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Core clinical problems > 105. Acute kidney injury > Flashcards

105. Acute kidney injury Flashcards

1
Q

what symptoms may ppl have with aki

A

reduced urine output
pulmonary and peripheral oedema (secondary to fluid overload)
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)
Nausea
Lethargy

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2
Q

what signs should you look for aki

A

Hypertension

Fluid status:
- Fluid overload with raised jugular venous pressure (JVP), pulmonary oedema and peripheral oedema.
- Hypovolemic if hypovolemic cause eg GI losses

Pericardial rub

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3
Q

why do ppl with aki get pericarditis

A

Uremic pericarditis is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins that accumulate in the body owing to kidney failure.

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4
Q

define aki

A

Rise in creatinine of more than 25 micromol/L in 48 hours

Rise in creatinine of more than 50% in 7 days

Urine output of less than 0.5 ml/kg/hour over at least 6 hours and more than eight hours in children and young people.

A 25% or greater fall in eGFR in children and young people within the previous 7 days.

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5
Q

risk factors aki

A

Older age (e.g., above 65 years)
Sepsis
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Cognitive impairment (leading to reduced fluid intake)
Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
Radiocontrast agents (e.g., used during CT scans)

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6
Q

General investigations aki

A

Bloods:
U&Es
albumin
lipid profile
VBG for acute ?hyperkalaemia

Urine:
Urine output
Urine dip
Urinalysis
Brown/black casts → ATN
Red casts → glomerulonephritis
White casts → acute interstitial nephritis
Urinary electrolytes, urea and creatinine (albumin:creatinine) ratio

Imaging:
ECG
USS for obstructive uropathy
CT
Biopsy for intrinsic cause

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7
Q

General management aki

A
  1. IV fluid resuscitation to promote renal perfusion (unless fluid overloaded)
  2. Hold nephrotic medications (DAMN) /risk vs benefit
    Diuretics
    ACEi/ARB/Antibiotics
    Metformin
    NSAIDs
  3. Correct electrolyte imbalances
    Hyperkalaemia (1. Calcium gluconate, 2. Insulin + dextrose)
  4. If obstructed → catheter if bladder outlet obstruction - monitor urine output and weight
  5. Renal replacement therapy if indicated eg
    Severe acidosis/hyperkalemia
    Drug intoxications
    Refractory
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8
Q

complications of aki

A

Fluid overload, heart failure and pulmonary oedema

Hyperkalaemia

Metabolic acidosis

Uraemia (high urea), which can lead to encephalopathy and pericarditis

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9
Q

what is aki (characterised by)

A

It is characterised by a decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte, and acid-base homeostasis

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10
Q

causes of pre-renal aki

A

hypovolemia
hypotension/shock
renal artery stenosis
aortic dissection
hf

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11
Q

what in the history and exam is suggestive of pre-renal aki

A

History:
vomiting/diarrhoea/burns
Heart failure
Examination
Hypovolemic status
Fluid overloaded if heart failure

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12
Q

what invetsigation finding is indicative of pre-renal aki

A

High urea>creatinine ratio

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13
Q

where is the pathology in renal aki

A

Involves damage at the level of the nephron

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14
Q

what is the normal pressure gradient across the nephron maintained by?

A

relative Afferent vasodilAtion and efferent vasoconstriction

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15
Q

Causes of renal aki

A

Change in pressure gradient
- NSAIDs
- ACEi/ARBs

Necrosis of tubule causing obstruction (acute tubular necrosis
- pre-renal injury
- rhabdomyolysis
- haemolysis
- drugs (AVRG)

Inflammation of glomerulus (glomerulonephritis)
nephrotic
- minimal change
- focal segmental glomerulosclerosis
- membraneous GN
nephritic
- post-strep GN
- IgA nephropathy (inc HSP)
- Lupus nephritis
nephritic rapidly progressing
- anti-GBM
- polyarteritis nodosum
- granulomatosis with polyangitis

Haemolytic uraemic syndrome

Acute interstitial nephritis
- Drugs PPN

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16
Q

causes of post-renal aki

A

External
- Benign prostatic hyperplasia (benign enlarged prostate)
- Tumours (e.g., retroperitoneal, bladder or prostate)

Internal
- Kidney stones
- Neurogenic bladder
- Strictures of the ureters or urethra

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17
Q

features of renal artery stenosis

A

hypertension
Renal hypoperfusion leads to hyperactivation of the renin-angiotensin-aldosterone axis, causing hypertension.

chronic kidney disease
‘flash pulmonary oedema’

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18
Q

causes of renal artery stenosis

A

acute (usually due to thromboembolism)

or chronic (usually due to atherosclerosis or fibromuscular dysplasia).

