Nephrology JC077: Renal Replacement Therapies Flashcards

1
Q

Renal replacement therapy

A

RRT: Therapy that replaces function of failed kidneys in patients with end stage renal disease (ESRD)

3 types:
1. Peritoneal dialysis (PD)
2. Haemodialysis (HD)
3. Kidney transplantation

Indication:
- Consider initiate in ESRD patients when:
1. **GFR <10
2. **
Develop uraemic symptoms (e.g. malaise, anorexia, nausea, vomiting, SOB)

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2
Q

Basic principles of dialysis

A

Uraemic toxins accumulation in circulation
—> Semi-permeable separate Patient’s circulation with Dialysis fluid
—> Uraemic toxins diffuse from circulations through semi-permeable membrane to Dialysis fluid
—> Replace dialysis fluid at regular intervals
—> Uraemic toxins removed from circulation continuously

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3
Q

Choice between PD / HD

A

Factors to consider when choosing between PD / HD:
1. CI to either PD / HD
- CI of PD: Extensive **scarring of peritoneal membrane due to previous major abdominal surgery (e.g. Colectomy for CA colon)
- CI of HD: Lack of suitable **
vascular access for HD, ***Poor cardiac function

  1. Local health care reimbursement system
    - HK: PD first policy (∵ less costly)
  2. Patient’s preference
    - PD usually performed by patient at home daily
    - HD usually performed by renal nurses in HD centre 2-3 times / week
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4
Q

Peritoneal dialysis (PD)

A

3 components:
1. Peritoneal membrane
- **thin + **vascularised + ***large SA —> used as a dialysis membrane

  1. Peritoneal dialysis catheter
    - aka **Tenckhoff catheter
    - specially designed plastic tube with many side-holes in one end (placed inside abdomen) + 2 fibrous cuffs (secure catheter in abdominal wall)
    - tip of catheter should be located inside **
    pelvis pointing ***downwards to facilitate drainage of PD fluid
  2. Peritoneal dialysis fluid
    - balanced salt solutions (devoid of K)
    - **glucose as osmotic agent (1.5% to 4.25% for different osmotic strength)
    - **
    lactate as buffer
    —> draw **excess water + **waste into PD fluid

2 main forms of PD:
1. Continuous ambulatory peritoneal dialysis (CAPD)
- Fill phase: fresh PD fluid (hanged above abdomen) instilled into abdominal cavity through PD catheter
- Dwell phase: PD fluid left inside cavity for 6-8 hours
- Drain phase: PD fluid drained through catheter into empty bag (below abdomen level)
—> repeat above cycle ***3-4 times a day

  1. Automated peritoneal dialysis (APD)
    - APD machine to help patient to perform PD exchanges, usually ***at night when patient sleeps
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5
Q

Comparison between CAPD and APD

A
  1. Need for APD machine
    - CAPD: No
    - APD: Yes
  2. Timing of PD exchange
    - CAPD: Throughout the day
    - APD: At night during sleep
  3. Need for daytime exchange
    - CAPD: Yes
    - APD: No for NIPD (nocturnal intermittent PD), Yes for CCPD (continuous cyclic PD)
  4. Dialysis efficacy
    - ***Similar
  5. QOL
    - ***Usually better in APD
  6. Cost
    - ***APD more costly
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6
Q

***Complications of PD

A
  1. PD catheter **exit site infection
    - redness + tenderness at exit site, may be associated with **
    purulent discharge
    - may predispose to ***PD peritonitis
  2. PD related ***peritonitis
  3. PD failure
    - chronic exposure (~10 years) to dextrose-containing PD fluid + repeated peritonitis —> ***fibrosis of peritoneal membrane (thickened) —> become ineffective as a dialysis membrane —> PD failure
  4. PD catheter malfunction / malposition
    - tip of catheter may occasionally migrate out of pelvis —> poor drainage of PD fluid
    - ***Omental wrap
  5. **Peritoneal leakage
    - normally PD fluid contained in peritoneal cavity —> PD fluid may leak out of peritoneal cavity occasionally —> into **
    pleural cavity (via pleuro-peritoneal communication), **anterior abdominal wall, **retro-peritoneal space

