Nephrology JC077: Renal Replacement Therapies Flashcards
Renal replacement therapy
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)
Basic principles of dialysis
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
Choice between PD / HD
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
- Local health care reimbursement system
- HK: PD first policy (∵ less costly) - Patient’s preference
- PD usually performed by patient at home daily
- HD usually performed by renal nurses in HD centre 2-3 times / week
Peritoneal dialysis (PD)
3 components:
1. Peritoneal membrane
- **thin + **vascularised + ***large SA —> used as a dialysis membrane
- 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 - 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
- Automated peritoneal dialysis (APD)
- APD machine to help patient to perform PD exchanges, usually ***at night when patient sleeps
Comparison between CAPD and APD
- Need for APD machine
- CAPD: No
- APD: Yes - Timing of PD exchange
- CAPD: Throughout the day
- APD: At night during sleep - Need for daytime exchange
- CAPD: Yes
- APD: No for NIPD (nocturnal intermittent PD), Yes for CCPD (continuous cyclic PD) - Dialysis efficacy
- ***Similar - QOL
- ***Usually better in APD - Cost
- ***APD more costly
***Complications of PD
- PD catheter **exit site infection
- redness + tenderness at exit site, may be associated with **purulent discharge
- may predispose to ***PD peritonitis - PD related ***peritonitis
- 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 - PD catheter malfunction / malposition
- tip of catheter may occasionally migrate out of pelvis —> poor drainage of PD fluid
- ***Omental wrap -
**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)
PD related peritonitis
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
Haemodialysis (HD)
3 components:
1. Vascular access
- Haemodialysis machine
- connected to patient via AV fistula
- blood pump drives blood through haemodialysis circuit - Haemo-dialyser
- where haemodialysis occurs
2 types of HD:
1. In-centre haemodialysis
- heamodialysis treatment in a haemodialysis centre (located in a hospital / community)
- Home heamodialysis
- patients usually younger + have day-time job
- perform HD by themselves at home
- ***Nocturnal home haemodialysis (sleep while HD in operation)
- Vascular access
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)
- ***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)) - 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
***Comparison between In-centre / Home HD
- Location of HD
- In-centre HD: HD centre
- Nocturnal home HD: Patient’s home - HD performed by
- In-centre HD: Renal nurses
- Nocturnal home HD: Patient - Frequency
- In-centre HD: 2-3 times / week
- Nocturnal home HD: 4-5 times / week - Duration
- In-centre HD: 4-5 hours / session
- Nocturnal home HD: 6-8 hours / session - Dialysis efficacy
- ***Higher in Nocturnal home HD - QOL
- ***Better in Nocturnal home HD - Cost
- ***Higher in Nocturnal home HD - Need to train patient
- ***Need in Nocturnal home HD
***Complications of HD
- 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) - 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) - Complications during HD
- Cardiovascular —> **Hypotension, Cardiac arrhythmia
- Neuromuscular —> **Muscle cramps
- Technical malfunctions —> ***Air embolism, Blood loss
Renal transplantation
***Treatment of choice for most ESRD patients (∵ QOL of renal transplant recipients»_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)
- 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
Kidney transplant operation
- Anastomosis of transplanted kidney’s **artery + vein to recipient’s **iliac blood vessels
- Transplanted ***ureter to recipient’s bladder
***Hockey stick Scar: in lower quadrant of abdomen
***Challenge of Renal transplantation
- ***Acute rejection (of transplanted kidney by host’s immune system) (major hurdle)
- 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) - 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) - Shortage of donor kidneys (advances in xeno-transplantation, gene editing technology, regenerative medicine may help in future)
***1. Acute rejection
- **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
