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MBBS VI - SpC - Medicine > Renal - Renal replacement therapy > Flashcards

Renal - Renal replacement therapy Flashcards

1
Q

Renal replacement therapy 3 main types? When to start?

A

Peritoneal dialysis Hemodialysis Kidney transplantation

Start when:

  1. GFR falls to <10mL/min/1.73m3
  2. Uremic symptoms
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2
Q

Mechanism of peritoneal dialysis

A

Diffusion

  • Process where molecules in solutions diffuse across semipermeable membrane using a concentration gradient
  • Pulls solutes out of blood from peritoneal capillary network through membrane into intraperitoneal dialysate
  • MOST effective for molecules that are not present in dialysis including urea, creatinine, K+, PO43- and other uremic toxins

Ultrafiltration
• Convective process where molecules pass through pores in the membrane using hydrostatic or osmotic pressure gradients
• Occurs across osmotic pressure gradient between dialysate and blood created by adding dextrose, icodextrin (glucose polymer solution) to dialysate

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3
Q

Factors that influence choice between peritoneal dialysis and hemodialysis

A
  1. Contraindications to PD or HD
  2. Local healthcare reimbursement - PD cheaper, used first
  3. Patient preference - PD at home or HD in hospital
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4
Q

Peritoneal dialysis

Indications

Contraindications

A

Indications:

  • Acute kidney injury
  • Chronic kidney injury with GFR < 10 mL/min/1.73 m2 (OR) Stage 5 CKD (AND) uremic symptoms

Contraindications:

 Previous extensive abdominal surgery (scarring)
 Frequent PD-related peritonitis
 Place of residence that does not permit peritoneal dialysis or residence lacking sanitary conditions

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5
Q

Peritoneal dialysis

Subtypes

A

Continuous ambulatory peritoneal dialysis (CAPD)

Automated peritoneal dialysis (APD):

  • Continuous cycling peritoneal dialysis (CCPD)
  • Nocturnal intermittent peritoneal dialysis (NIPD
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6
Q

Explain why the peritoneal membrane is chosen for dialysis

A
  • Thin semipermeable membrane
  • Large surface area
  • Highly vascularized
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7
Q

3 components of peritoneal dialysis

A

Peritoneal membrane

Peritoneal dialysis catheter

Peritoneal dialysis fluids

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8
Q

Peritoneal cavity access for PD

  • Name of catheter
  • Insertion and exit site
    • Placement inside cavity
A

Tenckhoff catheter: with many side holes and 2 fibrous cuffs

Insertion: Paramedian incision is created, insertion ≥ 2 weeks before start of dialysis

Exit: Lateral and caudal to entrance site, should be visible by patient and should not be located at the belt line, skin creases or skin folds

Placement: Tip should be pointing downwards inside pelvic cavity since the pelvis is the most dependent part of the body

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9
Q

Typical composition of peritoneal dialysis fluid

A

Balanced salt solutions with

  • No Potassium
  • Glucose as osmotic agent: in 1.5/ 2.5/4.25g per dL concentration for various osmotic strengths
  • Lactate as buffer agent
  • Salts: Sodium, Calcium, Magnesium, Lactate
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10
Q

Compare the timing between different types of peritoneal dialysis

A

Continuous ambulatory peritoneal dialysis (CAPD): Manual, multiple exchanges (3 times) during daytime + overnight dwell

Automated:

Continuous cycling peritoneal dialysis: Full 24 hour cycle

Nocturnal intermittent peritoneal dialysis: Only at night, with faster dwells

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11
Q

Compare CAPD and APD

  • Timing of PD exchange
  • Need for daytime exchange
  • Dialysis efficacy
  • QoL
  • Cost
A
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12
Q

4 types of osmotic agents in peritoneal dialysis solution

A

Glucose/ Dextrose: Most common, concentrations including 1.5% (小水)/ 2.5% (中水)/ 4.25% (大水)

Low GDP solution

Glucose-polymer-containing solution (Icodextrin*): Reduced carbohydrate dose provides some long-term metabolic advantages, good for DM

Amino-acid based solution: Improves nutritional status in PD patients

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13
Q

Disadvantages of using dextrose as osmotic agent in peritoneal dialysis solutions

A
  • Easily absorbed leading to short-lived ultrafiltration
  • Leads to metabolic complications including metabolic syndrome (hyperglycemia + hyperlipidemia + weight gain)
  • Presence of glucose degradation products (GDP) which affects peritoneal host defence mechanism by inhibiting phagocytosis and bactericidal activity
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14
Q

Reasons for different salts and ions additives in peritoneal dialysis solution

A

Replenish low ions:

  • Mg
  • Ca

Avoid worsening electrolyte imbalance

  • No Potassium (Patients are usually hyperkalemic, aim serum K+ at 4mEq/L)
  • Low Na prevents hyperNa due to fluid removal
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15
Q

