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

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

Jul 10, 2023 436 likes •827 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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SLIDE 1
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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

2

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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Mr Gangfløt – 50-year-old male Mr Hukkelberg – 50-year-old male Mr Mokkelbost – 50-year-old male

3

Layout for today’s session

1. No treatment 2. Dialysis 3. Kidney transplant

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History

You are a medical student on your elective in a developing country. Your next patient is Mr Gangfløt, a 50-year-old gentleman who visits the local doctor to complain about his swollen

  • ankles. He says that this has been bothering

him for many months. Past medical history includes HTN and T2DM. On examination, you note pitting oedema up to his knee level, as well as conjunctival pallor.

Observations

HR 64, BP 174/102, RR 11, SpO2 98%, Temp 37.3

4

Case-based discussion: 1

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History

You are a medical student on your elective in a developing country. Your next patient is Mr Gangfløt, a 50-year-old gentleman who visits the local doctor to complain about his swollen

  • ankles. He says that this has been bothering

him for many months. Past medical history includes HTN and T2DM. On examination, you note pitting oedema up to his knee level, as well as conjunctival pallor.

Observations

HR 64, BP 174/102, RR 11, SpO2 98%, Temp 37.3

5

Case-based discussion: 1

Peripheral oedema

Causes of bilateral:

  • Heart
  • Heart failure
  • Kidney
  • CKD
  • Nephrotic syndrome
  • Liver
  • Liver failure
  • Venous/lymphatic obstruction
  • Pelvic tumour
  • Not your first thought!
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Clerking cont.

  • Serum pro-NT-BNP - normal
  • Serum liver function test
  • Albumin – 36 (35-50)
  • Bilirubin – 4

(1-17)

  • ALT
  • 25 (<50)
  • Serum urea and electrolytes
  • Urea
  • 6.9 (2-7)
  • Creatinine
  • 200 (50-120)
  • Urine dipstick
  • Protein

++

  • Glucose

++

6

Case-based discussion: 1

eGFR calculation[1]

Calculated using the MDRD (modification of diet in renal disease), which uses the following parameters:

  • 1. Creatinine
  • 2. Age
  • 3. Gender
  • 4. Ethnicity

eGFR (ml/min/1.73 m2) =

175 × (Scr)-1.154 × (Age)-0.203 × (0.742 if female) × (1.212 if African American)

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Definition Progressive deterioration in renal function The KDIGO guidelines[2]:

  • Present for >3 months
  • With implications for health
  • Abnormalities of kidney structure or function
  • 1. This means ALL patients with an eGFR <60 or;
  • 2. ANY patient with markers of kidney damage:
  • Proteinuria
  • Haematuria
  • ACR >3 mg/mmol
  • Structural abnormalities (e.g. PKD)
  • Abnormalities on renal biopsy
  • History of renal transplant

7

Chronic Kidney Disease (CKD)

Epidemiology

  • It is estimated that 10% of the general

population are thought to have CKD

  • Risk factors:
  • Age
  • Ethnicity: Afro-Caribbean
  • Co-morbidities: HTN, T2DM, renal disease
  • Medications
  • Congenital abnormalities
  • Urinary tract pathology
  • CKD mortality is difficult to assess due to

the fact that patients with CKD will often die from linked cardiovascular disease prior to reaching end-stage renal failure.

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Staging

CKD grade GFR range G1 >90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests are normal, there is no CKD) G2 60-89 ml/min with some sign of kidney damage (if kidney tests are normal, there is no CKD) G3a 45-59 ml/min with a mild-moderate reduction in kidney function G3b 30-44 ml/min with a moderate reduction in kidney function G4 15-29 ml/min with a severe reduction in kidney function G5 <15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

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9

Staging

Urinary albumin : creatinine ratio (ACR) In addition, CKD is staged by urinary ACR to measure how leaky the glomerulus is to protein

  • A1 – ACR <3 (mg/mmol)
  • A2 – ACR 3-30 (mg/mmol)
  • A3 – ACR >30 (mg/mmol)

The higher the A grade in CKD, the poorer the prognosis, as proteinuria is considered a poor prognostic factor.

