AKI Flashcards

1
Q

Define AKI criteria

A

Rise in serum creatinine of 26 micro mol/L or greater within 48 hours

50% of greater rise in serum creatinine within past 7 days

Fall in urine output to <0.5 ml/kg/hour for more than 6 hours

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2
Q

Is creatinine or eGFR better for measuring AKI and why

A

Creatinine since it exclusively excreted by the kidneys
eGFR better for CKD
Urea also measured for AKI

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3
Q

Risk factors of AKI

A

Over 65y
History of AKI / CKD with GFR <60
Urinary obstruction symptoms
Heart failure
Liver disease
Diabetes
HTN
Neurological/cognitive impairment e.g. Stroke
Sepsis
Exposure to nephrotoxins / iodinated contrast agents
Perioperative

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4
Q

AKI signs and symptoms presentation

A

Reduced urine output - oligouria
Change in urine (frothy - proteinuria, dark, haematuria)
Possible dysuria
Signs of underlying cause - sepsis (pyrexia), rash from vasculitis
Signs of raised urea - Confusion/drowsiness, n+v, pruritis, fatigue
Fluid overload / Hypovolaemia signs - oedema and hypertension

Signs
- rapid rise in serum creatinine and urea

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5
Q

Name nephrotoxins

A

NSAIDs / COX2is
ACEi / ARB
Thiazide/loop diuretics
Potassium sparing diuretics
Metformin

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6
Q

Trimethoprim association with AKI

A

Trimethoprim is an antibiotic used for UTI
Interferes with creatinine secretion from tubules into urine - high creatinine may not be from AKI!!

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7
Q

How do you know raised creatinine is from AKI and not from CKD

A

If creatinine raise over a day or week is consistent with CKD instead of acute raise, it’s CKD

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8
Q

Pregnancy association with AKI

A

Creatinine may be raised post pregnancy and doesn’t mean AKI

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9
Q

What are the 3 different volume statuses

A

Dehydration/ hypovolaemia
Uraemia
Hypervolaemia

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10
Q

Components that can be checked in fluid balance assessment

A

Blood pressure
Urine output
Oedema - sacrum/peripheral
JVP

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11
Q

What are the 3 categories of AKI

A

Pre renal
Intra renal (intrinsic)
Post renal

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12
Q

Mechanism of pre renal AKI

A

Decreased renal perfusion

  • shock (hypovolaemic, cardiac, distributive)
  • decreased circulating volume e.g. dehydration
  • decreased cardiac output e.g. cardiac failure
  • liver failure / cirrhosis
  • systemic vasodilation e.g. sepsis, hypotension
  • arteriolar changes in the glomeruli e.g. from ACEi, ARBs or NSAID use
  • renovascular disease (renal artery stenosis) - more likely for CKD though
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13
Q

Causes of Hypovolaemia

A

Haemorrhage
Diuresis
GI loss (vomitting, diarrhoea)
Skin - sweating/burns
Reduced water intake / electrolyte intake
Medications

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14
Q

AKI characterisation

A

Increased creatinine and urea with oligouria (abnormally reduced urine output)

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15
Q

Renal artery stenosis presentation and clinical signs

A

Accelerated and difficult to control HTN
AKI post ACEi/ARB initiation
Progressive CKD
EPISODES OF FLASH PULMONARY OEDEMA

  • bruit on abdominal examination
  • narrowing on renal artery MRI with angiography
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16
Q

Diagnostic investigation for Renal artery stenosis

A

Renal arteriography
- can do CT or MRI though

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17
Q

Indications for acute dialysis

A

AEIOU
A - acidosis (pH under 7.2)
E - electrolyte imbalance (resistant hyperkalaemia)
I - intoxication (drug overdose, poisoning)
O - oedema
U - uraemia

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18
Q

What is Intra renal AKI

A

AKI caused by intrinsic renal pathology (damage or dysfunction to glomerulus, bowman’s capsule, and or tubules)

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19
Q

What is rhabdomyolysis

A

Skeletal muscle injury causing rapid breakdown and necrosis of skeletal muscle releases metabolic products e.g. myoglobin and potassium directly into blood

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20
Q

Causes of rhabdomyolysis

A

Trauma - elderly fall leading to prolonged immobilisation (anaerobic conditions for muscles leading to breakdown), crush injuries, burns, seizures, compartment syndrome

Ischaemia related to- embolism, surgery

Toxin induced - medications (statins, vibrates, neuroleptics), recreational drugs (ecstasy)

Strenuous / extreme physical activity e.g. intense spin class

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21
Q

What type of kidney issue can rhabdomyolysis lead to and why

A

Intra renal Acute kidney injury - metabolic products from skeletal muscle breakdown (myoglobin and potassium) damage glomeruli

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22
Q

Rhabdomyolysis symptoms

A

Muscle pain and swelling
Red / brown urinary - TEA OR COLA COLOURED - due to myoglobinuria
AKI occurs 10-12 hours after initial injury or pain onset

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23
Q

Rhabdomyolysis clinical signs and investigations

A

SERUM CREATININE FIVE FOLD RAISE FROM UPPER LIMIT - due to muscle breakdown
Raised lactate dehydrogenase
Hyperkalaemia, hyperphosphataemia, hyperuraemia, hypercalcaemia

Positive urine dipstick for blood due to myoglobinuria with no red blood cells on microscopy

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24
Q

Rhabdomyolysis treatment and management

A

Supportive management with IV fluid to excrete myoglobin and monitor electrolytes

treat hyperkalaemia - if not managed may need emergency dialysis (due to risk of acute renal failure)

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25
Q

What type of condition is nephritic and nephrotic syndromes?

