Acute Kidney injury

Question 1

Definition

Answer 1

• AKI is characterised by an abrupt reduction (usually within 48hrs) in kidney function
• This results in accumulation of nitrogenous and toxic waste products
• Many people become oliguric (low UO) with subsequent salt and water retention.
• The diagnostic classification is based on UO or serum creatinine increased

Question 2

KDIGO classification for AKI

Answer 2

Question 3

Classification and causes

Answer 3

• Classified into 3 main groups: Pre, intra and post renal
• A patient may have more than one category simaltaneously
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Question 4

Description of pre-renal AKI

Question 5

Pre-renal AKI

Pre-renal causes can be split into 2

Decreased Extracellular volume

Answer 5

• This is usally cause by impaired perfusion of the kidneys with blood and is usally a consequence of decreased intra-vascular pressures
• Decreased extracellular volume
  
  • Excessive sweating, diarrhoea/vomitting, diuretics, diabetes (osmotic diuresis), haemorrhage, burns
• Decreased Cardiac output
  
  • Acute MI, cardiac failure, hypotension
• Systemic dilation
  
  • Septicaemia with vascular bed oedma- Dec circulating volume, Anaphylaxis, pharmacological vasodilation

Question 6

Pre-renal AKI

Pre-renal causes can be split into 2

Altered renal vascular regulation

Answer 6

• Afferent arteriolar constriction (Pre-glomerular)
  
  • Sepsis
  • Hypercalcaemia
  • Drugs: NSAIDs, Amphotericin, Ciclosporin, NA, adrenaline
• Efferent arteriolar dilation (Post-glomerular)
  
  • ACEI, ARBs

Question 7

Hypovolaemia in Pre-renal AKI

Answer 7

• Hypovolaemia results from any condition that cause intravascular fluid depletion, either directly by haemorrhage or indirectly to compensate for extravascular loss
• Examples of this include diarrhoea, vomit, burns, dieuretics
• Hypotension is a secondary effect of hypovolaemia

Question 8

Hypotension

Answer 8

• In addition to hypovolaemia, hypotension can result from cardiac failure
• Septic shock- where there is peripheral vasodilation and low peripheral resistance which leads to profound hypotension despite a high CO

Question 9

Intra-renal AKI causes

Acute tubular necrosis

Answer 9

• Hypopefusion- reduced oxygen/nutrient supply
• Sepsis
• Rhabdomyolysis- Damaged muscle releases myoglobin, which can cause ATN through direct nephrotoxicity and a reduction in blood flow to the outer medulla
• Renal transplant- the procedure and conditions after surgery can cause ATN, which can be difficult to distinguish from the nephrotoxic effects of the immunosupressives
• Hepato-renal syndrome- renal vasoconstriction is frequently seen in patients with end-stage liver disease- progression to ATN is common

Question 10

Intra-renal AKI causes

Nephrotoxics

Answer 10

• Aminoglycosides- these are transported into tubular cells, where they exert a direct nephrotoxic effect. Current dosage regimens recommend OD, with frequent monitoring of drug levels, to minimise upto of AG
• Amphotericin- Direct nephrotoxcicity by disturbing the permeability of tubular cells
• Immunosupressants- Ciclosporin and tacrolimus cause intra-renal vasoconstriction that can result in ischaemic ATN
• NSAIDs- These inhibit production of vasodilatory prostaglandins (E2, D2, I2) which in presence of other co-morbidities (Hypovolaemia,tension, CO) can cause further AKI
• Cytotoxic chemo- cisplatin
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Question 11

Immune and inflammatory renal disease

Answer 11

• The kidney is vunerable to a range of immunological processes that can cause AKI
• Either Glomerulonephritis or Interstitial nephritis and rarely Pyelonephritis
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Question 12

Rapidly progressive glomerulonephritis

and Interstitial nephritis

Answer 12

• This is the inflammatory provess within the glomerulus
• If that process causes AKI it is called rapidly progressive glomerulonephritis (RPGN)
• Most cases are caused by small-vessel vasculitis
• Systemic lupus erythematosus, which usually effects young people are triggered by drugs, infections and tumours
• Interstitial nephritis- is thought to be a nephrotoxin-induced by hypersensitivity reaction associated with infiltration of inflammatory cells into the interstitium with secondary involvement of the tubules
  
