Acute Renal Failure

Question 1

What is ATN

Answer 1

Necrosis of tubular cells and occlusion of tubular lumen by casts and cell debri

Question 2

Causes of ATN

Answer 2

Ischaemia
- can be caused by severe prolonged pre-renal AKI
Sepsis
Nephrotoxins
- contrast (rise in creat 24-48 hours after exposure, peaks in 3-5 days, resolves in 1 week)
- antibiotics
- Chemotherapy
- endogenous toxins (rhabo, tumorlysis, multiple myeloma)

Question 3

Features of aminoglycoside kidney injury

Answer 3

Starts after 5-7 days of treatment
Resolves within 21 days
Usually have a concentrating defect, nonoliguric renal failure
Low magnesium common

Question 4

Causes of post renal AKI

Answer 4

Prostatic obstruction (BPH/malignancy)
Calculi
Structure
Malignancy
Blocked IDC
Retroperitoneal fibrosis

Question 5

Why do you get a post-obstructive dieuresis

Answer 5

Due to excretion of a large amount of accumulated salt and urea
Tubular injury and decreased concentrating ability

Question 6

What is acute interstitial nephritis

Answer 6

AKI due to inflammatory infiltrate in the interstitum

Question 7

Pathology of interstital nephritis

Answer 7

Intersitial inflammatory infiltrate not involving glomeruli or blood vessels
Mediated by a hypersensitivity reaction to an antigen
Often have systemic features - fever, rash, eosinophilia

Question 8

Common drug causes of acute interstitial nephritis

Answer 8

NSAIDs - can occur days to months after treatment, don't have eosinophillia
Omeprazole - usually insidious onset (2 months after exposure on average)
Mesalazine
Allopurinol
Penicillin
Cephalosporin
Rifampicin
Sulphonamide 
Anti-virals
Dieuretics

Question 9

What are some other non-drug causes of acute interstital nephritis

Answer 9

Infection
Autoimmune (Sjogrens, SLE, granulomatous, TINU )
Crystal deposition (urate in tumor lysis syndrome, oxalate in ethylene glycol toxicity, drug precipitation)
Cast deposition (in multiple myeloma)

Question 10

Causes of pre-renal AKI

Answer 10

Volume depletion
Hypotension
Decreased effective arterial volume (cirrhosis/CHF/nephrotic syndrome)
Drugs
- afferent arteriolar constriction = NSAIDs, calcineuron inhibitors
- efferent arteriolar diliatation = aCE-I, ARBs

Question 11

What is chronic tubulointerstital nephritis

Answer 11

Asymptomatic, slowly progressive renal impairment develops over months to years
AIN can progress to CIN
Biopsy shows cellular infiltrate in interstitum, tubular atrophy and fibrosis

Question 12

Causes of CIN

Answer 12

Autoimmune (Sjogrens, sarcoidosis, SLE)
Infections (BK virus, Tb, EBV, CMV)
Analgesic nephropathy
Calcineurin inhibitor - chronic vasoconstriction leads to fibrosis
Lithium
Lead
Hyperuricaemia
Reflux nephropathy
Balkan nephropathy