Acute Kidney Injury (aki)

Acute Kidney Injury (AKI)

Epidemiology of acute kidney injury (AKI) Staging (Kidney Disease Improving Global Outcomes grouping) – uses both serum creatinine and urine output STAGE SERUM CREATININE URINE OUTPUT 1 1.5–1.9 times baseline OR ≥0.3 mg/dl (≥26.5 mmol/l) increase <0.5 ml/kg/h for 6–12 hours 2 2.0–2.9 times baseline <0.5 ml/kg/h for ≥12 hours 3 3.0 times baseline OR Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 mmol/l) OR Initiation of renal replacement therapy OR, In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2 <0.3 ml/kg/h for ≥24 hours OR Anuria for ≥12 hours Grading of AKI directly is proportional to mortality Chertow, Glenn M., et al. "Acute kidney injury, mortality, length of stay, and costs in hospitalized patients." Journal of the American Society of Nephrology 16.11 (2005): 3365-3370. Costs approximately 1.2 billion pounds per year in the UK, not including those who go on to CRF http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf

Causes of acute kidney injury (AKI) AKI is NOT a diagnosis – it is a reflection of an unwell patient Nearly always signifies a systemically unwell patient rather than a primary renal injury- the history is very important! Classically broken into pre-renal, renal and post-renal There can often be a mixture of all aetiologies

Pre-renal causes of acute kidney injury (AKI) Renal blood flow is compromised causing a reduced glomerular filtration rate Fluid Hypovolaemia (bleeding, dehydration, burns, pancreatitis) Hypotension (e.g. septic shock) Heart failure – low cardiac output Liver cirrhosis causing low volume Vascular Renal artery stenosis Impairment of renal blood flow autoregulation Liver disease (hepatorenal syndrome - rare) ACE inhibitors and NSAIDs

Renal causes of acute kidney injury (AKI) Acute tubular necrosis Ischaemia Hypovolaemia, CCF, renal artery stenosis, hepatorenal syndrome Basically all the causes of pre-renal failure, hence why intrinsic and pre-renal disease overlap. Nephrotoxic Endogenous Haemoglobinaemia DIC and other causes of haemolysis Myoglobinuria: Rhabdomyolysis (NB have low ca in these and very high cr>ur) Myeloma kidney disease – light chain nephropathy and tubular cast damage Tubular crystal formation Exogenous Imaging contrast Nephrotoxic medication Drugs Aminoglycosides, Amphoteracin Contrast agents NSAIDs, Platinum drugs Acute tubulointerstitial nephritis Drugs: NSAIDS, penicillins, diuretics, antiretrovirals and many more Infections: TB, legionella, leptospirosis Autoimmune: Sarcoid and Sjorgen’s Acute glomerulonephritis Vascular Thrombotic micorangiopathies: Haemolytic Uraemic Syndrome, Thrombotic Trombocytopaenic Purpura, Pre-eclampsia, Malignant hypertension Vasculitis

Post-renal causes of acute kidney injury (AKI) These are all some form of obstruction either intraluminal, intramural or extrinsic obstruction Intraluminal Nephrolithiasis Tumours Sloughed papilla (post ATN, DM, sickle, analgesic nephropathy, amyloid and acute pyelonephritis) Clot retention Intramural Reflux Adynamic urethral segments Neurological disorder(MS, spinal cord injury, DM, PD, post-stroke Drugs: Anti-cholinergics and levodopa Tumours Strictures (worldwide post Schistomsomosa haematobium) Extrinsic Gravid uterus Benign and malignant masses Iatorgenic ureteric ligation Benign prostatic hypertrophy/prostate cancer Retroperitoneal pathology Retroperitoneal fibrosis – idiopathic, post inflammatory AAA, drugs (beta blockers and ergots)

