AKI

Question 1

When looking at eGFR in AKI we are assuming Cr production and filtration stay the same - what assumptions does this lead to?

Answer 1

• Cr production unchanged
• Slow rise in Cr does not mean continual change in eGFR
• urine output can add info about other kidney function as water and solute production

Question 2

How do we recognise an AKI?

Answer 2

> 50% increase in Cr or >25% fall in eGFR within 7 days or urine output <0.5ml/kg/hr for 6h

Question 3

Pathophysiology of pre-renal AKI

Answer 3

Ineffective perfusion in otherwise normal kidneys
Hypovolaemia - reduced ECV
Cardiac failure - reduced CO
Hypotension/sepsis - reduced blood flow
Vasoactive drugs - NSAIDs and immunosuppressants

Question 4

Acute tubular necrosis

Answer 4

PCT reabsorbs 70% of glomerular filtrate so high energy demand from mitochondria for active transport of Na and other solutes
Cellular processes lost by ischaemia through any of the pre-renal processes so AT lost. Also tight junctions allowing cells to attach to eachother are broken resulting in cell slough and necrosis
Sloughed/necrotic cells block the tubular lumen, increasing pressure, stopping glomerular filtration
Reduced sodium reabsorption due to tubular damage increases Na at macula densa, releasing adensoine and causing further VC

Delayed recovery due to secondary ischaemia in medulla due to cytokines release - usually recovers in 10-14 days

Question 5

Renal AKI

Answer 5

Damage to renal apparatus - glomerulus/tubules as a result of external toxin/antibody
Anti-GBM disease
ANCA postive vasculitis
Immune complexes
Tubular toxins - drugs, contrast, myoglobulin
Crystals
Allergic reaction infiltrating the interstitium of kidney
Gent accumulates in intracellular lysosomes and when toxic cause lysosomal rupture and cell death
RPGN - capillary wall necrosis and cells accumulating in Bowman’s capsule forming crescents

Question 6

AKI complications

Answer 6

Uraemia (raised urea in blood)
Anorexia/nausea/confusion/fatigue/oedema

Life threatening - pulomnary oedema, hyperkalaemia, pericarditis

Question 7

Hyperkalaemia

Answer 7

K>5.5
Increased risk in established CKD, metabolic acidosis, drug effects
cardiac arrhythmia

If >6.5 more cardiac depolarisation and therefore muscle contraction

Question 8

predisposing hyperkal drugs

Answer 8

ACE-i/ARB - impaured aldosterone secretion so reduced renal perfusion and so dec K excretion in DCT
NSAIDS - reduce renin, dec aldosterone, inhibit PGs
Spironolactone/eplerenone - aldosterone ants
K sparing diuretics and trimeth inhibit activity of epithelial sodium channels

Question 9

How do you treat serious hyperkalaemia?

Answer 9

Stop drugs if not severe
IV calcium if severe
Insulin-dextrose - insulin activates Na-K, binds to membrane, independent of effect on glucose, salbutamol increases efficacy
But these only holding measures - fluid resusitation re-establishes filtration of K
if anuric - needs dialysis