Renal Flashcards
Definition of AKI
Any of:
- Increase in creatinine by >26.5mmol/L within 48hr
- Increase in creatinine to ≥1.5x baseline which is presumed to have occurred within the last 7 days
- Urine volume <0.5ml/kg/h for ≥6 hours
Acute Tubular Necrosis
Ischaemic ATN essentially an extension of pre-renal AKI
Toxic ATN causes:
- Endotoxins: Myoglobin, Casts from MM, SLE
- Exotoxins: Aminoglycosides, IV contrast, chemo,
Oliguria = key predictor of need for RRT
Acute Interstitial Nephritis
Drugs: beta lactams, PPI, NSAIDs, Immunotherapy
Immune Mediated: Sjogren’s, Sarcoidosis, IgG4 Disease
Diffuse cellular infiltrate on biopsy
Urine Testing and Rhabdomyolysis
Positive dipstick for haematuria with absence of blood on microscopy is indicative of presence of myoglobin
Urine Casts
Hyaline: exercise, dehydration
Renal Tubular Epithelial Cells: suggests ATN
Granular: suggests ATN (appears muddy brown)
White Cell: Rarely isolated, suggests AIN
Dysmorphic Red Cells/RBC Casts: GN
Ultrasound features suggesting chronicity of kidney injury
Reduced kidney size
Reduced cortical thickness
Reduced echogenicity
Fluid Management in AKI
Restrictive fluid approach:
- Increased AKI in abdominal surgery
- No difference in ARDS or Cardiothoracic surgery
Fluid overload is associated with higher mortality
Modest benefit of crystalloid over normal saline for renal outcomes, similar for albumin
Renal Replacement Therapy in AKI
No different in mortality between early and late initiation
Delaying RRT can avoid RRT in 29% of patients
Urine Sodium in AKI
Urine Sodium and FENa used to distinguish Pre-Renal and ATN
Urine sodium >40 - ATN
FENa: >1% = ATN
FENa not confounded by volume state
These tests only indicated in oliguric AKI without diuretic use, CKD, obstructive cause, GN
Type 1 Renal Tubular Acidosis
- Hypokalaemic distal renal tubular acidosis
- Decreased distal tubule hydrogen ion secretion
- High urine pH
- Low urine pH → low urinary citrate → calcium phosphate stone formation
- Causes: Inherited, SLE, Sjogren’s, Drugs
- Management: Potassium citrate
- Can cause Osteomalacia and Rickets
Type 2 Renal Tubular Acidosis
- Proximal RTA
- Impaired bicarb reabsorption in proximal tubules → renal bicarb loss
- Causes: Fanconi Syndrome
- Low urine pH, raised urine glucose, protein, phosphate
- Mild hypokalaemia
- 1,25-Colecalciferol deficiency → hypocalcaemia and osteomalacia
- Treat cause as bicarb doesn’t work well
Type 4 Renal Tubular Acidosis
- Hyperkalaemic distal RTA
- Causes: Addison’s, other hypoaldosteronaemic states
- Potassium not secreted, ammonia not produced
- Management of hyperkalaemia corrects acidosis as it allows increased ammonia production
Fanconi Syndrome
Proximal tubular malfunction
Leads to loss of: amino acids, glucose, phosphate, bicarbonate
Causes: congenital, idiopathic, Wilson disease, Heavy metals, Gentamicin, Myeloma, Amyloid, Sjogren
Manage cause and replace losses to treat