Renal Revision Summary General Specific AKI Glomerulonephritis - - PowerPoint PPT Presentation

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Renal Revision Summary General Specific AKI Glomerulonephritis - - PowerPoint PPT Presentation

Nov 29, 2023 453 likes •870 views

Renal Revision Summary General Specific AKI Glomerulonephritis Causes Minimal change disease Investigation and management FSGS Complications Membranous nephropathy CKD MPGN IgA nephropathy

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General

  • AKI
  • Causes
  • Investigation and management
  • Complications
  • CKD
  • Causes
  • Investigation and management
  • Complications
  • Nephrotic vs nephritic syndrome
  • Causes
  • Investigation and management
  • Complications

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Renal Revision Summary

Specific

  • Glomerulonephritis
  • Minimal change disease
  • FSGS
  • Membranous nephropathy
  • MPGN
  • IgA nephropathy
  • Post-streptococcal glomerulonephritis
  • Amyloidosis
  • Polycystic kidney disease
  • Beware urology
  • SLE (lupus)
  • ANCA-associated vasculitides
  • Anti-GBM disease
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Mrs Lowe – 86 year-old female Mrs Bridney – 57 year-old female Mrs Post – 74 year-old female

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Layout for today’s session

1. Pre-renal 2. Renal / Intrinsic 3. Post-renal 4. Complications of all AKI Pre-renal Post- renal Renal

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History

Mrs Lowe is an 86-year-old female who lives in a nursing home. Half of the residents have been suffering from a norovirus outbreak, including Mrs Lowe. She has been vomiting multiple times a day and the staff have noted that she seems more confused than usual. Past medical history includes T2DM, HTN and AF.

Observations

HR 110, BP 89/72, RR 17, SpO2 96%, Temp 37.3

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Case-based discussion: 1

N.B. We will use Mrs Lowe to cover some general points about AKI, as well as one of the 3 types of AKI.

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Question: 1

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History

Mrs Lowe is an 86 year-old female who lives in a nursing home. Half of the residents have been suffering from a norovirus outbreak, including Mrs Lowe. She has been vomiting multiple times a day and the staff have noted that she seems more confused than usual. Past medical history includes T2DM, HTN and AF.

Observations

HR 110, BP 89/72, RR 17, SpO2 96%, Temp 37.3

6

Case-based discussion: 1

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Clerking continued.

Observations stabilise and the patient undergoes the following basic investigations over the next 6 hours: Bloods:

  • Urea
  • Creatinine
  • Serum U : Cr

Urine output

  • Hour 1

20ml

  • Hour 2

20ml

  • Hour 6

15ml Weight

  • 50kg

7

Case-based discussion: 1

20 mmol/L (2 – 7) 200 µmol/L (55-120) 100

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Definition

Abrupt and sustained decrease in kidney function The KDIGO guidelines[1]:

  • 1. Rise in serum creatinine >26μmol/L within

48h OR

  • 2. Rise in serum creatinine >1.5x baseline

(before AKI) within 7 days OR

  • 3. Urine output <0.5ml/kg/h for >6 consecutive

hours

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Acute Kidney Injury (AKI)

Epidemiology

  • Incidence: 13-18% of hospital admissions

have AKI [2]

  • Risk factors:
  • Age
  • Co-morbidities: HTN, T2DM, CKD
  • Medications
  • Hypovolaemia
  • Sepsis
  • High rates of morbidity and mortality (up

to 40%)

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Staging

  • Multiple
  • Beyond the scope of medical school
  • To be aware:

1. RIFLE – risk, injury, loss, failure, ESRD* 2. AKIN – stage 1, stage 2, stage 3

  • What does a higher stage mean?
  • Increased length of stay in hospital
  • Increased length of stay in ICU
  • Increased mortality
  • Reduced likelihood of renal recovery

*ESRD = end-stage renal disease

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Inflammation

Volum e loss Reduce d cardiac

  • utput

Systemic vasodilatati

  • n

Renal vasculature

Aetiology (pre-renal)

Decreased blood flow to glomerulus

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Pathophysiology

Decreased blood flow to glomerulus Decreased blood filtration Reduced urine output Raised urea Raised creatinine

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Clinical features (all AKIs)

Symptoms Signs

Oliguria Peripheral oedema Anuria Chest crackles (pulmonary oedema) Confusion Raised JVP Nausea Haematuria Shortness of breath Proteinuria

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Question: 2

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Management

First line

  • IV fluid bolus: treat hypovolaemia with 250-500ml boluses of crystalloid (e.g. saline or Hartmann’s)
  • Serial VBGs: monitor lactate for tissue hypoperfusion
  • Maintenance fluids: 1L of saline (+20mM K+) + 2L of 5% dextrose (+20mM K+)

