Acute Kidney injury Flashcards
Define:
An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes
What is the KDIGO criteria?
An increase of serum creatinine of >26umol/L within 48 hours.
An increase of 1.5 times serum creatinine from baseline in the last 7 days
Urine volume <0.5ml/kg/hr for >6hrs
Pre-renal causes:
Due to hypoperfusion:
Hypotension (e.g. shock, sepsis, anaphylaxis)
Hypovolaemia (e.g. haemorrhage, severe vomiting)
Renal artery stenosis, ACEi, NSAIDs, ARBs
Heart failure – cardiorenal syndrome
Cirrhosis – hepatorenal syndrome
Renal causes:
Renal - due to cellular or intrinsic damage:
o Glomerular - glomerulonephritis, haemolytic uraemic syndrome, autoimmune such as SLE, drugs
o Tubular - acute tubular necrosis (ATN) is commonest intrinsic renal cause; often occurs as a result of pre-renal damage or nephrotoxins (e.g. aminoglycosides)
o Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune), drugs, infiltration with lymphoma/infection/tumour lysis syndrome following chemotherapy
o Vascular - vasculitides (e.g. Wegener’s granulomatosis), large vessel occlusion
o Eclampsia
Post-renal causes:
URINARY TRACT OBSTRUCTION
o Luminal: stones, clots, sloughed papillae
o Mural: malignancy (ureteric, bladder, prostate), BPH, urethral strictures
o Extrinsic compression: malignancy (esp pelvic), retroperitoneal fibrosis, prostatic hypertrophy
Most common causes:
Sepsis, nephrotoxins and ischaemia
Risk factors:
o Age > 75 o Chronic kidney disease o Comorbidities (heart failure, peripheral vascular disease, chronic liver disease, diabetes mellitus) o Sepsis o Hypovolaemia o Use of nephrotoxic medications o Poor fluid intake/increased losses o Emergency surgery o History of urinary symptoms
Epidemiology:
- 18% of adults admitted to hospital will develop an AKI
* Most common in the ELDERLY
Symptoms:
• Depends on underlying CAUSE • Oliguria/anuria o NOTE: abrupt anuria suggests post-renal obstruction • Nausea/vomiting • Dehydration • Confusion
Signs:
- Hypertension
- Distended bladder – palpable
- May have palpable kidneys (suggests polycystic disease)
- May have renal bruit (sign of renovascular disease)
- Dehydration - postural hypotension
- Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
- Pallor, rash, bruising (vascular disease)
Investigations:
• Urinalysis o Blood - suggests nephritic cause o Leucocyte esterase and nitrites - UTI o Glucose o Protein – suggests glomerular disease o Urine osmolality • Bloods o FBC o Blood film o U&Es o Clotting o LFTs o CRP
Immunology
• Serum immunoglobulins and protein electrophoresis - for multiple myeloma
• ANA - associated with SLE
o Virology - check for hepatitis and HIV • Renal Ultrasound o Check for post-renal cause o CXR - pulmonary oedema o AXR - renal stones
Management:
• Begin with ABCDE approach along side checking for hyperkalaemia and treating if needed (10 ml 10% calcium gluconate, then 10 units actrapid in 50ml 50% glucose)
Assess volume status – BP, JVP, skin turgor, capillary refill, urine output
- Stop nephrotoxic drugs such as ACEi, NSAIDs, ARBs, gentamicin, amphotericin, metformin
- Monitor – fluid status, daily U&Es
- Nutrition is vital in critically unwell patient
- Treat the underlying cause
Complications:
- Pulmonary oedema
- Acidaemia
- Uraemia
- Hyperkalaemia
- Bleeding
Prognosis:
• Inpatient mortality varies depending on cause and comorbidities, and early recognition • Indicators of poor prognosis: o Age o Multiple organ failure o Oliguria o Hypotension o CKD • Patients who develop AKI are at increased risk of developing CKD
How would you treat underlying causes in AKI?
o Pre-renal: correct volume depletion with appropriate fluids/sepsis with antibiotics
Post-renal: catheterise and consider CT of renal tract and urology referral if obstruction likely cause – requires urgent relief
Intrinsic renal: refer to nephrology, check for signs of systemic disease
