Renal and post renal AKI Renal AKI Classified according to which structures are involved • Vascular causes o Vasculitis/GN o Haemolytic-uraemic syndrome (HUS) o Thrombosis • Glomerular • Tubular causes o ATN most common, due to ischaemia, drug toxicity or venom • Interstitial causes o Allergic interstitial nephritis  Common allergens are in antibiotics, NSAIDs, COX-2 inhibitors, sometimes PPIs  May be associated with rash or eosinophilia  Renal biopsy shows interstitial inflammation with eosinophil infiltration Hyperkalaemic ECG Changes • Peaked T waves • Broadened QRS • Sinus asystole • Sine wave ECG • Asystole/fibrillation • Severity depends on: o Associated hypocalcaemia o Rapidity of development o Absolute level of hyperkalaemia • Management o Diagnose and stabilise cardiac toxicity if present  ECG, cardiac monitor  IV calcium gluconate/chloride o Shift K into cells  Nebulised salbutamol  Insulin/dextrose bolus IV NaHCO3 if acidotic o Remove K from body using Ca or Na polystyrene resin and/or haemodialysis  Post Renal AKI • Unilateral complete obstruction o Loss of renal function on ipsilateral side o Hyperfiltration on contralateral side o Only causes AKI if:  Bilateral obstruction  Asymmetric function (single/dominant kidney) • Bilateral complete obstruction o Causes progressive and irreversible damage o Tubular damage affects concentrating ability of kidneys early in disease o Full recovery if relieved in <1 week o Minimal recovery if relieved >12 weeks • Causes of obstruction o Benign prostatic hyperplasia (BPH) o Blood clot o Blocked catheter o Neurologic diseases e.g. spinal injury o Pelvic tumour compressing ureters o Retroperitoneal fibrosis o Abdominal aortic aneurysm o Congenital lesions e.g. ureteropelvic junction (UPJ) obstruction o Bilateral ureteric calculi • Percutaneous nephrostomy: catheter inserted in collecting system of kidney to remove urine upstream of obstruction  Post obstructive diuresis: o Occurs after relief of complete obstruction due to the effects of obstruction on concentrating capacity of the kidney o K wasting can occur o Urine output >500mL/hr can occur Urinary Investigations in AKI • Urinalysis: blood + protein = GN until proven otherwise  Urine microscopy: o If glomerular cause: look for RBC casts and dysmorphic RBCs o If ATN: look for tubular cell casts o If unexplained: look for presence of oxalate or urate crystals  Urine electrolytes: o Can determine state of tubular function o In pre-renal phase: there is good Na reabsorption and urine concentration because the tubules are still viable o Will differentiate between a patient in pre-renal or ATN phase • Urinary myoglobin: if muscle necrosis or rhabdomyolysis is suspected Urinary Indices Pre-renal Phase ATN Phase Urine osmolarity (mOsm) High >310 Normal 290-310 Urine Na (mM) Low <10 High >40 Urine microscopy Bland hyaline casts Broad pigmented casts Fractional excretion of Na <0.01 >0.01 Fractional Excretion of Sodium • More elaborate way to measure tubular resorption of sodium • Less affected by diuretics • Measures proportion of filtered sodium that is excreted 𝑈𝑁𝑎 × 𝑃𝐶𝑟 𝐹𝐸𝑁𝑎 = 𝑃𝑁𝑎 × 𝑈𝐶𝑟 • FENa <0.01: pre-renal oliguria • FENa >0.03: renal cause (includes ATN)