(From bedside:
6. ***Encapsulating peritoneal sclerosis (EPS) (aka Sclerosing encapsulating peritonitis (SEP)) —> Intestinal obstruction —> Prednisolone / Tamoxifen / Surgery)

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7
Q

PD related peritonitis

A

Presentation:
- **Abdominal pain + **Fever + ***Turbid PD fluid

Causative agents:
- ***Gram +ve / -ve bacteria (usually)
- Fungi / Mycobacteria (occasionally)

(UpToDate:
- Gram +ve: **Coagulase-negative Staphylococcus spp. (60%) (e.g. Epidermidis), Streptococcus spp., Staphylococcus aureus, Enterococcus spp., Corynebacterium spp.
- Gram -ve: **
E. coli, ***Klebsiella spp., Pseudomonas aeruginosa)

Predisposing factors:
- Exit site infection
- Contamination of PD catheter during PD exchanges
- Constipation / Diarrhoea

Diagnosis:
- PD fluid microscopy: **↑ WBC count with **Neutrophil predominance (SpC Medicine: **>100 WBC / mm3, **>50% PMN)
- PD fluid culture: identification of causative organism
(- Clinical features consistent with peritonitis, i.e. abdominal pain and/or cloudy dialysis effluent (IM Handbook))

Treatment:
- Empirical **intraperitoneal antibiotics covering common Gram +ve / -ve bacteria (e.g. **Cefazolin (1st gen cephalosporin) + ***Amikacin (aminoglycoside))
—> Choice of antibiotics should be adjusted according to culture results
- Refractory peritonitis may need PD catheter removed + put on temporary HD
- New catheter inserted later after complete resolution of peritonitis

Complications:
- Frequent PD related peritonitis —> damage peritoneal membrane —> eventual PD failure —> cannot do PD

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8
Q

Haemodialysis (HD)

A

3 components:
1. Vascular access

  1. Haemodialysis machine
    - connected to patient via AV fistula
    - blood pump drives blood through haemodialysis circuit
  2. Haemo-dialyser
    - where haemodialysis occurs

2 types of HD:
1. In-centre haemodialysis
- heamodialysis treatment in a haemodialysis centre (located in a hospital / community)

  1. Home heamodialysis
    - patients usually younger + have day-time job
    - perform HD by themselves at home
    - ***Nocturnal home haemodialysis (sleep while HD in operation)
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9
Q
  1. Vascular access
A

Allows sufficiently ***high flow of blood from patient to pass through HD machine and then return to the patient

3 types:
1. **Arteriovenous fistula (AVF)
- anastomosis between radial artery and cephalic vein: **
radiocephalic AV fistula at wrist
- can detect thrills on palpation + bruit on auscultation of fistula
- vascular access of choice for **long-term HD (∵ made from native blood vessels with no foreign body involved —> **lowest risk of infection (+ **highest patency rate (from SpC Surg Bedside))
(- **
Allen test for blood flow: open + close hand as quickly as possible —> hold fist tightly —> compress radial + ulnar artery together —> release either one —> blood should fill back hand quickly —> artery is patent
- ***rule of 6 to assess maturity of fistula:
—> 6 weeks post-creation
—> diameter of body of fistula should be >=6mm
—> length of fistula should be 6cm to allow for a successful two-needle dialysis
—> depth <6mm from skin
—> blood-flow rate >=600mL/min)

  1. ***Arteriovenous graft (AVG)
    - synthetic material directly connect artery + vein
    - used when infeasible to create an AVF
    (- readily available
    - no need to wait it to mature unlike AVF (from SpC Surg Bedside))
  2. Tunneled cuffed double lumen ***central venous catheter
    - inserted into right IJV
    - fibrous cuff just inside exit site beneath clavicle
    - catheter runs through a SC tunnel before entering IJV
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10
Q

