Renal: Acute Kidney Injury Flashcards
What are the three types of AKI?
Pre renal
Intra renal
Post renal
Is there normally higher levels of urea or creatanine in the blood?
Urea levels are higher as some urea is reabsorbed whereas almost no creatanine is (ration of about 10:1)
Describe pre renal AKI?
Decreased blood flow into the kidney leads to a lower volume of blood being filtered and a lowered GFR. This can be due to:
1. Absolute loss of body fluids (Hypovolaemia, burns, D & V)
2. Relative loss of body fluid (Distributive shock - fluid moves from the blood vessels into the tissues, congestive heart failure,
3. Renal artery stenosis
4. Renal artery embolus.
This leads to activation of the RAAS system and higher sodium and creatanine reabsorption and oliguria which is very concentrated.
What is intrarenal AKI?
Caused by damage to the tubules, the glomerulus or the interstitium.
1. Tubules
Acute tubular necrosis (most common cause of intra renal AKI) is when the epithelial cells of the renal tubule die. This can happen due to ischaemia, nephrotoxins etc. When these cells dye they are released into the tubules and block it. This then leads to high pressure in the tubules which reduces GFR. This leads to oliguria, hyperkalaemia, acidosis. Casts can also be excreted in the urine. People can recover from this type of AKI as these cels can regenerate.
2. Glomerulonephritis
Typically caused by antigen - antibody complexes in the glomerulus. This then activates the complement system which releases enzymes which damage the podocytes. This then allows large molecules to be filtered into the urine (eg protein and red blood cells.) this also reduces the GFR as the pressure difference is reduced. This leads to oliguria and oedema.
3. Interstitium
Acute interstitial nephritis due to infiltration of immune cells (neutrophils, eosinophils) that develops over days and weeks and is a response to medications such as NSAIDs, penicillins and diuretics. It is a type 1 or type 4 hypersenstivity. This usually stops if the drug is stopped but if it doesn’t then renal papillary necrosis can occur
What are some things that can cause acute tubular necrosis ?
Aminoglycoside antibiotics (Gentamicin)
Heavy metals such as lead
Myoglobin
Radiocontrast dye (giving fluids before can reduce this)
Ethylene glycol (anti freeze)
Uric acid (by product of cell breakdown in cancer treatment - tumour lysis syndrome)
What is hydration so important and chemotherapy?
reduces risk of tumour lysis syndrome which can lead to acute tubular necrosis
Why is allopurinol given with some chemotherapy?
Reduces build up of uric acid to reduce the risk of an AKI?
What is post renal AKI?
Obstruction to the outflow due to:
1. Compression
2. Blockage
If this only occurs in one and the other kidney is fine then usually renal function is usually preserved but if there is obstruction of both or the other kidney is damaged then AKI occurs.
The obsturction increases the pressure in the tubules which leads to decreases GFR.
What are the potentially life threatening consequences of AKI?
Volume overload (pulmonary oedema) Hyperkalaemia Metabolic acidosis
What is the definition of AKI?
An abrupt (less than 48 hours) reduction in kidney function defined by:
- An absolute increase in serum creatanine by more than 26.4 u mol/l
- Increase in creatanine by over 50%
- Reduction in urine output.
What are some risk factors for AKI?
Elderly CKD Diabetes Heart failure Liver disease Previous AKI Peripheral vascular disease
What is the treatment of pre renal AKI?
Fluid challenge for hypovolaemia ( Saline)
What initial investigations would you do if you suspected a renal AKI?
- U & E’s
- FBC and Coag screen
- Urinalysis
- Ultrasound
- Antibodies
- Protein electrophoresis and Bence Jones proteins
What are some indications for a renal biopsy?
- Urgent
- Suspected rapidly progressive GN
- Positive immunology and AKI - Semi urgen
- Unexplained AKI
- Rule out ATN
What would be contraindications to a renal biopsy?
Abnormal clotting
Hydronephrosis
Warfarin
Abnormal clotting
