Acute Kidney Injury Flashcards
Definition
Abrupt decrease in kidney function- rise in serum creatinine by 26.4 micro mols or 50%
Fall in urine output <0.5ml/kg/hour >6 hours
Most common cause of AKI
Acute tubular necrosis
Pre- renal causes
Hypovolaemia- burns, D+V, Haemorrhage
Hypotension- cardiogenic shock, sepsis, anaphylaxis
Hypoperfusion- NSAIDS, COX inhibitors, hepatorenal syndrome
Renal causes
Vascular- thrombosis, embolism, vasculitis, polyarteritis nodosa
Glomerular- acute GN, acute vasculitis, SLE, HSP, good pastures
Interstitial nephritis - drug induced (NSAID, Cephalosporins), TB, Sarcoidosis, lymphoma
Tubular injury- contrast, rhabdomyolysis, hypercalcaemia
Post renal causes
Stones
Cancer
Strictures
External compression
Pathophysiology of pre-renal AKI
Volume depletion leads to decreased effective intravascular volume
Increased ADH + aldosterone leads to salt and water retention –> oliguria + AKI
Pathophysiology of renal AKI
inflammation/damage to cells
Pathophysiology of post-renal AKI
Obstruction of urine flow leading to hydronephrosis + loss of contracting ability
Symptoms of AKI
Decreased urine output Fluid retention - oedema Anorexia, weight loss, fatigue vomiting SOB, palpitations
Signs of AKI
Hypertension Pulmonary oedema Plural effusions Uraemia- itch, pericarditis Oliguria
Investigations
U+Es FBC + Coagulation screen Urinalysis USS KUB Immunology Biopsy
When is a biopsy indicated
suspected rapidly progressing GN
+ve immunology + AKI
Stage 1 classification of AKI
Creatinine >26.4 or increase by 150-200%
Stage 2 classification of AKI
Creatinine increase by 200-300%
Stage 3 classification of AKI
Creatinine increase by 300% or >350micromols or need for renal replacement therapy