AKI /CKD

Question 1

What is the definitio of AKI?

Answer 1

A rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis.

One of the following should be met:

• Rise in serum creatinine over 26 sithin 48h
• 50% greater rise in serum creatinine known or presumed within past 7 days
• All in urine output under** 0.5ml/kg/h for >6h **

Question 2

What are the criteria of AKI Stage 1?

Answer 2

Increase ≥26 µmol/L; or by 1.5-1.9x the reference sCr

OR
Urine output under 0.5 ml/kg/h for 6-12h

Question 3

What is the definition for AKI stage 2?

Answer 3

Increase 2.0-2.9x the reference sCr

OR
Urine output <0.5 ml/kg/h for >12h

Question 4

What is the definition for AKI stage 3 ?

Answer 4

Increase ≥354 µmol/L; or by ≥3x the reference sCr

OR
Urine output <0.3 ml/kg/h for >24h or Anuria

Question 5

What is a pre-renal AKI?

Answer 5

AKi due to reduced renal perfusion (generalised or selective renal ischaemia)

–> usually no structural abnormalty in kidnes
–> usually responds to volume replacements

Question 6

What are causes of pre-renal AKI?

Answer 6

• Volume depletion (dehydration)
• Hypotension
• Oedematous states
• selecive renal ischaemia
• drugs affecting flomerular blood flow (ACEi and ARB reduce efferent consttriction)

Question 7

How do NSAIDs cause AKI?

Answer 7

Decreased afferent arteriolar dilatation –> decreased glomerular blood flow and renal filtration

Question 8

How do ACE i and ARB cause AKI?

Answer 8

Cause Pre-renal AKI due to
reduced efferent constriction –> less pressure to filtrate

Question 9

What 4 mechanisms can cause intrarenal AKIs?

Answer 9

Damage to any part of the nephron can caus intrarenal AKIs
1. Vessels –> vasculitis (vascular disease)
2. Glomerulus –> Glomerular disease (e.g. glomerulonephritis)
3. Tubules –> tubular disease (e.g. ATN)
4. Interstitium –> Interstitial disease (e.g. analgesic nephropathy)

Question 10

What is the most common cause of intrarenal AKI?

What are the most common aetiologies?

Answer 10

Acute tubular necrosis or Acute Tubular Injury

2 Main causes
1. Hypovolaemia → Pre-renal ARF/ AKI → Ischaemia of nephrons (EMQ: cured hypovolaemia but persistent ARF)

2. Nephrotoxins – drugs (aminoglycosides, NSAIDs), radiographic contrast agents, myoglobin (e.g. secondary to rhabdomyolysis), heavy metals.

Question 11

What is the pathophysiology of acute tubular necrosis? How does it cause AKI?

Answer 11

Damage, particularly to **short segments of tubule **of nephron leading to

1. necrotic proximal tubular cells shed fall into the tubular lumen → debris obstructs tubules → decreased GFR → sequence of pathophysiological events similar to prerenal failure

Question 12

What can cause Immune mediated intrarenal AKI?

Answer 12

Immune disfunction causing renal inflammation

Main structures involved
* Glumerus –> Glumerulonephritis
* Vasculature –> Vasculitis

Question 13

What can cause Infliltration intrarenal AKI?

Answer 13

• Amyloidosis
• Lymphoma
• Myeloma

Question 14

What are causes of post-renal AKI?

Answer 14

Anything obstructive
* BPH (Prostatic/ureteral obstruction)
* Renal stones/ other ureteric obstruction
* Blocked urinary catheter

Leading to hydronephrosis + Sky high Creatinine

Question 15

What is the prognosis of AKI presenting in Hospital

Answer 15

• 40% fully recover
• 20% die
• Other have mild-severe long term complications

Question 16

What are the indications for hamodyalisis for an AKI?

Answer 16

AEIOU

1. Acidosis
2. Electrolyte discurbance (e.g. hyperkalaemia)
3. Intoxcation (e.g. lithium/ aspirin)
4. Overload (fluid), e.g. Pulmonary oedema
5. Uraemic encephalopathy

Question 17

What are the stages of CKD?

Answer 17

Question 18

What are the main causes of CKD?

Answer 18

Diabetes
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis

–> expected to continue to increase

Question 19

What are the homeostatic consequences of CKD?
How are they managed?

Answer 19

1. Acidosis (reduced excretion of H+) –> Management with oral sodium bicarb
2. Hyperkalaemia (dietary restriction)

Question 20

What are the Hormonal consequences of CKD?

Answer 20

• Anaemia (normochromal normocytic) (Epo reduction –> epo injections)
• Renal Bone disease (1,25 alpha hydroxylase deficiency –> 1-alpha calcidiol administration)

Question 21

What are the Cardiovascular consequences of CKD?

Answer 21

Generally most severe consequence likely leading to death
* Leading to Atherosclerosis + Calcification
* Uraemic Cardiomyopathy

Question 22

What are the Uraemic consequences of CKD?

Answer 22

Uraemia and Death

Question 23

What Bone changes does Renal disease lead to?

Answer 23

1. Osteitis fibrosa cystica (increased osteoclast absorbtion –> Brown’s tumour)
2. Osteomalacia
3. Adynamic bone disease (PTH supression due to e.g. overtreatment –> decreased osteoblast activity)

Question 24

How is renal Bone disease managed?

Answer 24

• Phosphate control (bring it down) dietary, phosphate binders
• Vitamin D receptor activators:(1-alpha calcidol,Paricalcitol)
• Direct PTH suppression (e.g. Cinacalcet (increases sensitivity of the calcium-sensing receptors)