AKI pt.1

Question 1

What is an AKI?

Answer 1

A rapid deterioration in kidney function

Question 2

How often do AKIs occur in hospitals?

Answer 2

Up to 20% of hospital admissions

Question 3

How is GFR maintained?

Answer 3

• Maintained by sufficient blood flow into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney. If there are alterations to this system, an AKI can occur
• At the glomerular level, GFR is dependent on a pressure gradient between the incoming blood at the afferent capillaries and the pressure in Bowman’s space

Question 4

Relationship between GFR and serum creatinine and in the context of AKI

Answer 4

in the early stages of an AKI, the reduction in GFR may coexist with a normal serum creatinine
Be aware that there may be a delay in creatinine rise in a patient with worsening renal function– urine output responds more quickly to acute kidney injury. GFR is not a tool for measuring acute kidney injury – it is derived from an equation that has only been validated for chronic kidney disease, so do not rely on it in the acute setting.

Question 5

What can the causes of AKI be divided into?

Answer 5

Into pre-renal, intra-renal, and post-renal

Question 6

When do pre-renal AKI occur?

Answer 6

• Pre-renal AKI occurs when there is reduced perfusion to the kidney.
• This can occur in hypovolaemic, euvolaemic or hypervolaemic states

Question 7

Causes of prerenal AKI

Answer 7

• Absolute hypovolaemia: haemorrhage, over-diuresis, vomiting and diarrhoea
• Low effective arterial blood volume (EABV): heart failure, cirrhosis, sepsis, third spacing of fluid
• Anatomical: renal artery stenosis
  Drug-induced: NSAIDs, ACE inhibitors, diuretics

Question 8

When does intra-renal AKI occur?

Answer 8

• Intra-renal AKI occurs when there is a structural or functional change at the level of the nephron
• This can occur independently or as a transformation of a pre-renal AKI

Question 9

Causes of intra-renal AKI

Answer 9

• Acute tubular necrosis (most common cause and due to ischemic or toxxic injury to the cells of the proximal convoluted tubules )
• Acute interstitial nephritis (AIN)
• Glomerular disease
• Intra-tubular obstruction (multiple myeloma with paraprotein, pigment (e.g. rhabdomyolysis))
• Other: scleroderma renal crisis, malignant hypertension

Question 10

AKI acute interstitial nephritis causes

Answer 10

Most often eosinophilic nephritis that can be drug-induced (e.g. NSAIDs, penicillin), infection-induced (e.g. tuberculosis, legionella) or immune-mediated (e.g. sarcoidosis, SLE or IgG-related disease (IgG4-RD))

Question 11

Glomerular disease AKI causes

Answer 11

Includes nephrotic and nephritic syndromes which may be primary renal disease (e.g. anti-glomerular basement membrane (anti-GBM), or part of systemic disease with immune complex deposition (e.g. IgA vasculitis) or without immune complex deposition (e.g. granulomatosis with polyangiitis (GPA))

Question 12

Post renal causes of AKI

Answer 12

• Post-renal AKI is associated with an obstructive pathology leading to congestion of the kidneys
• Causes of post-renal AKI can be divided anatomically:
  Ureters: nephrolithiasis, retroperitoneal fibrosis
  Bladder: bladder cancer
  Prostate: benign prostatic hyperplasia (BPH), prostate cancer
  Urethra: urethral stricture
  External: retroperitoneal mass, ovarian tumours

Question 13

What can obstruction distal to the level of bladder cause?