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Aetiology

Diabetes mellitus Hypertension Glomerulonephritis Other:

  • PKD
  • Renal artery

stenosis

  • SLE
  • Amyloidosis
  • RA
  • HIV

1 2 3

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Pathophysiology (Diabetes)

Mechanism of kidney damage:

  • 1. Excessive glucose in the blood results in

glycosylation of proteins

  • 2. In particular, the efferent arteriolar surface

proteins are prone to this

  • 3. This leads to hyaline arteriole sclerosis,

creating a stiff and narrow arteriole

  • 4. This raises the pressure in the glomerulus

and causes hyperfiltration and mesangial cell expansion

  • 5. Over many years, this leads to reduced

filtration and leakiness of the glomerulus

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Pathophysiology (Hypertension)

Mechanism of kidney damage:

  • 1. In hypertensive states, the renal arteries

become stenosed

  • 2. Reduced blood supply to the glomerular

arterioles means the glomeruli undergo ischaemic injury

  • 3. This results in deposition of macrophages
  • 4. These release growth factors, which cause

mesangial cell regression to mesangioblasts

  • 5. These precursor cells produce excess

extracellular matrix, causing glomerulosclerosis and lowered eGFR

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Pathophysiology (Glomerulonephritis)

Definition:

  • Collective term for any condition that causes

inflammation of the glomerulus

  • Can present as AKI, CKD or nephrotic/nephritic

syndrome Nephrotic

  • Minimal change
  • FSGS
  • Membranous

nephropathy Nephritic

  • IgA nephropathy
  • Post-infectious GN
  • Anti-GBM disease
  • MPGN

[3]

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Pathophysiology (other causes)

Other:

  • PKD
  • SLE
  • RA
  • Amyloidosis
  • HIV
  • NSAIDs
  • Toxins
  • Etc.

Regardless of the aetiology, the end result is glomerular scarring and resultant kidney failure

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Clinical features

Symptoms Signs

Lethargy Hypertension Pruritis Peripheral oedema Nausea Pulmonary oedema Anorexia Uraemic sallow: yellow/brown colour to skin Frothy urine (secondary to proteinuria) Evidence of a specific underlying cause, e.g. butterfly rash in lupus More features to come when we introduced dialysis and transplant*

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Investigations

Bloods

  • FBC
  • U&Es
  • HbA1c
  • Bone profile

Urine

  • Dipstick
  • ACR

Imaging

  • Renal US
  • CT KUB

Specialist tests

  • Renal biopsy
  • The “renal workup”
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17

Management

Lifestyle

  • Encourage

regular exercise, achieve a healthy weight and stop smoking

  • Offer dietary advice about potassium, phosphate,

calorie and salt intake (keep these low)

  • Low protein diets are NOT required

Pharmacological

  • ACE-inhibitor or ARB if:
  • Diabetic + ACR of 3mg/mmol or more
  • Hypertensive + ACR of 3mg/mmol or more
  • An ACR of 7mg/mmol or more
  • Offer statin and anti-platelet

Renal replacement therapy (RRT)

  • Dialysis – haemodialysis vs peritoneal dialysis
  • Kidney transplant

Why ACE-inhibitors? “Stop them in AKI, start them in CKD” 1) They reduce the intraglomerular pressure and thus reduces hyperfiltration à less proteinuria 2) They reduce the blood pressure à a cause of CKD 3) Other – poorly studied, e.g. ATII causes renal injury

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18

Complications

System Description

Cardiovascular Cardiovascular disease is the leading cause of death in CKD, e.g. IHD or heart failure Musculoskeletal CKD-metabolic bone disease (CKD-MBD) Endocrine Secondary hyperparathyroidism à Tertiary hyperparathyroidism Haematological Anaemia (usually normocytic and normochromic). Caused by: 1) Low EPO production; 2) Reduced iron absorption; 3) Uraemia causing anorexia / reduced erythropoiesis Metabolic Metabolic acidosis, hyperkalaemia, uraemic encephalopathy/pericarditis [3]

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Definition Also known as renal osteodystrophy, this is a bone disorder that results in:

  • Bone and joint pain
  • Bone deformation
  • Bone fractures
  • Reduced mobility

19

CKD-MBD

Mechanism

1. Active vitamin D = 1,25- dihydroxycholecalciferol 2. Reduced 1-alpha hydroxylase activity in CKD 3. Leads to reduced vitamin D activation 4. Less vitamin D means:

  • A. Reduced renal excretion of phosphate (rises)
  • B. Reduced absorption of calcium in gut
  • C. Reduced release of calcium from bone
  • 5. Results in hypocalcaemia and

hyperphosphataemia

  • 6. Low calcium à raised PTH

Manage with phosphate binders & vitamin D analogues Expected laboratory results Serum calcium ↓ Serum phosphate ↑ Serum vitamin D ↓ Serum PTH ↑ Alkaline phosphatase (ALP) ↑

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Recap

CKD is a progressive deterioration in renal function

  • 1. >3 months and;
  • 2. eGFR <60 or markers of kidney damage (e.g. haematuria,