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19
Q

what drugs affect the haemodynamics and therefore can cause renal aki

A

NSAIDs cause afferent vasoconstriction

ACEi and ARBs cause efferent vasodilation

These reduce the pressure gradient and therefore reduce eGFR

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20
Q

what drugs are nephrotoxic

A

Acute tubular necrosis causing drugs: (AVRG)
Aminoglycosides
Vancomycin
Radio contrast
Gentamicin

Acute interstitial nephritis causing drugs: (PPN)
PPI
Penicillin
NSAID

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21
Q

what drugs should you hold during aki

A

DAMN

Diuretics
ACEi/ARB/Antibiotics esp aminoglycosides
Metformin, lithium, digoxin, opiates (narrow TW) (may have to be stopped)
NSAIDs

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22
Q

why do you soemtimes stop metformin in aki

A

increased risk of toxicity (but doesn’t usually worsen AKI itself)

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23
Q

causes of acute tubular necrosis

A

Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)

Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin) (eg, aminoglycosides, radiocontrast media, myoglobin, cisplatin, heavy metals, light chains in myeloma kidney).

Myoglobin : rhabdomyolysis, haemolysis

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24
Q

what invetsigation confirms ATN

A

Muddy brown casts on urinalysis confirm acute tubular necrosis

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25
Q

prognosis ATN

A

The epithelial cells can regenerate, making acute tubular necrosis reversible. Recovery usually takes 1-3 weeks.

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26
Q

what is nephrotic syndrome

A

Nephrotic syndrome occurs when the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria. It refers to a group of features without specifying the underlying cause.
It involves:
Proteinuria (more than 3g per 24 hours)

Low serum albumin (less than 25g per litre)

Peripheral oedema

Hypercholesterolaemia

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27
Q

what is the most common cause of nephrotic syndrome in children

A

Minimal change disease

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28
Q

what is the most common cause of nephrotic syndrome in adults

A

Membranous nephropathy

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29
Q

presentation nephrotic syndrome

A

Frothy urine due to excess protein in the urine

Generalised oedema due to a combination of a decrease in oncotic pressure from hypoalbuminemia, as well as a primary renal sodium retention

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30
Q

complications of nephrotic syndrome

A

thrombosis, hypertension and high cholesterol

relapse

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31
Q

how does nephrotic syndrome cause thrombosis

A

due to loss of proteins that normally prevent blood clotting, and because the liver responds to the low albumin by producing pro-thrombotic proteins.

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32
Q

how does nephrotic syndrome cause infection

A

due to loss of immunoglobulins, complement, and other compounds in the urine. Immunotherapy may exacerbate the infection risk.

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33
Q

how does nephrotic syndrome increase the pts risk of cvs disease

A

Patients become hypoalbuminemic due to the urinary loss of albumin. The liver tries to compensate for this protein loss by increasing the synthesis of albumin, as well as other molecules including lipids. These lipid abnormalities increase the patient’s risk of cardiovascular disease.

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34
Q

triad of minimal change disease? with values

A

oedema

proteinuria
proteinuria > 3.5 grams/24 hours OR urine ACR > 300 mg/mmol* or PCR > 300g/mol*

hypoalbuminaemia
serum albumin <2.5 g/dL

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35
Q

gold standard invetsigation for proteinuria

A

24-hour urine collection to quantify proteinuria (gold standard)

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36
Q

nephrotic range proteinuria is?

A

proteinuria > 3.5 grams/24 hours

OR urine ACR > 300 mg/mmol*

OR PCR > 300g/mol*

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37
Q

what blood tests would you do ?minimal change

A

U&Es

albumin

lipid profile

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38
Q

defintive diagnosis of minimal change?