A

Intra renal AKI

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26
Q

List nephritic syndrome conditions

A

IgA nephropathy - Berger’s disease - type of glomerulonephritis
Post infectious glomerulonephritis
Vasculitis
Lupus nephritis
Infective endocarditis driven immune complex mediated

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27
Q

Typical presentation of nephritic syndrome

A

Sudden onset - pt acutely unwell
Some oedema
RAISED BP
some proteinuria and hypoalbuminaemia
HAEMATURIA - cola coloured
Oligouria
May or may not hypercholesterolemia

28
Q

Typical presentation of nephrotic syndrome

A

Gradual onset - pt more acutely well
OEDEMA
PROTEINURIA
HYPOALBUMINAEMIA
may or may not have haematuria
HYPERCHOLESTEROLEMIA

29
Q

What are the differences in nephritic and nephrotic syndrome presentations !!!

A

Nephritic - sudden onset so pt acutely unwell, RAISED BP, not much oedema, only some proteinuria and hypoalbuminaemia, lots of haematuria, may not have hypercholesterolemia

Nephrotic - gradual onset so pt acutely well, lots of OEDEMA, NORMAL blood pressure, lots of PROTEINURIA and hypoalbuminaemia, HYPERCHOLESTEROLEMIA

30
Q

Nephritic syndrome mechanism

A

Endothelial wall of Glomerular capillary wall damage from immune complex formation - sediments seen on microscopy

IMMUNE SYSTEM MEDIATED

31
Q

Investigations for nephritic syndrome

A

Urine dip for leukocytes (due to immune relation) proteins and blood
Urine protein creatininratio (PCR)
Acute renal screen

32
Q

Management of nephritic syndrome

A

Urgent renal referral
BP control - may have diuresis
Treatment for underlying infection after confirming on microscopy / renal biopsy

33
Q

What is IgA nepropathy and its mechanism

A

Most common type of glomerulonephritis (nephritic syndrome - Intra renal AKI)

  • glomerular deposits of immunoglobulin A lodges in glomerulus, IgA activates complement pathway and cytokines release
  • this all leads to glomerular injury
34
Q

IgA nephropathy presentation

A

Recurrent / episodic haematuria
Teen - thirties
Common after URTI, resp or gastrointestinal infection
Hypertension
Mild proteinuria

35
Q

IgA nephropathy investigations

A

Urinalysis - blood and protein
Microscopy - dysmorphic red blood cells showing glomerular damage
Urgent referral to renal
Gold standard - renal biopsy
Serum IgA raised in 50% of pts

36
Q

IgA nephropathy management

A

Supportive management - salt restriction, hypertension management, proteinuria management (ACEi and ARB)

37
Q

What is post infectious glomerulonephritis

A

Nephritic syndrome - Intra renal AKI
Immune complex mediated glomerulonephritis

38
Q

Presentation of post infectious glomerulonephritis

A

Children
Sudden onset of haematuria 1-3 weeks after group A streptococci infection (URTI, throat or skin infection, infective endocarditis)
Oedema 1-3 weeks after infection
Hypertension

39
Q

Post infectious glomerulonephritis investigations

A

Urinalysis - for blood, maybe protein
Microscopy - dysmorphic red blood cells (sign of glomerular / renal bleeding)
FBC - resided WBC due to infection
Urea and electrolytes- sign of AKI

Gold standard - renal biopsy - humps

40
Q

What is vasculitis

A

Auto immune condition - nephritic syndrome - inflammation of small blood vessels and immune cell infiltration causing vessel wall damage e.g. haemorrhage / aneurysm or vessel occlusion

41
Q

Vasculitis presentation

A

65-74

Systemic symptoms - weight loss, fevers, malaise, polyathralgia (pain in several joints)

Depending on which blood vessels affected - in lungs (haemoptysis, pulmonary haemorrhages), ENT (epistaxis, sinusitis), eyes (conjunctivitis, episcelritis), cardiac (myocarditis)

RENAL (HAEMATOPROTEINURIA, HYPERTENSION, PROGRESSIVE AKI)

ANCA associated

42
Q

Vasculitis management

A

Urgent same day referral for biopsy
Immunosuppression depending on severity and frailty