Complications of peritoneal dialysis

A

Catheter:

  • Pericatheter leakage
  • Bleeding, Injury to visceral organs
  • Mechanical flow dysfunction: catheter failure, kinking, malposition
  • Dialysis Failure
  • Catheter migration

Catheter-associated infections:

  • Exit site infections
  • Tunnel infections

Metabolic:

  • Metabolic syndrome (Hyperglycemia + Hyperlipidemia + Weight gain)
  • Hypoalbuminemia
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16
Q

PD-related peritonitis

  • Causative pathogens
  • Predisposing factors
A

Microbiology:

o Gram +ve: Staphylococcus sp. (Particularly coagulase -ve)
o Gram -ve: E. coli/ Campylobacter/ Pseudomonas aeruginosa
o Mycobacterium tuberculosis
o Fungal infections

Predisposing factors:

  • Catheter-associated infection (exit-site and tunnel infections)
  • Contamination of catheter during exchange
  • Underlying GI pathology (cholecystitis/ appendicitis/ diverticulitis)
  • Constipation or diarrhea
  • Recent invasive interventions (colonoscopy/ cystoscopy/ hysteroscopy)
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17
Q

PD-related peritonitis

Diagnostic tests

Treatment

A

Diagnostic:

  • Clinically features indicative of peritonitis such as fever, abdominal pain or cloudy effluent
  • WBC count ≥ 100 cells/mm3 and percentage of neutrophils (PMNs) > 50% in peritoneal fluid after dwell time ≥ 2 hours
  • +ve Peritoneal dialysate effluent culture

Treatment:

  • Gram +ve: 1st generation cephalosporin (cefazolin) or Vancomycin
  • Gram -ve: Aminoglycoside or 3rd or 4th generation cephalosporin (ceftazidime/ cefepime)
  • Cover both: e.g. Cefazolin + Amikacin
  • Remove catheter for recurrent infections
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18
Q

Peritoneal dialysis failure

Cause

A

Chronic exposure to dextrose in PD fluid, Repeated peritonitis >> Fibrosis of peritoneal membrane and marked thickening of membrane

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19
Q

Peritoneal dialysis catheter leakage

Possible cavities involved

A

Leak out of peritoneal cavity to:

Pleural cavity

Anterior abdominal wall

Retro-peritoneal space

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20
Q

Main components of hemodialysis

A

Vascular access:

  • Arteriovenous fistula (AVF)
  • Arteriovenous Graft (AVG(
  • Tunneled cuffed double lumen central venous catheter

Hemodialysis machine

Hemo-dialyzer

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21
Q

Choice of vascular access for chronic hemodialysis?

Reasons?

A

AV fistula most preferred

AV fistula > AV graft > Central hemodialysis catheter

Reasons:

lowest morbidity and mortality, lowest need for intervention and best long-term patency

22
Q

Central hemodialysis catheter for HD

Risks

Indications

A

Risks: worse complication and survival rates than AV fistula or AV graft

Indications:

o AV access is exhausted
o AV access is contraindicated (e.g. severe heart failure)
o Expected duration of dialysis < 1 year

23
Q

Compare AV fistula with AV graft

  • Likelihood of failure
  • Long-term patency
  • Time to mature
  • Ease of cannulation
  • Complication rate
A
24
Q

List 2 types of hemodialysis

Compare:

  • frequency
  • Duration
  • Efficacy
  • QoL
  • Cost
  • Training
A
25
Q

Types of AV fistula and AV graft

A

AVF: vein-to-artery anastomosis

  • Radial-cephalic AVF
  • Brachial-cephalic AVF
  • Brachial-basilic AVF

AVG: Constructed by interposing a prosthetic graft between an artery and vein with expanded polytetrafluoroethylene (ePTFE)

  • Looped forearm (Brachial artery to cephalic vein)
  • Straight forearm (Radial artery to cephalic vein)
  • Looped upper arm (Axillary artery to axillary vein
  • Straight upper arm (Brachial artery to axillary vein)
26
Q

Complications of hemodialysis

Vascular access, catheter-related, dialysis-related complications

A

Vascular access:

Stenosis, thrombosis, upper limb ischemia

Catheter access:

Exit site infection, Bacteremia, Catheter malfunction (clot)

During dialysis:

CVD: hypotension, arrhythmia

Neuromuscular: Muscle cramps

Technical: Air embolism, blood loss

27
Q

Central vascular access for HD

Which veins are used?