***Comparison between In-centre / Home HD

A
  1. Location of HD
    - In-centre HD: HD centre
    - Nocturnal home HD: Patient’s home
  2. HD performed by
    - In-centre HD: Renal nurses
    - Nocturnal home HD: Patient
  3. Frequency
    - In-centre HD: 2-3 times / week
    - Nocturnal home HD: 4-5 times / week
  4. Duration
    - In-centre HD: 4-5 hours / session
    - Nocturnal home HD: 6-8 hours / session
  5. Dialysis efficacy
    - ***Higher in Nocturnal home HD
  6. QOL
    - ***Better in Nocturnal home HD
  7. Cost
    - ***Higher in Nocturnal home HD
  8. Need to train patient
    - ***Need in Nocturnal home HD
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11
Q

***Complications of HD

A
  1. Vascular access complications
    - Vascular access **stenosis (e.g. AVF stenosis —> ↓ effective bloodflow through HD circuit)
    - Vascular access **
    thrombosis
    - Upper limb **ischaemia (elderly + DM patients with severe **atherosclerosis are prone to develop ischaemia in the limb bearing the AV fistula)
  2. Catheter access complications
    - Catheter **exit site infection (usually localised to skin / soft tissue around exit site with erythema + pustular discharge, uncontrolled infection may spread along the SC tunnel into systemic circulation —> **bacteraemia / septicaemia)
    - Catheter associated **bacteraemia
    - Catheter **
    malfunction (∵ formation of blood clot / thrombosis inside catheter lumen —> blockade of catheter)
  3. Complications during HD
    - Cardiovascular —> **Hypotension, Cardiac arrhythmia
    - Neuromuscular —> **
    Muscle cramps
    - Technical malfunctions —> ***Air embolism, Blood loss
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12
Q

Renal transplantation

A

***Treatment of choice for most ESRD patients (∵ QOL of renal transplant recipients&raquo_space; dialysis patients)

2 types of kidney donors:
1. Living donor
- **1st degree relative / spouse
- should be healthy + have **
normal renal function / ***structure —> need to undergo repeated pre-transplant workup to ensure fit to donate a kidney
- Donor nephrectomy: Laparoscopic nephrectomy (smaller surgical scar + shorter hospital stay)

  1. Deceased donors
    - irreversible brain damage leading to brainstem death (e.g. severe head injury)
    - should have no known history of **kidney diseases, **long-standing HT, **DM, have **normal renal function
    - Donor nephrectomy: Open nephrectomy
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13
Q

Kidney transplant operation

A
  1. Anastomosis of transplanted kidney’s **artery + vein to recipient’s **iliac blood vessels
  2. Transplanted ***ureter to recipient’s bladder

***Hockey stick Scar: in lower quadrant of abdomen

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14
Q

***Challenge of Renal transplantation

A
  1. ***Acute rejection (of transplanted kidney by host’s immune system) (major hurdle)
  2. Early allograft dysfunctions
    - Urological complications (e.g. urine leakage)
    - **Vascular complications (e.g. renal vein thrombosis)
    - **
    Infections (e.g. UTI, viral infection)
    - ***Drug toxicity (e.g. Calcineurin inhibitor nephrotoxicity)
  3. Long term complications of renal transplant
    - **Infections (CMV, Pneumocystis jirovecii, BK virus, M. Tb)
    - **
    Malignancy (PTLD)
    - CVS disease
    - Drug-related SE
    - **Chronic allograft injury
    - **
    Recurrence of primary disease (IgA nephropathy, membranous nephropathy, FSGS)
  4. Shortage of donor kidneys (advances in xeno-transplantation, gene editing technology, regenerative medicine may help in future)
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15
Q

***1. Acute rejection

A
  • **T-cell + **Ab-mediated mechanisms
  • risk of rejection highest in first ***3-6 months after transplantation