ACR >3) Staging:

  • G1 to G5 – based on eGFR
  • A1 to A3 – based on ACR

Management:

  • Lifestyle
  • ACE-inhibitors / ARBs
  • Renal replacement therapy (RRT) – when the time comes

Complications:

  • Cardiovascular disease
  • CKD-MBD
  • Hyperparathyroidism (2º or 3º)
  • Anaemia
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History Mr Hukkelberg, a 50-year-old Afro-Caribbean male, is diagnosed with CKD in 2015 having presented with mild oedema. Over the next 5 years, he undergoes regular monitoring, as well as management with lifestyle advice, ACE-inhibitors and sevelamer for known CKD- MBD. Despite best efforts, by 2020 he has an eGFR of 19ml/min/1.73. Observations HR 86, BP 145/82, SpO2 97%, temp 37.2

21

Case-based discussion: 2

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Referral

NICE guidelines[5]:

People with CKD in the following groups should normally be referred for specialist assessment:

  • GFR <30 ml/min/1.732
  • Urinary ACR of 30 or more, with haematuria
  • Urinary ACR of 70 or more (w/o diabetes)
  • Sustained decrease in GFR of 15 ml/min/1.73

m2 or more within 12 months

  • Hypertension that remains poorly controlled

despite the use of at least 4 antihypertensive drugs at therapeutic doses

  • Known or suspected rare cause of CKD
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23

Dialysis

General:

  • Relies upon the principle of diffusion
  • Movement of solutes from an area of high

solute concentration to an area of low solute concentration…

  • …through a semi-permeable membrane
  • 1. Haemodialysis
  • 2. Peritoneal dialysis
  • In both of these renal replacement

therapies (RRT), the patient’s blood is filtered by passing in close proximity to dialysate fluid and separated by a semi- permeable membrane

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A V

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Haemodialysis

Details:

  • Blood from the body is ran into an artificial kidney

(haemodialyser) ~3 times a week Access:

  • Central line (jugular, femoral)
  • AV fistula

Dialysate includes:

  • Similar electrolytes to blood
  • Slightly raised bicarbonate

Complications:

  • Hypotension
  • Dialysis disequilibrium
  • AV fistula thrombosis / steal syndrome
  • SIRS

Hand

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25

Peritoneal dialysis

Details

  • Dialysate is slowly infused into the peritoneal cavity via

a catheter.

  • The peritoneal membranes act as a natural filter for

dialysing the blood.

  • It can be used as a stop-gap to HD or for younger

people Dialysate includes

  • Similar sodium/potassium to blood
  • Raised bicarbonate
  • 1.5%, 2.5% and 4.25% glucose – for ultrafiltration

Complications

  • Constipation can compress the catheter and

prevent fluid from returning to the dialysis machine

  • Sclerosing peritonitis – rare, potentially fatal
  • Peritonitis – Staph epidermidis
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OSCE Presentation: the dialysis patient

Signs of disease:

  • Peripheral oedema
  • Raised JVP
  • Neuropathy
  • Joint disease
  • Conjunctival pallor

Signs of dialysis

  • AV fistula – palpate, auscultate
  • Tunnelled line
  • Peritoneal dialysis catheter
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27

Recap

CKD is a progressive deterioration in renal function

  • 1. >3 months and;
  • 2. eGFR <60 or markers of kidney damage (e.g. haematuria,

ACR >3) Haemodialysis (HD):

  • Blood from the body is run into an artificial kidney

machine

  • Requires vascular access, e.g. central line / AV fistula
  • Patients have a lower mortality rate than for PD

Peritoneal dialysis (PD):

  • Dialysate fluid is introduced into peritoneal cavity with

peritoneal membrane acting as natural semi-permeable membrane

  • Does not require vascular access
  • Patients have a higher mortality rate than for HD
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History Mr Mokkelbost is a 50-year-old male who has been

  • n haemodialysis for 5 years, whilst awaiting a kidney

transplant. Today, the patient received a call that they have reached the top of the list and must come in for a pre-operative assessment. Observations HR 98, BP 139/84, SpO2 98%, Temp 37.2

28

Case-based discussion: 3

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Kidney transplant

  • Introduction of a donor kidney (deceased or live)
  • Given at the point of ESRD - 15ml/min/1.73m2
  • Selecting an allograft donor:
  • Match ABO and HLA (A,B,C, DP, DR, DQ)
  • Donor kidney is placed into the iliac fossa and