A

Internal jugular vein (IJV) (most common)
o Right IJV is preferred since it takes a straight path into SVC

External jugular vein (EJV)

Common femoral vein
o Indicated in bilateral occlusion of central thoracic vein

Subclavian vein
o Indicated if internal and external jugular veins are occluded and common femoral vein is not a good option

28
Q

MHC

Genes contained in Major Histocompatibility complex

Expression of genes in MHC

A
  • MHC Class I: HLA-A,B,C - Present on all nucleated cells and platelets
  • MHC Class II: HLA-DP,DQ,DR - Expressed on APCs (antigen presenting cells)
  • MHC Class III: TNF, C4 - Does not code for HLA but contains genes for other components involved in inflammation and other immune complexes
29
Q

HLA genes

Function

Inheritance

Variability

A

HLA genes are blueprints to show how cells should organized amino acids to make proteins and are located on chromosome 6

Inheritance:

Each person gets two copies of each gene, one from father and one from mother

4 possible combinations from parents to children

Variability: highly polymorphic

Individual can express 6 different types of MHC Class I molecules and 6 different types of MHC Class II molecules on the cell surface

30
Q

Reason for HLA matching before renal transplant

A

Matched HLA antigens at serological level required including HLA-A, HLA-B and HLA-DR

Anti-HLA antibodies will target against HLA antigens expressed on surface of allograft

Crossmatch is performed prior to transplantation to evaluate for any evidence of preformed antibodies with specificity for the potential donor that could lead to hyperacute or acute antibody-mediated rejection (AMR)

31
Q

Pre-requisites for living and deceased donor for renal transplant

A

Requirements for living donor
• Good past health
• Normal renal structure and function

Requirements for deceased donor
• Irreversible brain damage leading to brainstem death
• Normal renal structure and function
• No known history of kidney disease
• No known history of long-standing HT or DM

32
Q

Patient pre-requisites for renal transplant

A

Acute kidney injury (AKI)
• A = Acidosis: Metabolic acidosis with HCO3- < 10 mmol/L
• E = Electrolyte disturbance: Uncontrolled hyperkalemia > 6 mmol/L
• I = Intoxication
• O = Oedema: Fluid overload/ Uncontrolled pulmonary edema
• U = Uremia: Uremic pericarditis/ Uremic encephalopathy/ Intractable uremic symptoms

Chronic kidney disease (CKD)
• Patients with GFR < 10 mL/min/1.73 m2 (OR) Stage 5 CKD
• Patients becomes symptomatic of uremia

33
Q

List uremic symptoms

Does it correlate with serum BUN or creatinine?

A

anorexia, nausea, vomiting, pericarditis, peripheral neuropathy and CNS abnormalities such as loss of concentration, lethargy, seizures and coma

NO direct correlation exists between the absolute serum levels of blood urea nitrogen (BUN) or creatinine and the development of symptoms

34
Q

Nephrectomy techniques for renal transplantation

A
  • Laparoscopic nephrectomy for living donor
  • Open nephrectomy for deceased donor
35
Q

Implantation of renal allograft

  • Incisions
  • Indications for removal of native kidney(s)
  • Locations for placement of allograft
A

Incisions:

  • Gibson incision - Curvilinear incision in the lower quadrant of the abdomen
  • Hockey stick incision- Inverted J-shaped incision

Indications for removal of native kidneys:

  • Renal cell carcinoma (RCC)
  • Polycystic kidney disease (PKD)
  • Pyelonephritis

Placement:

  • Right iliac fossa (RIF)
  • Extraperitoneal (retroperitoneal) position
36
Q

Renal transplantation

3 Anastomosis

A

Renal artery (donor) anastomosis to internal or external iliac artery (recipient)

Renal vein (donor) anastomosis to external iliac vein (recipient)

Anastomosis of ureter to the bladder by ureteroneocystostomy

37
Q

Methods to monitor renal allograft function

A

Serum creatinine and GFR

Urine dipstick (Urinalysis) for proteinuria/ Spot urine albumin-to-creatinine ratio (ACR)

Allograft renal biopsy (if allograft dysfunction)

38
Q

Types of organ rejection after transplantation according to timing

A

Hyperacute (7mins) - Pre-existing antibodies and complement activation to donor tissue

Acute (8-11 days) - CD4-controlled, CD8 mediated, NK cells and macrophage-mediated

Chronic rejection (3 months to 10 years) - Mixed CD4 and antibody

39
Q

Short-term/ acute complications of renal transplant

A

Acute transplant rejection

Side-effects to Rejection prophylaxis drugs

40
Q

Rejection prophylaxis in renal transplant

Purpose

Choice of prophylaxis drugs

A

Long-term immunosuppressant is needed to prevent rejection of transplanted kidney by recipient’s immune system

3 immunosuppressants are used concurrently to minimize the side effects of individual drugs while achieving adequate immunosuppression
• Corticosteroids (e.g. Prednisolone) (AND)
• Calcineurin inhibitors (e.g. Cyclosporine/ Tacrolimus) (AND)
• Any of the following: Azathioprine/ Mycophenolate mofetil (MMF)/ mTOR kinase inhibitors (e.g. Sirolimus)

