, list at least 5
Age > 65 history of AKI CKD urological history cardiac failure DM Sepsis hypovolaemia Nephrotic drug use contrast agents
causes of acute tubular necrosis
ischaemic
nephrotoxic: medication (aminoglycosides, chemotherapies), contrast, myoglobin (i.e. rhabdomyolysis) and multiple myeloma
Presentation of pre-renal AKI
reduced CRT dry mucous membranes reduced skin turgor thirst dizziness reduced urine output orthostatic hypotension
cardiac failure
- ankle swelling
- orthopnoea
- paroxysmal nocturnal dyspnoea
- dyspnoea
- raised JVP
- ascites
Investigations for AKI
Bedside: fluid status and balance, urine dipstick and microscopy, urine osmolality and electrolytes, ECG
Bloods: FBC, U+E, bone profile, VBG
- other bloods based on suspicion: creatinine kinase, vasculitis screen, clotting, blood film, complement, immunoglobulins, serum electrophoresis, virology
Imaging: USS, CXR, renal dopplers, magnetic resonance angiography
When should you discuss AKI with a specialist
- Stage 3 AKI or in patients that might require specialist intervention (renal)
- within 48hrs
- Obstructive AKI: consider discussing with urology