“plumbed” into the host vasculature

  • Usually the donor renal artery and renal vein are

connected to the common iliac vessels

  • “A third kidney”
  • Patients will have a J shaped (hockey) scar
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Immunosuppression regimen

Must immunosuppress for life to avoid host rejection [6] Initial induction:

  • KDIGO recommend starting a combination of

immunosuppressive medications, including biological (IL2-RA)

  • E.g. basiliximab and tacrolimus

Maintenance therapy:

  • KDIGO recommend a combination of immunosuppressive

medications as maintenance therapy, including a CNI and an anti-proliferative agent (+/- steroids)

  • E.g. ciclosporin/tacrolimus with MMF

Side effects:

  • Ciclosporin – gum hypertrophy / hyperlipidaemia
  • Tacrolimus – physiological tremor
  • Mycophenolate mofetil (MMF) – GI upset and marrow

suppression

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Early complications

Delayed graft function

  • Requires dialysis
  • Risk factors include renal disease in donor, obese

recipients and prolonged ischaemic time Infection

  • CMV is the most common viral infection of solid organ

transplant Acute tubular necrosis of graft

  • Death of the graft for a number of reasons (not just

immune) General surgical

  • Bleeding, infection, thrombosis

Acute rejection

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Rejection

Hyperacute rejection

  • Type 2 hypersensitivity reaction
  • Pre-formed antibodies attack the allograft immediately
  • E.g. ABO incompatibility

Acute rejection

  • Weeks to months (~3)
  • Clinical features akin to infection (fever, tender graft,

↓GFR)

  • 15-25% of patients will experience this
  • Requires a biopsy
  • Reversible with steroids
  • Living donor transplants get rejected less.

Chronic rejection

  • Months to years
  • Progressive occlusion or intimal hyperplasia of the

blood vessels

  • Less reversible

[6][7]

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Late complications

Cardiovascular disease

  • Tacrolimus and ciclosporin can cause hypertension,

hyperlipidaemia and hyperglycaemia.

  • Dialysis à risk of IHD

Renal failure

  • Nephrotoxic effects of tacrolimus and ciclosporin
  • Chronic graft rejection
  • Recurrence of original disease in transplanted kidney

Malignancy

  • Skin cancer – all types
  • Educate patients about minimising sun exposure

Post-transplant lymphoproliferative disorder (PTLD)

  • One of the commonest malignancies following transplant
  • Seen most in those who are heavily immunosuppressed
  • Driven by EBV donated by the donor
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OSCE Presentation: the transplant patient

Signs of disease

  • Peripheral oedema
  • Raised JVP
  • Neuropathy
  • Joint disease
  • Conjunctival pallor

Signs of transplant / immunosuppression

  • Defunctioned AV fistula – palpate, auscultate
  • Peritoneal dialysis catheter scars
  • Palpable abdominal mass in iliac fossa
  • J shaped (“hockey stick”) scar
  • Gum hypertrophy – ciclosporin
  • Tremor – tacrolimus
  • Bruising and skin malignancies –

steroids/immunosuppressants

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Recap

CKD is a progressive deterioration in renal function

  • 1. >3 months and;
  • 2. eGFR <60 or markers of kidney damage (e.g. haematuria,

ACR >3) Transplant

  • Donor allograft introduced into abdomen without removing
  • riginal kidneys
  • Requires lifelong immunosuppression

Early complications

  • Infection and bleeding
  • Delayed graft function
  • Rejection

Late complications

  • Skin cancer
  • Renal failure
  • CVD
  • PTLD
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References

1.

  • NIDDK. Estimating glomerular filtration rate. https://www.niddk.nih.gov/health-

information/professionals/clinical-tools-patient-management/kidney-disease/laboratory- evaluation/glomerular-filtration- rate/estimating#:~:text=The%20Modification%20of%20Diet%20in,patients%20age%2018%20and%20over. 2. KDIGO CKD guidelines - https://kdigo.org/wp-content/uploads/2017/02/KDIGO_2012_CKD_GL.pdf 3. KDIGO glomerulonephritis guidelines - https://kdigo.org/wp-content/uploads/2017/02/KDIGO-2012-GN- Guideline-English.pdf 4. BiteMedicine CKD textbook - https://app.bitemedicine.com/textbooks/chronic-kidney-disease 5. NICE guidelines. Chronic Kidney Disease - https://www.nice.org.uk/guidance/cg182/chapter/1- Recommendations 6. KDIGO Kidney transplant guidelines - https://kdigo.org/wp-content/uploads/2017/02/KDIGO-2009-Transplant- Recipient-Guideline-English.pdf 7. Elizabeth Ingulli (2010). Paediatric nephrology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778785/

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