Answer 13

Obstruction at or distal to the level of the bladder can cause a post-renal AKI in both kidneys

Question 14

AKI in patients with one kidney vs two kidneys

Answer 14

Unless there is a solitary kidney, a unilateral obstruction may not cause post-renal AKI as the unaffected kidney may be able to compensate for the reduced function of the affected kidney. This puts patients with a solitary kidney at increased risk of AKI

Question 15

Risk factors for AKI

Answer 15

Risk factors for acute kidney injury include:

• Chronic kidney disease (adults with an eGFR < 60 ml/min/1.73 m2 are at high risk)
• Heart failure
• Liver disease
• Diabetes
• History of acute kidney injury
• Oliguria (< 0.5 ml/kg/hour)
• Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
• Hypovolaemia
• Use of drugs that can cause or exacerbate kidney injury (Table 1)
• Use of iodine-based contrast media within the past week
• Symptoms or history of urological obstruction, or conditions that may lead to obstruction
• Sepsis
• Deteriorating early warning scores
• Age 65 years or over

Question 16

Commonly used medication with potentially nephrotoxic side effects

Answer 16

Question 17

Why do NSAIDs cause renal impairement?

Answer 17

• Pre-renal: NSAIDs block prostaglandin mediated vasodilation of the afferent arteriole, which limits the kidney’s ability to regulate local blood flow
• Intra-renal: NSAIDs can cause acute interstitial nephritis (AIN)
• Post-renal: long term NSAID use can cause renal papillary necrosis where the medullary papilla sloughs off, causing obstruction to urine flow

Question 18

Timeline of AKI

Answer 18

The timeline of AKI occurs over hours to days

Question 19

Symptoms of AKI

Answer 19

• Often asymptomatic or can present with non-specific symptoms of fatigue, nausea and confusion.
• These symptoms can often be mistaken as symptoms of the underlying condition that is causing the AKI (e.g. sepsis)

Question 20

Important areas in patient history to cover when suspecting AKI

Answer 20

Important areas of the history to cover include:

• Reason for admission to hospital (e.g. sepsis, burns)
• Underlying medical conditions (e.g. heart failure, cirrhosis, SLE)
• Use of medications known to be nephrotoxic (e.g. NSAIDs, diuretics, penicillin, cisplatin)
• Recent imaging investigations using iodinated contrast, particularly if delivered arterially (e.g. CT with contrast, angiogram)
• Lower urinary tract symptoms (e.g. frequency, urgency, incomplete emptying)
• Known to have a solitary kidney
• Clinical examination

Question 21

Clinical findings in AKI

Answer 21

Typical clinical findings of AKI may include:
- Oliguria or anuria
- Signs of hypovolaemia
- Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
- Signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy (e.g. asterixis, confusion, seizures)
- Signs of post-renal obstruction: palpable or tender distended bladder

Question 22

Signs of hypovolemia/dehydration

Answer 22

Dry mucous membranes, reduced skin turgor, tachycardia, hypotension

Question 23

Investigations in AKI

Answer 23

• AKI is detected biochemically by checking urea and electrolytes.
• Other relevant laboratory investigations include BUN, FBC ( anaemia, leukocytopenia, thrombocytopenia), LFTs (serum albumin), calcium, phosphate, potassium, sodium, and VBG (to assess for acidemia)
• Urine analysis
• Imaging

Question 24

Urine studies in patients with AKI

Answer 24

Relevant urine studies may include:

= Urine analysis: proteinuria, albuminuria, haemoglobinuria, haematuria, WBC, glucose
- Urine volume measurement: oliguria, anuria
- Urinary microscopy and sediment: casts, crystals
- Urine osmolarity and specific gravity: dehydration, less commonly used in clinical practice
- Urinary eosinophil count: useful in the evaluation of AIN (rare), less commonly used in clinical practice

Question 25

Imaging studies in AKI

Answer 25

Relevant imaging investigations include:
- Post-void residual volume (PVR): can be assessed rapidly using a bedside bladder scanner
- Ultrasound of the kidneys, ureters and bladder (KUB): assess kidney size, hydronephrosis, postrenal obstruction, renal lesions
- CT non-contrast: radiopaque and non-radiopaque calculi, ureteric obstruction
- CT urogram: investigate for urinary tract bleeding
- CT triphasic kidneys: dedicated cross-sectional imaging for renal lesions (often used to clarify masses seen on ultrasound)

Question 26

Investigations

Answer 26