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Acute Kidney Injury (Risk Factors (Peripheral Vasc disease, Chronic Liver…
Acute Kidney Injury
Risk Factors
Peripheral Vasc disease
Chronic Liver disease
Cardiac Failure
Diabetes
CKD
Drugs (newly started esp). Nephrotix : NSAIDS, aminoglycosides, ARBS, AVE-I, diuretics. Iodinated contrast agents. witih last week
= 75 y.o (65)
Sepsis
Poor fluid intake or increased fluid loss (D&V). think neurlogical impairment, reliance on carer etc
History of urinary symptoms. or AKI
Intrinsic Renal
May require biopsy for diagnosis
Tubular
Acute Tubular Necrosis (most common)
the result of prerenal damage (ischaemia) or nephrotoxins: aminoglycosides, heavy metal contrast agents, myoglobinuria in rhabdomyolysis, crystal damage(ethylene glycol
antifreeze
, uric acid - build up from dead cells in Cancer tx, TLS), myeloma and increase in calcium
Proximal tubule and medullary thick ascending LoH very sensitive
Interstitial
. acute interstitial nephritisdrugs, infiltration with, lymphoma, infecion, tumour lysis syndrome following chemo ( see above re uric acid. keep hydrated give, allopurinol/urate oxidase)
AIN: days to weeks. infiltration of immune cells; neutrophils and eosinophils (Type I or IV hypersensitivity). NSAIDS, Penicillin, diuretics. first symptoms Oliguria, eosinophilurea, fever, rash. STOP meds. ( if not stoped, renal papillary necrosis occurs --> haematuria and flank pain
Glomerular
Autoimmune such as SLE, HSP. drugs, infections, primary glomerunlonephritides (important not to miss)
GN: antibody complexes, complement cascade activated, macrophages and neutrophil attracted and damage podocyts (-ve charge). Proteinuria, haematuria, lower GFR(pressure difference decreases), oliguria, oedema, hypertension, azotemia
Vascular
Vasculitis, malignant hypertension, thrombus or cholesterl emboli from angiography, HUS/TTP(thrombotic thromboctyopenia purpura
Glomerulonephritis
tubes becomes "plugged" and therefore there is a high back pressure and the GFR falls. oligouria, Azotemia, hyperkalaemia, metabolic acidosis. Brown cast
#
Blood urea: Cr < 15:1. FeNa >2%, urine osm < 300ml. water cannot be reabsorbed. Na, urea can't be reabsorbed.
Post renal.
Obstruction to outflow
Intra-abdominal tumours
BPH
Kidney stones
Unilateral: normal can't tell
Bilateral/urethra obstruction = post renal AKI
backup. reduced pressure gradient. reduced GFR. Azotaemia, oliguria. more reabsorption of Na, water, urea (not creatinine) due to high pressure in tubules. high reabsorptions levels, relative to Creatinine gives blood urea:Cr > 15:1. Urine Na is low. FeNa <1%. concentration urine Osmo/kg >500.
#
but high pressure in the tubules, damages epithelium. less urea gets reabsorbed. BUN:Cr < 15:1, FeNa >1%. urine becomes less concentration < 350.
Symptoms and Signs
may experience no symptoms
reduced urine output
pulm/peripheral oedema
arrythmia (K+/acid-base)
Features of uraemia : pericarditis or encephalopathy
Drugs
Safe to continue
Warfarin
Aspirin (75mg OD)
Paracetamol
Clopidogrel
B Blockers
Statins
Stop: may worsen
ACE- I
ARBs
NSAIDs
Aminoglycosides
Diuretics
Stop: may be toxic due to AKI
Lithium
Digoxin
Metformin
Not recommended : loop diuretics and low-dose dopamine (boost renal circulation). Loop diuretics may play a role in fluid overload
Pre:Renal
Normal. Blood urine: Creatinine is 5-20:1
in this AKI less Urea and Cr is filtered and more stays in the blood (Azotemia (nitrogen containing). Oliguria also
Due to decreased blood flow into the kidneys
Absolute fluid loss
vomitting
Diarrhea
Major haemorrhage
Severe burn
Relative fluid loss (moves from blood to other comparments)
Distributive shock
Congestive heart failure
renal stenosis etc
RAAS. aldosterone released from adrenal gland. Na is then reabsorbed (water reabsorption) and urea is also reabsorbed.
blood urea:creatinine ratio >20:1
#
Urine sodium is low <1% of FeNa
Urine osm > 500mOsm/kg. less water excreted, mostly urea in concentrated urine.
Diagnosis AKI
Rise in Cr > 26umol/L in 24 H
Rise in Cr >1.5 x baseline, within last 7 days
Urine output <0.5ml/kg/hr > 6 consecutive hours
Commonest Causes
Sepsis
Nephrotoxins
Ischaemia
Hyperkalaemia
short term shift in potassium from extracell-intracell fluid:
combined insulin/dextrose infusion . nebulised salbutamol
Removal of potassium from the body:
calcium resonium (oral,enema), loop diuretics, dialysis
Stabilise cardic membrane:
IV calcium gluconate
Staging: KDIGO
1: >26umol/l in 48H or increase 1.5* baseline. <0.5ml/kg/hr >6H
2. increase 2-2.9 from baseline. <0.5ml/kg/hr for >12H
3. increased >3 x baseline or required RRT. <0.3ml/kg/hr or anuria fo 12H
40-70%
10-50%