Suspend common medications that will worsen AKI

  • ACE-inhibitors (e.g. ramipril): dilates efferent arteriole
  • Diuretics (e.g. bendroflumethiazide): reduce flow through tubular capillaries
  • NSAIDs (e.g. naproxen): constricts afferent arteriole

Second line

  • KDIGO recommend the use of vasopressors in patients with vasomotor shock
  • KDIGO do NOT recommend using low-dose dopamine
  • KDIGO do NOT recommend using diuretics to treat AKI, except in the management of volume
  • verload
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Recap

  • AKI is an abrupt and sustained decrease in kidney function
  • Divided into pre-renal, renal and post-renal causes
  • Pre-renal causes:
  • Volume loss
  • Reduced cardiac output
  • Systemic vasodilatation
  • Excessive constriction of afferent arteriole
  • Distinguishing features:
  • History
  • High urea : creatinine ratio
  • Low urine sodium – kidney can still reabsorb
  • Management:
  • Fluid responsive
  • ICU – if features of vasomotor shock
  • Stop exacerbating medication, e.g. diuretics, NSAIDs, ACE-i/ARB
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History Mrs Bridney is a 57-year-old female who is being treated in hospital for sepsis

  • f

unknown origin. Past medical history includes T2DM. In the last 12 hours, she has been noted to have a urinary

  • utput
  • f

0.4ml/kg/hour. Despite regular IV fluids and catheterisation this has not improved. Observations HR 104, BP 100/77, SpO2 96%, temp 37.6

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Case-based discussion: 2

  • Metformin
  • Enoxaparin
  • Amoxicillin
  • Metronidazole
  • Amikacin
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Question: 3

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History Mrs Bridney is a 57 year-old female who is being treated in hospital for sepsis

  • f

unknown origin. Past medical history includes T2DM. In the last 12 hours, she has been noted to have a urinary

  • utput
  • f

0.4ml/kg/hour. Despite regular IV fluids and catheterisation this has not improved. Observations HR 104, BP 100/77, SpO2 96%, temp 37.6

18

Case-based discussion: 2

  • Metformin
  • Enoxaparin
  • Amoxicillin
  • Metronidazole
  • Amikacin
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Aetiology (renal/intrinsic)

  • 1. Glomerular
  • 3. Tubular
  • 2. Interstitial
  • 4. Kidney vascular supply
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Pathophysiology

Glomerular

  • Glomerulonephritis conditions
  • IgA nephropathy
  • FSGS
  • MPGN
  • SLE (lupus nephritis)
  • Amyloidosis
  • May present as acute kidney injury
  • More commonly will present with

nephrotic or nephritic syndrome

  • Beyond the scope of a single lecture on

AKI Interstitium

  • Acute interstitial nephritis (AIN)
  • Neutrophils/eosinophils infiltrate

the interstitium of the kidney

  • NSAIDs
  • Penicillin
  • Diuretics
  • May present as acute kidney injury
  • More commonly will present with:
  • Rash
  • Joint pain
  • Eosinophilia
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Pathophysiology (cont.)

Tubular

  • Acute tubular necrosis (ATN)
  • Death of the tubular cells results in a

clogged tubule and loss of pressure gradient

  • Causes:
  • Ischaemia
  • Rhabdomyolysis (e.g. myoglobin)
  • Aminoglycoside antibiotics

(e.g. amikacin, gentamicin)

  • Lead
  • Ethylene glycol (anti-freeze)
  • Good prognosis as tubular cells

continually replace within 1-3 weeks Renal vascular supply

  • NOT to be confused with glomerular

blood supply (for ultrafiltration)

  • Blood supply to kidney tissue
  • Can be compromised à infarct
  • E.g. TTP, HUS
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Question: 4

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Investigations (“the renal workup”)

Bloods

  • Serum urea : creatinine ratio
  • Serum free light chains (FLCs)
  • Serum complement (C3, C4)
  • ANCA, ENA, anti-dsDNA
  • Blood-borne virus serology

Urine

  • Dipstick
  • Microscopy: 400x magnification reveals muddy

brown casts

  • Sodium

Imaging

  • Renal US

Specialist tests

  • Renal biopsy

Type Urea : Creatinine ratio Pre-renal > 100 : 1 Renal < 40 : 1 Post-renal 40-100 : 1 Worked example: Urea = 10mmol/L Creatinine = 250µmol/L 10,000 : 250 40 : 1 [3]

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Management

One size does not fit all!

  • Specific to the underlying cause
  • Some general tips:
  • Glomerulonephritis will likely require

various immunosuppressive medications à à à

  • ATN will likely recover with suspension of

toxic agent, e.g. suspend amikacin

  • Call the renal team and get help!