A

Renal biopsy

Definitive diagnosis of MCD relies on renal biopsy in adults, with light microscopy typically showing normal glomeruli, and electron microscopy revealing diffuse podocyte foot process effacement. In children, renal biopsy is generally avoided.

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39
Q

indications for renal biopsy ?minimal change

A

Aged < 12 months >10 years
Steroid resistant
Low serum C3
Clinical evidence of systemic disease e.g. HSP, SLE
Concern regarding ciclosporin nephrotoxicity
Persistent renal impairment, persistent hypertension or family history of FSGS

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40
Q

Management minimal change disease

A

High dose steroids (i.e. prednisolone) for 4 weeks (60mg/m2/day) and then gradually weaned over the next 8 weeks

Low salt diet
Diuretics may be used to treat oedema
Albumin infusions may be required in severe hypoalbuminaemia
Antibiotic prophylaxis may be given in severe cases

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41
Q

biopsy results membraneous nephropathy

A

the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

M looks like spike and dome

42
Q

causes of membraneous nephropathy

A

idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

43
Q

Management membraenous nephropathy

A
  1. ACEi or ARB (to reduce proteinuria)

+ ONLY IF SEVERE…immunosuppression

44
Q

biopsy reuslts focal segmental glomeruloscleorsis

A

focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

45
Q

management of focal segmental glomerulosclerosis

A

steroids +/- immunosuppressants

46
Q

causes of focal segmental glomeruloscleoris

A

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

47
Q

what is nephritic syndrome

A

Nephritic syndrome refers to a group of features that occur with nephritis:

Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible)

Oliguria (significantly reduced urine output)

Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)

Fluid retention

48
Q

epidemiology post strep glomerulonephritis

A

The most commonly affected age group are children between the ages 5-12years, with an increased risk also present for older adults >60years.

Boys appear to be affected twice as commonly as girls.

49
Q

pathophysiology post strep glomerulonephritis

A

nephritogenic streptococcal antigens become lodged in glomerular membrane → anti-streptococcal antibodies bind to form immune complexes → activation of complement and inflammation → damage to glomerulus

type 3 hypersensitivity

50
Q

3 year old frothy urine, generalised oedema and pallor

A

minimal change disease

51
Q

nephritis developing 1-3 weeks after URTI/tonsilitis

A

Post-streptococcal glomerulonephritis

52
Q

management of post strep glomerulonephritis

A

self limiting

supportive
- monitor BP –> diuretics
- monitor oedema –> diuretics

Antibiotic therapy should be given if there is any evidence of a persistent streptococcal infection. Early antibiotics reduce the incidence and severity of PSGN.

53
Q

what tests should you get to support a diagnosis of post strep glomerulonephritis

A

evidence of infection!
- A throat or skin swab for culture should be taken to help confirm the presence of GAS.
- Streptozyme test (includes ASO titre)

complement
- low C3 levels duirng first 2 weeks (as it has been deposited)

54
Q

Renal biopsy features of strep glomerulonephritis

A

subepithelial ‘humps’

Immunofluorescence: diffuse granular deposits of complement (C3) and immunoglobulin G (IgG).

55
Q

young male, recurrent episodes of macroscopic haematuria
typically associated with a very recent respiratory tract infection

A

IgA nephritis (bergers disease)

56
Q

Management IgA nephroathy/bergers disease

A

isolated hematuria, no or minimal proteinuria and normal eGFR
- no treatment needed

persistent proteinuria above 500 to 1000 mg/day, a normal or only slightly reduced eGFR
+ ACE inhibitors

falling eGFR or not responding to ACEi:
+ corticosteroids

57
Q

how to differentiate strep glomer from IgA neph

A

Age: SG young, IgA teenage
Timing of URTI: SG 1-3 weeks ago, IgA days ago
Complement levels: SG low
Proteinuria: SG has worse
Haematuria: IgA has worse

58
Q

Histology IgA nephropathy

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

59
Q

markers of prognosis iga nephroapthy

A

markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

60
Q

causes of rapidly progressing glmerulnpehritis

A

Goodpasture’s disease

Polyarteritis nodosum
Wegener’s granulomatosis (granulomatosis with polyangitis)
Microscopic polyangitis

61
Q

invetsigations ?vasculitis causing glomerulonephritis

A

cxr
renal biopsy
antibodies (c-ANCA, p-ANCA, anti-GBM)
angiography

62
Q

what is goodpastures disease

A

antibodies attack the alpha-3 subunit of type IV collagen found in the basement membrane of the lungs and kidneys.

