Renal - AKI Flashcards Preview

Year 3 - Medicine Block 2 > Renal - AKI > Flashcards

Flashcards in Renal - AKI Deck (18)
Loading flashcards...
1
Q

what is AKI?

A

Acute decrease in GFR (hrs-days) due to abrupt loss of kidney function. Results in:

  • disruption in ECF volume, electrolyte and acid-base homeostasis
  • accumulation of nitrogenous waste products (urea and creatinine)
2
Q

what is the most common cause of AKI?

A

90% develop in community due a pre-renal state, typically hypotension associated with sepsis and/or fluid depletion (e.g. diarrhoea, vomiting).

3
Q

describe the causes of pre-renal AKI

A

Involve decreased renal perfusion.

  1. True hypovolaemia
    - volume depletion, e.g. haemorrhage, severe vomiting/diarrhoea, burns, inappropriate diuresis
  2. Relative hypovolaemia
    - septic, anaphylactic or neurogenic shock (systemic vasodilation… hypotension)
    - oedematous states: HF (causing decreased CO), cirrhosis, nephrotic syndrome
    - renal hypoperfusion: drugs (NSAIDs, ACEi), renal artery stenosis or occlusion, hepatorenal syndrome
4
Q

how do NSAIDs and ACEi affect renal perfusion?

A

Override intrinsic autoregulatory mechanisms:

  • NSAIDs: prevent vasodilatory effects of prostaglandins on afferent arteriole
  • ACEi/ARBs: prevent vasoconstrictive effect of AngII on efferent arteriole
5
Q

describe the causes of post-renal AKI

A

Significant urinary obstruction causes increased intraluminal pressure… urine backup into kidneys… hydronephrosis. If affects both kidneys (or single functioning kidney), causes decreased GFR.

Causes of obstruction include:

  1. within lumen (kidney, ureter, bladder, urethra): calculi, blood clots, tumours
  2. within wall (usually causes CKD rather than AKI): congenital megaureter, post-TB stricture
  3. pressure from outside: BPH, abdo. tumour
6
Q

name the 3 types of causes of intrarenal AKI

A
  1. Acute tubular necrosis (ATN) = damage to renal tubule epithelium
  2. Acute interstitial nephritis = damage to interstitum
  3. Glomerular disease
7
Q

describe the causes of ATN

A

a) pre-renal AKI: decreased perfusion to kidney results in epithelial cell ischaemia… depletion of cellular ATP, cell damage and loss of function
b) nephrotoxins: myoglobin (in rhabdomyolysis), uric acid (e.g. released in tumour lysis syndrome), bilirubin, endotoxins, radiocontrast dye, aminoglycoside antibiotics (e.g. gentamicin)
c) sepsis

8
Q

describe the causes of acute interstitial nephritis

A

a) toxin-induced, e.g. NSAIDs, penicillins, diuretics: infiltration of immune cells… inflammation (type I or IV hypersensitivity)… renal papillary necrosis
b) can also be caused by infection or autoimmune disease

9
Q

explain how types of glomerular disease can result in AKI

A
  1. glomerulonephritis (e.g. causes of nephritic syndrome): Ag-Ab complexes deposited in glomerulus… activation of complement system… inflammation and podocyte damage
  2. thrombotic microangiopathy (haemolytic-uraemic syndrome, malignant HTN, scleroderma, pre-eclampsia): endothelial cell damage results in platelet thrombi formation and RBC destruction (microangiopathic haemolytic anaemia)… glomerular damage
10
Q

what parts of the nephron are especially prone to ischaemic injury?

A

Terminal PCT and TAL:

i. located in renal medulla - relatively low O2 saturation at baseline due to geometry of vasa recta
ii. highly metabolically active - substantial amounts of reabsorption and secretion occur

11
Q

describe the clinical consequences of AKI

A

Occur as a result of decreased GFR:

  1. decreased urine production (oliguria) and thus build-up of metabolites such as creatinine and BUN (azotaemia)
  2. acid-base disturbance: metabolic acidosis due to decreased excretion of metabolic acids and decreased HCO3- reabsorption and regeneration in PCT
  3. electrolyte disturbances: hypernatraemia due to reduced Na+ excretion, hyperkalaemia due to decreased K+ excretion (risk of arrhythmias) and hyperphosphataemia due to insufficient excretion of plasma phosphate +/- phosphate release from damaged cells
12
Q

what is uraemia?

A

Endpoint of loss of kidney function as a result of decreased GFR. Includes consequences of AKI plus:

  1. secondary HTN (increased ECF volume)
  2. secondary hyperparathyroidism
  3. normocytic anaemia (decreased EPO synthesis)
  4. acute pericarditis (unclear pathogenesis)
13
Q

describe the common symptoms of AKI

A
  1. oliguria or anuria
  2. nausea and vomiting
  3. confusion
14
Q

describe the common signs of AKI

A
  1. dehydration
  2. HTN (unless hypotension/pre-renal AKI is cause)
  3. fluid overload with raised JVP, pulmonary oedema and peripheral oedema
  4. pericardial rub
15
Q

what would blood Uand Es show in AKI

A

raised urea, creatinine, Na+, K+ and Pi

16
Q

how would you distinguish between pre-renal AKI and ATN

A

Urine biochemistry:
1. in pre-renal AKI, kidney is functional so high osmolality (>500 mOsm/kg) and specific gravity (>1.018) as trying to excrete waste products in as little solute as possible (as state of hypovolaemia). Low urinary Na+ (<10 mmol/L) as trying to retain water.

  1. in ATN, damaged kidney cells unable to concentrate urine, causing low osmolality (<250 mOsm/kg) and specific gravity (<1.012), and unable to reabsorb Na+, so high urinary Na+ (>20 mmol/L).
17
Q

how would you manage a pt with AKI

A
  1. Treat underlying cause:
    • pre-renal: fluid resuscitation or treatment of organ failure to restore renal perfusion
    • renal: restrict dietary Na+ and water (<1L/day) if volume overload, may require immunosuppression
    • post-renal: urological intervention
  2. Supportive management, e.g. stop nephrotoxic drugs where possible
  3. Monitoring:
    • measure UO
    • monitor creatinine, Na+, K+, Ca+, Pi and glucose (insulin therapy may be required in critically ill pts to avoid hyperglycaemia, and has effect of driving K+ into cells)
18
Q

in which cases is RRT considered?

A

If any of the following not responding to medical management:

  • hyperkalaemia (>6.5 mmol/L)
  • pulmonary oedema
  • severe metabolic acidosis (pH <7.2) due to kidney failure
  • progressive renal failure (creatinine >300 umol/L and/or rise in creatinine >100 umol/L/day)
  • uraemic complications (pericarditis or uraemic encephalopathy)
  • CKD stage 4 or 5
  • renal transplant
  • pt suspected of intrinsic renal disease (vasculitis, primary glomerulonephritis, interstitial nephritis)