AKI Flashcards
Definition?
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.
RF?
- Older
- Underlying kidney disease
- DM
- Sepsis
- Nephrotoxins
- Surgery
- Fluid loss/Sodium retention
- CT/cancers
- Cardiac arrest. Trauma, pancreatitis, kidney stones
ddx?
CKD
Reduced kidney function and high creatinine, hypocalcaemia, anaemia, hyperphosphatemia, small kidneys
Increased muscle mass
Minor elevation, non-acute, normal 24 urine creatinine normal
Drug SE
Drug hx, normalises
Epidemiology?
P:AKI rate of 10,400 per million population
A?
pre renal
intrinsic
post-renal
Pre-renal?
Prerenal causes includeany condition leading todecreased renalperfusion.
• Hypovolemia
• Volume depletion: e.g.,hemorrhage, vomiting,diarrhea, sweating,burns,diuretics, poor oral intake,acute pancreatitis
• Decreased circulating volume:e.g.,hepatorenal syndrome,cirrhosis,liverfailure,nephrotic syndrome,congestive heart failure
• Hypotension: e.g.,sepsis,dehydration,cardiogenic shock(decreasedcardiac output),anaphylactic shock
• Renal artery stenosis
• Drugsaffectingglomerularperfusion: e.g.,cyclosporine,tacrolimus,NSAIDs,ACE inhibitors
Intrinsic?
Intrinsic causes includeany disease that leads to severedirectkidneydamage.
• Acute tubular necrosis(causes∼85%of intrinsic AKIs): most commonly caused bysepsis, infection,ischemia, and/ornephrotoxins
• Glomerulonephritis(e.g.,rapidly progressive glomerulonephritis)
• Vascular
• Hemolytic uremic syndrome(HUS)
• Thrombotic thrombocytopenic purpura(TTP)
• Malignant hypertension
• Vasculitis
• Acute tubulointerstitial nephritis
• Drug-induced
• Infectious
• Immunological
Post-renal?
Postrenal causes include any condition that results inbilateral obstructionof urinary flow from therenal pelvisto theurethra.
• Congenitalmalformations(e.g.posterior urethral valves)
• Acquired obstructions
• Benign prostatic hyperplasia(BPH)
• Iatrogenic/catheter-associatedinjuries
• Tumors
• Stones
• Bleedingwith blood clot formation
• Neurogenic bladder(e.g.,multiple sclerosis,spinal cord lesions, orperipheral neuropathy)
CP?
- May be asymptomatic.
- Oliguriaoranuria
- Signs ofvolume depletion(inprerenal AKIcaused by volume loss)
- Orthostatic or frankhypotensionandtachycardia
- Reducedskinturgor
- Signs of fluid overload(from Na+and H2O retention)
- Peripheral andpulmonary edema
- Hypertension
- Heart failure
- Shortness of breath
- Signs ofuremia
- Anorexia, nausea
- Encephalopathy,asterixis
- Pericarditis
- Platelet dysfunction
- Signs of renal obstruction (inpostrenal AKI)
- Distendedbladder
- Incomplete voiding
- Painover thebladderor flanks
- Fatigue,confusion, andlethargy
- In severe cases:seizuresorcoma
- Affected individuals have a higher risk of secondary infection throughout all phases(most common reason for fatalities).
Staging?
1
Increase >26µmol/L in 48h OR increase > 1.5 × baseline
<0.5mL/kg/h for >6 consecutive hours
2
Increase 2–2.9 × baseline
<0.5mL/kg/h for >12h
3
Increase >3 × baseline OR >354 µmol/L OR commenced on RRT irrespective of stage
<0.3mL/kg/h for >24h or anuria for 12h
What do the kidneys usually do?
- Kidneys regulate what’s in the blood by removing waste, keeping electrolyte levels stable, regulate water levels and make hormones
- Blood enters via the renal artery into glomeruli-contents filtered into the renal tubule-some are reabsorbed and some can be secreted
- Urea and creatinine is excreted-ratio of blood urea nitrogen to creatinine is 5-20:1
- Filtrate becomes urine, is released into the ureter to be stored in the bladder and blood drains into renal vein
What happens in pre-renal?
- Decreased blood flow
- Absolute loss of body fluid-haemorrhage, vomiting, diarrhoea, burns
- Relative loss of fluid-
- distributive shock-fluid moves into tissues from blood-total body fluid is same but blood vol is less
- CHF-blood pools in heart-less is sent to kidneys
- Renal artery stenosis or blocked by embolus-
- less blood into kidney and glomeruli-less is filtered so decreased GFR-less urea and creatinine are filtered out so they build up in the blood (azotemia)-oliguria
- Activation of RAAS-more aldosterone-more water and sodium reabsorption-more urea absorption
- Less sodium excreted gives a low urine sodium and low ratio-more concentrated and smells of urea
What is intrinsic?
- Damage to tubules, glomeruli or interstitium
- ATN-epithelial cells lining tubules necrose
- Ischaemia-pre-renal acute injury meaning less blood is sent to the kidneys-so less transport can occur
- Cells in the PCT and ALoH are esp sensitive
- Nephrotoxins-damage cells-eg aminoglycosides, heavy metals, myoglobin, ethylene glycol, dyes, uric acid (tumour lysis syndrome)
- Cells slough and plug tubules, creating a higher pressure so less of a pressure gradient in the arterioles
- Less fluid is secreted-less GFR-less urine produced and azotemia
- Less exchange of molecules causes hyperkalaemia and metabolic acidosis
- Brown glandular cast-residue from cells
What happens in GN?
- Inflammation of glomerulus
- Deposition of antigen-antibody complexes in the glomerulus, whcih activates teh complement system-macrophages and neutrophils are attracted to the site-lysosomal enzymes released-damage podocytes
- This increases membrane permability so large molecules filter through-proteinuria and haematuria
- The leakage also reduces pressure differences bt the blood vessel and tubule-lower GFR-less blood filtered-oliguria and oedema and hypertension, azotemia
What happens in AIN?
- Inflammation of interstitium over days/weeks
- Cuased by infiltrattion of neyutrophls or eosinophils-type I/IV hypersensitivity to meds like NSAIDs, penicillin, diuretics
- Oliguria and eosinophilis, fever and med-stop when meds too
- Renal papillary necrosis if not stopped or on chronic analgesia, DM sickle cell and pyelonephritis-papillae destroyed-haematuria and flank pain