43
Q

Triad for diagnosing nephrotic syndrome

A

Fluid overload
Low albumin
Heavy proteinuria

44
Q

What is nephrotic syndrome

A

Glomerular protein leakage - increased permeability to serum proteins in glomerulus due to damaged basement membrane

45
Q

Presentation of nephrotic syndrome (symptoms and clinical signs)

A

Frothy urine - proteinuria
Oedema

Signs
Hypoalbuminaemia
HYPERLIPIDAEMIA (hypercholesterolemia)
Lipiduria
Pro-thrombotic tendency - venous thrombosis - blood clots

46
Q

Causes of nephrotic syndrome

A

Lupus
Amyloid
Minimal change disease
Membranous nephropathy

47
Q

Investigation and management of nephrotic syndrome

A

Ix
Urine dipstick - protein
Urinalysis- albumin creative ratio raised
Renal biopsy , acute renal screen to find cause

Tx
High dose corticosteroids

Reduce proteinuria - ACEi and ARBs - proteinuria is risk factor for progression to CKD

Depends on cause and symptoms - immunosuppression for lupus, BP management, diuresis for fluid overload/oedema

prophylaxis for VTE

48
Q

Multiple myeloma investigations

A

Bone profile - calcium levels
FBC - anaemia and low platelets
CT skeleton
Serum protein electrophoresis
Serum free light chains

49
Q

Multiple myeloma treatment

A

IV hydration and correcti9n of hypercalcaemia

Haematology referral
Bone marrow biopsy
Chemotherapy + dexamethasone

50
Q

What is multiple myeloma and how does it cause kidney damage

A

Bone marrow cancer

Hypercalcaemia and light chain deposition in glomerulus causes renal damage - Intra renal AKI

51
Q

Lupus nephritis presentation + clinical signs

A

More often in women
Afro-Caribbean and Asian predisposed
Young adulthood

Weight loss, fever, rash, Alopecia, pericarditis, headache, seizure, stroke, thrombocytopenia, athralgia, arthritis

Clinical signs
- proteinuria (due to autoimmune complex formation and deposition)
Low grade haematuria
Low albumin and raised PCR
Raised ESR!!!
Positive ANA

52
Q

What is obstructive uropathy

A

Type of post renal AKI
Obstruction increases Intra tract pressure as urine builds up causing hydronephrosis

53
Q

What is hydronephrosis

A

Swelling and inflammation of obstructed kidney

54
Q

When does obstructive uropathy lead to renal failure

A

Only present of single functioning kidney or is obstruction is bilateral (obstruction may be in bladder and below)

55
Q

What are the 3 classifications of obstructive uropathy

A

Level of obstruction (upper is ureter and above so more likely unilateral , lower is bladder and below so more likely bilateral)

Complete or partial obstruction (urine output varies in partial but complete causes ANURIA)

Intrinsic or extrinsic (intrinsic cause within tract like stones, extrinsic cause outside of tract like BPH or ovarian mass)

56
Q

Symptoms and clinical signs of obstructive uropathy

A

Pain (flank pain)
Haematuria
Changes to urine volume
ANURIA!!!
Dysuria

Clinical findings
Palpable bladder (full or urine) - dull on percussion
Loin tenderness
Flank mass - rare

57
Q

Obstructive uropathy investigations

A

Urine MCS and urine dipstick
Creatinine (may be normal if one kidney normal and compensating during unilateral obstruction)
CRP, WBC and blood cultures

PSA for men with lower urinary tract symptoms

Ultrasound- - appearance may be delayed

58
Q

Obstructive uropathy treatment - done by urology / renal team

A

Relieve obstruction - catheter
- nephrostomy (if site of obstruction is further up then stent and block)

Manage underlying cause

Antibiotics due to stasis of urine

59
Q

What is reflux nephropathy

A

Reflux of urine up ureters as bladder contracts during micturition

60
Q

Complicati9ns of reflux nephropathy

A

UTIs
Tubules scarring / atrophy
If not resolved into adulthood will present as CKD / proteinuria

61
Q

Reflux nephropathy presentation

A

Childhood most commonly due to abnormally developed urinary tract - becomes better when developed

Prolonged bed wetting
Frequent UTIs!!! - leukocytes and nitrates may be present on investigations

Resolves in adulthood after urinary tract development or if not may present as CKD or unexplained proteinuria

62
Q

What is pyelonephritis

A

Acute infection of ascending urinary tract and kidney

63
Q

Diagnosis of pyelonephritis

A

Clinical diagnosis

Only US if other symptoms e.g. incomplete bladder emptying, obstruction, stones , abscess

64
Q

Pyelonephritis treatment

A

Urine MCS and Blood cultures then start antibiotics

Manage AKI

65
Q

Indications for emergency dialysis

A

Acidosis despite management
Electrolytes - hyperkalaemia despite management
Intoxication - drugs
Overload - pulmonary oedema - remove extra fluid
Uraemia - pt may be confused / drowsy