Renal

Question 1

AKI definition

Answer 1

We can diagnose AKI with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:

A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

Question 2

AKI staging with KDIGO

Answer 2

Question 3

Drug safety in AKI

Answer 3

Question 4

Prerenal AKI pathophysiology

Answer 4

Reduction in renal perfusion without primary damage to kidney tissue

This diminished perfusion leads to decreased glomerular filtration, triggering the release of renin, aldosterone, and antidiuretic hormone to conserve fluid and maintain perfusion pressure

Prolonged prerenal states, if not rectified, can progress to ATN, causing intrinsic renal damage.

Question 5

Intrinsic renal AKI pathophysiology

Answer 5

Acute Tubular Necrosis:

Ischaemic ATN occurs due to prolonged prerenal states, leading to tubular epithelial cell death. Cells slough off and can form casts, obstructing tubules.
Toxic ATN results from direct toxin exposure, leading to necrosis and apoptosis of tubular cells

Glomerulopathies: Immune-mediated injury to the glomeruli results in inflammation and often crescent formation, diminishing the filtering capacity of the glomerulus

Interstitial Diseases: Inflammatory infiltration of the interstitium disrupts tubular function and can cause tubular atrophy

Vascular Causes: Compromise of the renal vasculature leads to ischaemic injury or inflammation, damaging the renal parenchyma

Question 6

Postrenal AKI pathophysiology

Answer 6

Obstruction results in increased intratubular pressure. Initially, this increases tubular reabsorption, but if prolonged, it can diminish glomerular filtration rate (GFR).
Backflow of urine can cause tubular damage and expose the kidney to infection

Question 7

AKI investigations

Answer 7

urine dipstick

urinary tract infection: leucocytes +/- nitrites
glomerulonephritis: haematuria + leucocytes
acute interstitial nephritis: leucocytes by themselves
microscopy, culture and sensitivity
protein:creatinine ratio if glomerulonephritis is suspected

Bloods

urea and electrolytes (?hyperkalaemia)
FBC, CRP and bone profile

if the cause is not known further blood tests should be considered including:
creatinine kinase
ANA
ANCA
anti-GBM (glomerular basement membrane)
complement levels
immunoglobulin levels
antistreptolysin O titre (checks for group A strep infection)
HIV

Ultrasound (urgent if obstructive uropathy or pyelonephritis is suspected, within 24hrs if no clear cause)

Question 8

Pre-renal uraemia vs acute tubular necrosis

Answer 8

Question 9

Dehydration renal profile

Answer 9

Increased creatinine and urea

increase in urea is proportionally higher than the rise in creatinine

Urea/(creatinine(umol)/1000)

Pre-renal >100
Post-renal or normal 40-100
Renal <40

Question 10

Hyperkalaemia treatment

Answer 10