[4]

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Recap

  • AKI is an abrupt and sustained decrease in kidney function
  • Divided into pre-renal, renal and post-renal causes
  • Renal causes:
  • Glomerular
  • Interstitial
  • Tubular
  • Vascular
  • Distinguishing features:
  • Unresponsive to fluids or catheterization
  • Complex medical history
  • Nephrotoxic agent use
  • Low urea : creatinine ratio
  • High urine sodium
  • Management:
  • Varying
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History

Mrs Post is a 74-year-old female who is admitted to hospital with suprapubic pain and is passing very little urine in the past 24 hours. She denies dysuria or haematuria. Past medical history includes osteoarthritis and HTN. She takes amlodipine and amitriptyline. Examination reveals suprapubic tenderness. A catheter is easily inserted and Mrs Post cries with immediate relief.

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Case-based discussion: 3

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Question: 5

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Aetiology (post-renal)

General:

  • Urinary tract infection
  • Kidney stones
  • Malignancy
  • Strictures

Specific:

  • Enlarged prostate (BPH)
  • Phimosis
  • Occluded indwelling catheter (common)
  • Pharmacological
  • Anti-cholinergics, e.g. amitriptyline
  • α-adrenergic agonists
  • Calcium channel blockers
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Investigations (urology)

Bloods

  • Serum urea : creatinine ratio
  • WCC
  • CRP
  • Cultures

Urine

  • Dipstick
  • MC&S

Imaging

  • Renal US
  • Bladder scan
  • CT KUB (non-contrast)
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Management

First line (if indicated)

  • Flush catheter OR;
  • Replace catheter OR;
  • Insert new catheter
  • Stop medications, e.g. amitriptyline

Treatments (specific to cause)

  • UTI: empirical antibiotics whilst awaiting sensitivities
  • Ureteric stones:
  • <5mm: wait to pass
  • 5-10mm:

tamsulosin

  • r

nifedipine à lithotripsy à ureteroscopy

  • >5-10mm: ureteroscopy à lithotripsy
  • Malignancy: surgery and/or chemotherapy
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Recap

  • AKI is an abrupt and sustained decrease in kidney function
  • Divided into pre-renal, renal and post-renal causes
  • Post-renal causes:
  • Urinary tract infection
  • Kidney stones
  • Malignancy
  • Strictures
  • BPH
  • Pharmacological
  • Blocked catheter
  • Distinguishing features:
  • May be responsive to catheterization
  • Urea : creatinine ratio (40-100 : 1)
  • LUTS
  • Management:
  • Varying
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An example of the complexity

History You are an FY1 covering nights on a surgical assessment unit. You are bleeped to see Mr Jones, a 54-year-old man recovering on the ward 1-day post-op. Today:

  • The nurse tells you that his urine output has been

dropping for some hours

  • You allowed a medical student to change his catheter

this morning

  • You started him on gentamicin and losartan

Observations HR 110, BP 88/72, RR 16, SpO2 96%, Temp 37.3

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An example of the complexity

History You are an FY1 covering nights on a surgical assessment unit. You are bleeped to see Mr Jones, a 54 year old man recovering on the ward 1 day post-op. Today:

  • The nurse tells you that his urine output has been

dropping for some hours

  • You allowed a medical student to change his catheter

this morning

  • You started him on gentamicin and losartan

Observations HR 110, BP 88/72, RR 16, SpO2 96%, Temp 37.3

Post-renal cause? Renal cause? Pre-renal cause?

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Complications

Most common Description

Acidosis Metabolic acidosis due to loss of renal acid handling & compensatory mechanism to hyperkalaemia. Hyperkalaemia Changes in normal tubular reabsorption and secretion leads to a loss of renal potassium handling. Oedema Loss of normal glomerular filtration leads to fluid accumulation. Encephalopathy Secondary to uraemia (raised blood urea nitrogen – BUN). Pericarditis Secondary to uraemia (raised blood urea nitrogen – BUN). [2]

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Top-decile question

[5]

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References

  • 1. KDIGO AKI guidelines - https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-

Guideline-English.pdf

  • 2. NCEPOD - adding insult to injury - https://www.ncepod.org.uk/2009aki.html
  • 3. LITFL – urea to creatinine ratio - https://litfl.com/urea-creatinine-ratio/
  • 4. KDIGO glomerulonephritis guidelines - https://kdigo.org/wp-

content/uploads/2017/02/KDIGO-2012-GN-Guideline-English.pdf

  • 5. NICE. AKI guidelines -

https://www.nice.org.uk/guidance/ng148/chapter/Recommendations#managing-acute- kidney-injury

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