This anti-glomerular basement membrane (anti-GBM) disease leads to small vessel vasculitis in the kidneys and lungs causing bleeding in the lungs and renal failure.

63
Q

investigations goodpastures

A

anti-GBM antibody titre

renal biopsy (cresenteric glomerulonephritis)

64
Q

management of goodpastures

A
  1. intensive plasmapherisis
    +immunosupression:
    - prednisolone
    - cyclophosphamide
65
Q

classic presentation goodpastures

A

patient with no history of lung or renal dysfunction who presents after noticing an abrupt onset of haemoptysis, cough, shortness of breath, peripheral oedema, dark urine and oliguria.

66
Q

features microscopic polyangitis

A

purpura
p-anca
alveolar haemorrhage
mononeuritis
glomerulonephritis

67
Q

investigations microscopic polyangitis

A

p-ANCA antibodies

renal biopsy

cxr

68
Q

management of microscopic polyangitis

A

cyclophospahmide with high dose steroids

69
Q

features granulomatosis with polyangitis

A

saddle nose
haemoptysis
epistaxis

c-anca
wegners
mononeutiits
mononeuritis
glomerulonephritis

70
Q

autoantibodies in graulomatosis with polyangitis

A

c-ANCA

71
Q

cxr granulomatosis with polyangitis

A

many diff but
cavitating lesions are common

72
Q

renal biopsy granulomatosis with polyangitis

A

epithelial crescents in bowmans capsule

73
Q

management granulomatosis with polyangitis

A

steroids
cyclophosphamide
plasma exhcnage

74
Q

features of polyarteritis nodosa

A

skin - livedo reticularis
neuro
renal

other - ass w hep B, CVS events, HTN

75
Q

features of eosinophilic granulomatosis with polyangiitis

A

resp inc asthma
ENT

NO bleeding
NO RENAL

76
Q

urianlysis interpretation of ‘casts’

A

Brown/black casts → ATN
Red casts → glomerulonephritis
White casts → acute interstitial nephritis

77
Q

features acute interstitial nephritis

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

78
Q

investigation findings acute interstitial nephritis

A

bloods:
eosinophilia

urinalysis:
sterile pyuria
white cell casts

79
Q

complcation of AIN

A

Tubulointerstitial nephritis with uveitis

Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.

80
Q

which cause of aki is associated with malignancy

A

Membranous nephropathy is frequently associated with malignancy making this the most likely diagnosis.

81
Q

what is rhabdomyolysis

A

Rhabdomyolysis is caused by skeletal muscle breakdown.
This causes the release of intracellular contents such as myoglobin and potassium into the blood stream.
Excess myoglobin can precipitate in the glomerulus causing renal obstruction, direct nephrotoxicity and acute kidney injury.

82
Q

triad rhabdomyolysis - symptoms

A

dark urine, generalised weakness and myalgia.

83
Q

features of rhabdomyolysis blood tests etc.

A

acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
myoglobinuria
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis

84
Q

causes of rhabdomyolysis

A

seizure
collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)

Ischaemia: embolism, surgery
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)

85
Q

diagnosis of rhabdomyolysis

A

A creatine kinase >5x the normal range is typically diagnostic.

86
Q

management rhabdomyolysis

A

IV fluids to maintain good urine output

Correction of electrolyte disturbances

urinary alkalinization is sometimes used

87
Q

electrolytes in rhabdomyolysis

A

Hyperkalaemia (liberated from the damaged muscle)

Hyperphosphatemia (liberated from the damaged muscle)

Hyperuricaemia (liberated from damaged muscle)

Hypocalcaemia (calcium is taken into the damaged muscle by several mechanisms).

88
Q

What is the pathophsyiology of SLE?

A

SLE is characterised by anti-nuclear antibodies (ANA). These are autoantibodies against proteins within the cell nucleus. These antibodies generate a chronic inflammatory response, leading to the condition’s features.

89
Q

Presentation SLE?