Treatment of acute kidney injury (AKI) Avoidance of AKI Identify high risk patients: Elderly, CKD, cardia failure, liver disease, diabetes, vascular disease, on nephrotoxic medications Monitor patients appropriately: fluid balance, bloods tests Maintain circulation: Hydration, resuscitation and oxygenation Minimise renal insult: nephrotoxics, contrast hospital acquired infection Manage acute illness Optimise volume status BP, CRT, pulse, oedema, sats, urine output Should have iv fluid protocol If fluid deplete: Crystalloid (500ml) stat bolus THEN REASSESS Maintenance: Hartmanns Need 25-30ml/kg water, 1mmol salt and 50-100g glucose per day Evidence of crystalloid or colloid Volume needed to resuscitate someone is comparable between crystalloid and colloid - SAFE study (2007) showed only 1.3x more crystalloid than colloid needed No evidence from RCTs that colloid is better at all and may cause harm. They are also more expensive. NB. CRISTAL study actually found that colloids (inc HES) improved mortality at 90 days post-ITU admission relative to crystalloid. So a confusing area. Saline or Hartmanns Plasma-lyte better outcomes than saline Stop nephrotoxics ACE-I, diuretics, metformin, allopurinol etc. Also consider stopping antihypertensives Avoid contrast if possible Dialysis or haemofiltration Renal ward Further treatment Treat sepsis – antibiotics should be given within 1 hour of suspicion of sepsis Steroids (in AIN) Cyclophosphamide (vasculitis) Plasma exchange (HUS/TTP)

Complications of acute kidney injury (AKI) Hyperkalaemia Calcium gluconate 10mls of 10% if ECG changes Insulin and dextrose 10units of actarapid in 50ml of 50% dextrose over 15 minutes (if potassium >6.5 mmol/L or ECG changes) Salbutamol 5mg nebulised (caution in tachycardia or heart disease) Insulin and salbutamol work for roughly 4 hours or less Furosemide is useful if the patient is passing good volumes of urine but ONLY IF THE PATIENT IS FLUID OVERLOADED Cation exchange resins are overused – moderate effect with high rates of constipation which might paradoxically make the situation worse – rectal route is preferable if must be used. Renal replacement therapy if refractory Longer term review diet, avoid potassium sparing diuretics/ACE-I, ARBS, NSAIDs. Be wary of the potassium load in blood transfusions Pulmonary oedema Sit patient up High-flow oxygen unless contraindicated – consider CPAP Opiates e.g. IV diamorphine 1.25-2.5 mg or morphine 2.5mg-5mg as both an anxiolytic and a venodilator – don’t give too often due to accumulation in renal failure If haemodynamically stable give 80mg furosemide IV and consider further boluses or infusion of 10mg/hour If haemodynamically stable GTN infusion titrating up from 1mg/hour as tolerated by blood pressure (systolic above 100mmHg) If unstable will need transfer to high dependency setting for urgent filtering If hyperkalaemic with bicarbonate <22mmol/L and not fluid overloaded then can consider 1.26% sodium bicarbonate over 1 hour (can be given via peripheral cannula but avoid in cannula that calcium gluconate was given through) Acidosis Bicarbonate use should be reserved for hyperkalaemia pending specialist help pH<7.15 will need immediate critical care input for filtration Uraemic encephalopathy Acute setting presents as coma Chronically: fatigue, weakness, anorexia, nausea, metallic taste, pruritis, impotence Will need emergency renal replacement therapy in the acute setting Uraemic pericarditis Will need RRT Hypertension (more of a problem in CRF – but acute renal failure can present with hypertensive emergency and needs aggressive treatment, e.g. nitroprusside, beta blockers, ACE-I slowly over 24-48h) Sepsis – avoid or adjust doses of nephrotoxic drugs (e.g. vanc and gent) Electrolyte derangement – fluid, sodium and potassium restriction, and RRT if it is still there.

Questions concerning acute kidney injury (AKI) A 50 year old alcoholic male presents with sepsis secondary to klebsiella pneumonia. His background includes IHD, previous pneumonia, hypercholesterolaemia and hypertension. Medications include: furosemide, enalapril, aspirin, clopidogrel, co-amoxiclav (current) and simvastatin He is treated with IV antibiotics and is managed on an ITU setting for 1 week On step down to a medical ward routine bloods reveal: Sodium 132 Potassium 5.0 Urea 24 (from 8) Creatinine 390 (from 60) Clinically he is mildly dry, with a BP 135/83, HR 90, he is catheterised with a U/O 35ml/hr His management plan should include which of the following? Switch to high dose IV furosemide, stop enalapril, give IV fluids to maintain urine output, daily bloods Stop furosemide, stop enalapril, add in dopamine and maintain adequate hydration to maintain urine output, daily bloods Stop furosemide, stop enalapril, adequate fluids to maintain urine output, daily bloods Continue furosemide, stop enalapril, high dose corticosteroids and continue adequate fluids to maintain urine output, daily bloods None of the above Answer – 3