AKI Flashcards
PRERENAL ETIOLOGY of aki ?
reduced perfusion to the kidney
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Absolute hypovolaemia: haemorrhage
vomiting, diarrhea,
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Low effective arterial blood volume (EABV): heart failure, cirrhosis, sepsis, ACE inhibitors Angiotensin receptor blockers (ARBs) (vascular tone of the afferent and efferent arterioles, ) ======
Anatomical: renal artery stenosis
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Drug-induced: NSAIDs, ACE inhibitors, diuretics
Intra-renal AKI etiology ?
Acute tubular necrosis (ATN): the most common cause of AKI which occurs due to ischaemic or toxic injury to the cells of the proximal convoluted tubules
Aminoglycosides
Amphotericin B
Contrast-induced
Myoglobinuria due to rhabdomyolysis
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Acute interstitial nephritis (AIN):
most often eosinophilic nephritis that can be drug-induced (e.g. NSAIDs!!!!! penicillin),
infection-induced (e.g. tuberculosis, legionella)
or immune-mediated (e.g. sarcoidosis, SLE or IgG-related disease (IgG4-RD))
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Glomerular disease: includes nephrotic and nephritic syndromes which may be
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Intra-tubular obstruction: multiple myeloma with paraprotein,
pigment (e.g. rhabdomyolysis)
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Other: scleroderma renal crisis, malignant hypertension
etiology of post renal ?
obstructive pathology
Ureters: nephrolithiasis,
Bladder: bladder cancer
Prostate: benign prostatic hyperplasia (BPH), prostate cancer
Urethra: urethral stricture
External: retroperitoneal mass, ovarian tumours
4 phases of AKI ? !
Oliguric or anuric phase
oligo 400 mL or 500 mL per 24h
anurea = < 50 ml/24 hr
pulmonary edema , hyperkalemia ,
metabolic acidosis
uremia
uremic encephalopathy
ecchymosis due to platelet dysfunction
Asterixis
azotemia - Asterixis decreased alertness and confusion ====== Polyuric/diuretic phase tubular reabsorption remains disturbed.
dry mucous membranes, reduced skin turgor, tachycardia,
hypotension
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recovery phase = months to years
Kidney function and urine production normalize
if there is post renal AKI what are the clinical manifestation ?
Distended bladder
Incomplete voiding
Pain over the bladder or flanks
diagnosis of AKI ?
rapid deterioration in kidney function marked by elevated serum creatinine and urea or reduced urine output.
KDIGO system confirms an AKI with any of the following present:6
Urine output less than 0.5ml/kg/hr for 6 hours
Serum creatinine increase 1.5x the baseline over 7 days
Serum creatinine increase by 0.3mg/dL in 48 hours
diagnosis if it is pre renal ?
BUN: Creatinine ratio >20:1
Fraction of excreted sodium (FENa) <1 %
Fractional excretion of urea <35%
Rapid response to isotonic fluid (0.9% NaCl) resuscitation strongly favours a pre-renal AKI.
management of AKI ?
A-E
C - Fluid resuscitation can rapidly improve renal function in hypovolaemia/hypotension
Diuretics may benefit volume overloaded patients
Urinary catheterisation can be used where there is difficulty in measuring urine output or to relieve urinary obstruction
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Withdrawal of nephrotoxic medication
evidence of sepsis and initiate the sepsis six care bundle if required
glucocorticoids can be considered in AIN or RPGN
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if obstruction
urinary stones - percutaneous nephrostomy tubes
Hydration
Analgesia (NSAIDs, IV morphine)
Medical expulsive therapy: alpha-blockers (e.g., tamsulosin) or calcium-channel blockers (e.g., nifedipine)
nephrostomy tubes
Change urinary pH: depends on stone composition
Extracorporeal shock wave lithotripsy
ureterorenoscopy
bladder catheter,
BPH - Alpha blockers
5-alpha reductase inhibitors (5-ARIs) - finestride
ureteric stent insertion depending on the site and cause of the obstruction
when is renal replacement therapy indicated ?
cidosis pH < 7.15 or worsening acidaemia
Refractory electrolyte abnormalities (hyperkalaemia >6.5mmol)
Presence of dialysable toxins (toxic alcohols, aspirin, lithium)
Refractory fluid overload (diuretic resistant fluid overload in setting of AKI)
End-organ uraemic complications (e.g. pericarditis, encephalopathy, uraemic bleeding)