A

Hair loss
Mouth ulcers
Fatigue
Fever
Photosensitive malar rash

Lymphadenopathy
Shortness of breath
Pleuritic chest pain
Weight loss
Splenomegaly

Arthralgia (joint pain)
Non-erosive arthritis
Myalgia (muscle pain)
Raynaud’s phenomenon

Oedema (due to nephritis)

90
Q

what makes malar rash in SLE worse?

A

triggered or worsened by sunlight.

91
Q

Invetsigation findings SLE

A

Autoantibodies
ANA - 85% will have positive - other things can make it positive
Anti-dsDNA - 50% will have positive - specific

Full blood count may show anaemia of chronic disease, low white cell count and low platelets
CRP and ESR may be raised with active inflammation
C3 and C4 levels may be decreased in active disease
Urinalysis and urine protein:creatinine ratio shows proteinuria in lupus nephritis
Renal biopsy may be used to investigate for lupus nephritis

92
Q

Complications of lupus?

A
  • CVS disease
  • Infection (from disease and immunosupp drugs)
  • Anaemia of chronic disease
  • pericarditis
  • pleuritis
  • lupus nephritis
  • neuropsychiatiric (optic neuritis, transverse myelitis, psychosis)
  • recurrent miscarriage
  • VTE - due to antiphospholipid secondary to SLE
93
Q

Management SLE

A

First-line options include:
Hydroxychloroquine
NSAIDs
Steroids (e.g., prednisolone)

Treatment options for resistant or more severe SLE include:
DMARDs (e.g., methotrexate, mycophenolate mofetil or cyclophosphamide)
Biologic therapies

Biological therapies include:
Rituximab (a monoclonal antibody that targets the CD20 protein on the surface of B cells)
Belimumab (a monoclonal antibody that targets B-cell activating factor)

94
Q

Presentation HSP

A

Purpura (100%)
Joint pain (75%) usually knees and ankles
Abdominal pain (50%)
Renal involvement (50%) - microscopic or macroscopic haematuria and proteinuria, oedema

95
Q

most common trigger HSP

A

URTI 1-3 weeks prior, streptococcus

96
Q

what type of hypersensitivity is HSP

A

type 3 - immune complex mediated

97
Q

Invetsiagtions HSP

A

To rule out other things:
- Sepsis : blood culture, CRP
- Thromboytopaenia (inc leukaemia) : coagulation studies
- Other vasculidities: Autoantibody screen: antinuclear antibodies, antineutrophil cytoplasmic antibodies, and complement levels

To help support HSP diagnosis
- ESR raised in 75% of patients
- Serum IgA may be high

To test for complications:
- urinalysis : haematuria, proteinuria
- Serum creatinine and electrolyte levels
Elevated creatinine indicates renal impairment or renal failure
Electrolyte abnormalities may occur in patients with severe gastrointestinal symptoms.
- blood pressure

If non-typical presentation :
- skin/renal biopsy for confirmation of diagnosis

If severe abdo pain:
- abdo USS

98
Q

Management HSP

A

Supportive (fluid, rest, symptomatic relief)

  • paracetamol (avoid ibruprofen if abdo pain)
  • steroids may be used in severe cases

Monitoring
- 6 months periodic urinalysis and BP monitoring
- abnormlaity on urinalysis –> test serum cretainine
- if persistent - refer to nephrologist

99
Q

monitoring post HSP

A
  • 6 months periodic urinalysis and BP monitoring
  • abnormlaity on urinalysis –> test serum cretainine
  • if persistent - refer to nephrologist
100
Q

cause HUS? exacerbating factors?

A

The most common cause is a toxin produced by the e. coli 0157 bacteria, called the shiga toxin. Shigella also produces this toxin.

The use of antibiotics and anti-motility medications such as loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS.

101
Q

features HUS

A

Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Oedema
Hypertension
Bruising

102
Q

management HUS

A

supportive
- antihypertensive
- blood transfusion
- dialysis

HUS is a medical emergency and has a 10% mortality. It needs to be managed by experienced paediatricians under the guidance of a renal specialist. The condition is self limiting and supportive management is the mainstay of treatment:

Urgent referral to the paediatric renal unit for renal dialysis if required
Antihypertensives if required
Careful maintenance of fluid balance
Blood transfusions if required

70 to 80% of patients make a full recovery.

Core clinical problems (94 decks)

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