Renal - intrinsic renal AKI Flashcards
Name intrinsic causes of AKI
- Glomerulonephritis
- Acute tubular necrosis (ATN)
- Acute interstitial nephritis (AIN)
- Rhabdomyolysis
- Tumour lysis syndrome
What is acute interstitial nephritis?
Inflammation of interstitium (cell, extracellular matrix and fluid surrounding renal tubules)
What are features of acute interstitial nephritis?
- Variety of signs and symptoms, many nonspecific
- Systemic upset: ever (esp with drug induced nephritis), nausea, vomiting, fatigue, wt loss, anorexia
- Flank pain
- Dysuria
- visible haematuria
- rash and arthralgia
- mild renal impairment
- eosinophilia/eosinophil casts in urine
- HTN
Name a few causes of acute interstitial nephritis
- idiopathic
- drugs: penicillin, rifampicin, NSAIDs, allopurinol, furosemide
- Infection: staphylococci
Rhabdomyolysis: features
- Acute renal failure with disproportionately raised creatinine
- elevated CK
- myoglobinuria
- hypocalacaemia (myoglobin binds calcium)
- elevated phosphate (released from myocytes
- Coca-cola urine
Rhadobyomylysis: causes
- Seizures
- Collapse/coma
- ecstasy
- crush injury
- drugs: statins
Rhabdomyolysis: management
- IV fluids to maintain good urine output
- Urinary alkalinisation sometimes used
What is acute tubular necrosis? What finding I’d pathognomonic?
- Death of tubular epithelial cells (most common form of AKI)
- Presence of muddy brown casts of epithelial cells in urine are pathognomonic
What types of ATN are there?
- Ischaemic: hypoperfusion of kidneys during shock, renal artery stenosis and increased renal metabolism. (Should cause ski lesions because medullary region is at higher ischaemic risk)
- Toxic insult caused by haemoglobin, myoglobin, aminoglycosides, statins, anti-freeze. The tubular epithelium necrosis (but shape is preserved) due to toxic substance, it falls in lumen and turns into cast. Glomeruli are not affected.
Name a few drugs that should be stopped in AKI because they worsen renal function
- NSAIDs
- Aminoglycosides
- ACEi
- AngII antagonists
- Diuretics
Name drugs that have to be stopped in AKI due to increased risk of toxicity (but don’t worsen AKI itself)
- Metformin
- Lithium
- Digoxin
How can you try and distinguish between acute tubular necrosis and prerenal uraemia?
- Pre-renal uraemia/AKI will have a urinary sodium < 20 mmol/L because the kidneys try and hold onto sodium to preserve water and mitigate the effect of pre-renal injury
- Acute tubular necrosis will have a urine sodium > 30 mmol/L
Name a few drugs that are usually safe to continue in AKI
- Paracetamol
- Warfain
- Statins
- Aspirin - at cardioprotective dose 75mg
- Clopidogrel
- Betal blockers
How can you try and differentiate between ATN, AIN and Glomerulonephritis based on an urine dipstick?
- Protein: if protein is present, can rule out a pre-renal or post-renal cause
- Nitrites: if absent rule out infection. If present consider infection because nitrites are made by reduction from nitrates by gram negative bacteria (Eg E. coli)
- Acute interstitial nephritis is an inflammatory process: higher white cell content (leukocytes)
- Acute tubular necrosis is not inflammatory - urine has no cellular component (would expect leukocyte and blood levels to be same and both low)
- Glomerulonephritis would induce nephritic syndrome t/f blood would be present in urine.