Rejection prophylaxis:
***Long-term immunosuppressive treatment
- heaviest during first 3-6 months
- several immunosuppressive drugs used together
—> minimise SE of individual drug
—> while achieving adequate level of immunosuppression

Drugs (記: PCMMA):
1. Prednisolone
2. **
Azathioprine
3. Cyclosporine A, Tacrolimus (
Calcineurin inhibitors CNIs)
4. Rapamycin (
**mTOR inhibitors)
5. ***Mycophenolate mofetil

SE:
1. Prednisolone: Cushingoid facies, **hyperglycaemia, HL, peptic ulcers, HT
2. Cyclosporine: **
nephrotoxicity, **HT, HL, **gum hypertrophy, gout
3. Tacrolimus: **nephrotoxicity, HT, **new onset DM, tremors, GI upsets
4. Mycophenolate mofetil: diarrhoea, vomiting, **anaemia, **leukopenia, viral infections
5. Rapamycin (Sirolimus): synergistic nephrotoxicity with CNIs, proteinuria, HL, impaired wound healing, interstitial pneumonitis
6. Azathioprine: GI upsets, ***hepatotoxicity, anaemia, leukopenia, thrombocytopenia

From JC066:
- Steroid: moon face, osteonecrosis, impaired glucose tolerance
- Cyclosporine: **hairy face (hirsutism), **gum hypertrophy, **nephrotoxicity
- Tacrolimus (FK506): **
neurotoxicity (idiosyncratic), **nephrotoxicity
- Mycophenolate mofetil: **
leukopenia
- Sirolimus: ***hyperlipidaemia

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16
Q

Biologic agents

A

Polyclonal / Monoclonal Ab
- used either as **Induction therapy / **Treatment of acute rejection

Example:
1. **Anti-thymocyte globulin (ATG)
2. **
Monoclonal Anti-IL2 receptor Ab

17
Q
  1. Early allograft dysfunctions
A

Causes:
1. Urological complications (e.g. urine **leakage)
2. Vascular complications (e.g. renal vein **
thrombosis)
3. **Infections (e.g. UTI, viral infection)
4. **
Drug toxicity (e.g. Calcineurin inhibitor nephrotoxicity)

18
Q
  1. Long term complications of renal transplant
A
  1. ***Infections
    - Renal transplant recipients are immunocompromised + prone to opportunistic infections
    - organisms: CMV, Pneumocystis jirovecii, BK virus, M. Tb
  2. Malignancy
    - ↑ risk of developing most types of malignancies (∵ immunocompromised)
    - e.g. ***PTLDs (post-transplant lymphoproliferative disorders)
  3. CVS disease
    - **most important cause of death with a functioning graft in renal transplant recipients
    - transplant recipients have multiple CVS risk factors e.g. DM, HT, HL (usually **
    associated with use of immunosuppressive drugs)
  4. Drug-related SE
    - Cushingoid features (prenisolone)
    - Gum hypertrophy (cyclosporine A)
  5. Chronic allograft injury
    - Clinico-pathological syndrome characterised by:
    —> **Slow progressive decline in renal graft function, proteinuria, HT
    —> Histological features of **
    interstitial fibrosis, **tubular atrophy
    —> caused by both immune + non-immune factors
    - leading cause of **
    late graft failure after renal transplantation
  6. Recurrence of primary disease
    - cause of original kidney disease may recur in transplanted kidney
    - recurrence of **IgA nephropathy, **membranous nephropathy, ***FSGS are not uncommon in transplant patients
19
Q

Pneumocystis pneumonia (PCP)

A

Clinical presentation:
1. Acute onset of fever
2. Cough
3. SOB
4. Severe ***type 1 respiratory failure

CXR:
- Diffuse, **Bilateral, **Interstitial infiltrates

Diagnosis:
- Microscopy with staining of BAL fluid

Treatment:
- High dose ***Septrin (Cotrimoxazole)
—> Septrin prophylaxis of PCP for transplant recipients