  • Drugs: NSAIDs, antibiotics, PPI, furosemide, allopurinol, azathioprine

Question 13

Clinical manifestations

AKI injury with volume depletion

Answer 13

• In those patients with volume depletion, a classic pathophysiolgical picture is likely to be present, with tachycardia, postural hypotension, reduced skin turgor
• Oliguria- 0.5mL/Kg/hr
  
  • This is less than the vol required to remove waste products of metabolism to maintain normal function
• AKI is normally first diagnosed with a blood test or oliguria
  
  • Inc: creatinine, K, H+ (acidosis), phosphate

Question 14

Clinical manifestations

AKI with volume overload

Answer 14

• In those patients with AKI who have maintained a normal or increased fluid intake as a result of oral or IV administration, look for signs of fluid overload
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Question 15

Investigation of AKI

Answer 15

Question 16

Diagnosis and clinical evaluation

Answer 16

• Changes in serum creatinine can be slow (50-100 mmol/L/day) therefore is not always sufficient to severe as a rapid practical indicator of a rapidly changing GFR
• AKI is most likely to happen in people with pre-existing CKD
• Must check the root cause of AKI: ATN, Glomerulnephritis, interstital nephritis, multiple myeloma, or UT obstruction
• Often fluid balance charts can be inaccurate- try and use daily weight but this is dependent on patient mobilty

Question 17

Clinical assessments

Answer 17

1. Measure BP
2. Auscultation of the heart for the presence of third (and fourth) heart sounds, the presence of which indicates cardiac strain associated with fluid overload
3. Presence of added sounds in the chest, in particular fine inspiratory crackles that are found in some patients with pulmonary oedema
4. A CXR for pulmonary oedema
5. Pulse oximetry to assess SaO2
6. Pitting oedema of the legs- fluid overload
7. Evaluation of skin turgor- decreased skin tugor0 sign of fluid loss

Question 18

ACEI/ARB in AKI

Answer 18

• ACEI and ARBs are not inherinetly nephrotoxic
• However, profound hypotension can occur if they are initiated in susceptible patients such as those who are receiving high-dose diuretics as treatment for fluid overload
• ACEI is contra-indicated in patients with bilateral renal artery stenosis or renal artery stenosis (RAS) when they have a single kidney
• In these patients efferent vascular tone created by RAAS system is increasing blood pressure to maintain perfusion. If we inhibit this perfusion will be reduced resulting in pre-renal AKI
• Many patients with RAS, have not been identified which is why we do the monitoring for ACEI

Question 19

Management
Overview

Answer 19

• Withdrawal and avoidance of nephrotoxic agents
• Optimisation of renal perfusion
  
  • Correction of electrolytes and fluid balance
  • Use of crystalloids- potential fluid challange
  • Ionotropic + vasoconstricting drugs?
• Establishing and maintaining adequate diuresis
  
  • Furosemide (Fluid overload and hyperkalaemia)
  • Metolazone has been used as a diuretic- NB synergistic effect can be to profound (Hypovol/tension)
• Drug therapy and renal auto-regulation
  *

Question 20

Uraemia and Intravascular volume overload

Non-dialysis treatment of established AKI (NDT- AKI)

Answer 20

• In AKI symptoms of uraemia include N&V as a result of accumulation of products of metabolism
• Often these patients can’t tolerate oral diet and catabolic. Therefore need TPN/enteral feeding
• IV fluid overload must be managed, salt restriction 1-2g/day if the patient is not hyponatraemic

Question 21

Hyperkalaemia

Non-dialysis treatment of established AKI (NDT- AKI)

Answer 21

• Hyperkalaemia is a particular problem in AKI- due to reduced excretion and increased release of K
• Acidosis also exacerbates hyperkalaemia by provoking K release from cells
• Cause arrythmias, MI and are life-threatening
• Follow hospital guidelines on hyperkalaemia management

Question 22

Acidosis

Non-dialysis treatment of established AKI (NDT- AKI)

Answer 22

• The inability of the kdiney to excrete hydrogen ions may result in a metabolic acidosis
• This may contribute to hyperkalaemia
• Can treat with oral bicarbonate
• NB- bicarbonate can exacerbate K release

Question 23

Infection

Non-dialysis treatment of established AKI (NDT- AKI)

Answer 23

• Patients with AKI are prone to infection and sepsis which can cause death
• Catheters and IV lines should be used with care to reduce chance of bacterial invasion
• Fever/ signs of sepsis or infection should be immediately treated with broad-spectrum antibiotics