MOST common combination = Prednisolone + Tacrolimus + MMF

41
Q

Long-term complications of renal transplant

A

Opportunistic infections: CMV, Pneumocystis pneumonia, BK virus, TB

Malignancy: e.g. Post-transplant lymphoproliferative disorders

Cardiovascular disease *most deadly

Drug-related S/E

Chronic allograft injury *most common cause of late graft fallure

Recurrence of primary disease: e.g. IgA nephropathy, membranous nephropathy, FSGS

42
Q

Definition of Chronic allograft injury in renal transplant

A

Slow, progressive decline in renal graft function, proteinuria, hypertension

With histological features of interstitial fibrosis, tubular atrophy

43
Q

Pneumocystis pneumonia

  • S/S
  • Prophylaxis treatment
A

Acute onset of fever, cough and SoB with type I respiratory failure

High-dose Septrin prophylaxis

44
Q

Cyclosporine

Class

MoA

S/E

A

Class: Calcinuerin inhibitor

MoA:

 Bind to cytoplasmic receptor protein called cyclophilin (CpN)
 Inhibits calcineurin phosphatase
 Prevent activation of nuclear factor (NFATc)
 Inhibits synthesis of IL-2
 ↓ Cell-mediated immunity

S/E:

 Nephrotoxicity

 Gum hyperplasia
 Hyperkalemia
 Hypertension
 Hyperlipidemia

45
Q

Tacrolimus

Class

Drug interactions

MoA

S/E

A

Calcineurin inhibitor

D/D: Cyclosporine, additive nephrotoxicity

MoA:

 Binds to FK-binding protein
 Inhibits calcineurin phosphatase
 Prevent activation of nuclear factor (NFATc)
 Inhibits synthesis of IL-2
 ↓ Cell-mediated immunity

S/E:

 Nephrotoxicity
 Neurotoxicity

 Hyperkalemia
 Hypertension
 Hyperlipidemia
 DM

46
Q

Sirolimus

Drug interaction

MoA

S/E

A

D/D: Aggravates cyclosporine-induced renal dysfunction

MoA:

 Binds to FK-binding protein
 Interfere with mTOR signal
 Block T-cell proliferation in response to IL-2 stimulus

S/E:

 Pancytopenia

 Hypertension
 Hyperlipidemia

47
Q

Azathioprine

Class

MoA

S/E

A

Anti-metabolite (Folate antagonist)

MoA:

 Azathioprine is converted into 6-MP
 6-MP is converted into thioinosine monophosphate (TIMP)
 TIMP inhibits de novo purine ring synthesis which is required for lymphocyte proliferation
 TIMP is converted into 6-thioguanine (6-TG)
 6-thioguanine (6-TG) is incorporated in DNA as a false nucleotide

S/E:

 Hepatotoxicity
 Bone marrow toxicity
(Myelosuppression)
• Anemia
• Leukopenia
• Thrombocytopenia
 Pancreatitis

48
Q

Mycophenolate mofetil

MoA

S/E

A

MoA:

 Inhibits inosine monophosphate dehydrogenase
 Block purine synthesis (guanosine phosphate) which is required for lymphocyte proliferation
 Deprive B and T cells of a key component of nucleic acids

S/E:
GI disturbances:
 Abdominal pain
 Diarrhea
 Constipation
 Nausea and vomiting

Myelosuppression:
 Anemia
 Leukopenia

49
Q

IL-2 antagonists

Examples

MoA

S/E

A

Basiliximab
Daclizumab

MoA:

 Anti-CD25 antibodies block IL-2 receptor on activated T-cells
 Inhibits IL-2 mediated T-cell activation and proliferation

S/E:

None

50
Q

Prednisolone for organ transplant

MoA

S/E

A

MoA:

 Inhibition of nuclear factor kappa B activation (NFκB)
 Binding to glucocorticoid response elements in cytokine genes
 Inhibits cytokine production by T cells and macrophages
 Disrupt T-cell activation and macrophage-mediated tissue injury

S/E:

 Cushingoid changes

 Cataracts
 Peptic ulcer disease (PID)
 Proximal myopathy
 Thinning of skin
 Osteoporosis/ AVN
 Hypertension
 Hyperlipidemia
 Glucose intolerance
 Immunosuppression

51
Q

Causes of early renal allograft dysfunctions

A
  1. Urological complication (e.g. leakage)
  2. Vascular complication (e.g. renal vein thrombosis)
  3. Infection (e.g. UTI, viral infection)
  4. Drug toxicity (e.g. rejection prophylaxis drugs)

MBBS VI - SpC - Medicine (80 decks)

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