Principles of renal replacement therapies - haemodialysis and peritoneal dialysis

What dialysis does and does not replace

Dialysis replaces solute clearance and volume control only
- It does NOT replace erythropoietin, 1-alpha-hydroxylation, or the endocrine and metabolic functions - hence the persisting anaemia and CKD-MBD
Native GFR of a well-dialysed patient is equivalent to ~10-15 mL/min - dialysis is a poor kidney

	Diffusion	Convection (ultrafiltration)
Driving force	Concentration gradient	Pressure gradient (hydrostatic or osmotic)
Removes	Small solutes (urea, K+, creatinine)	Middle molecules (beta-2 microglobulin) + water
Modality	Haemodialysis	Haemofiltration; PD ultrafiltration
Efficiency falls with	Increasing molecular weight	Membrane pore size

Haemodiafiltration = both; better middle-molecule clearance and improved survival vs high-flux HD (CONVINCE trial)

~15,000 Australians on dialysis (ANZDATA); ~80% haemodialysis, ~20% peritoneal dialysis
Home therapies (home HD + PD) ~25-30% - among the highest rates internationally
Annual mortality on dialysis ~15%; 5-yr survival ~40-50%

Blood flow rate (Qb) - 250-400 mL/min; limited by vascular access
Dialysate flow rate (Qd) - typically 500-800 mL/min, counter-current to blood
Membrane surface area and permeability (KUf) - high-flux vs low-flux
Time - the variable most often under-prescribed
Kt/V: K = dialyser clearance, t = time, V = volume of distribution of urea

The peritoneum is the membrane (~1-2 m2); solute crosses by diffusion, water by osmosis
Dextrose (glucose) creates the osmotic gradient that drives ultrafiltration from blood into dialysate
- Glucose is absorbed over the dwell, dissipating the gradient - hence the dwell-time limit
- Icodextrin (a glucose polymer, poorly absorbed) sustains ultrafiltration over long dwells - used for the overnight/day dwell
Peritoneal equilibration test (PET) classifies transport status:
- High transporter - fast solute equilibration, poor ultrafiltration -> short frequent dwells (APD)
- Low transporter - good ultrafiltration, poor clearance -> long dwells, large volumes (CAPD)

Removed well: low molecular weight, low protein binding, small volume of distribution, water-soluble
- Lithium, salicylate, methanol, ethylene glycol, metformin, theophylline, valproate, phenobarbitone, carbamazepine (with charcoal HP)
Not removed: high protein binding, large Vd, lipophilic
- Tricyclic antidepressants, digoxin, benzodiazepines, beta blockers (except atenolol and sotalol), phenytoin, warfarin, opioids
Rebound after dialysis is characteristic of drugs with a large Vd (lithium) - re-check levels

	Target
Haemodialysis	spKt/V >=1.2 per session (3x/week), URR >65%
Peritoneal dialysis	Weekly Kt/V >=1.7

*Residual renal function contributes to both, and preserving it matters more than pushing Kt/V* - it independently predicts survival
- Avoid nephrotoxins and volume depletion; continue ACEi/ARB and loop diuretics while urine output persists
Volume status, BP and nutrition predict survival better than Kt/V

Monthly: UEC, Ca/PO4/PTH, FBE, iron studies, albumin
Access surveillance: fistula flow, recirculation, venous pressures; PD catheter function
Annual: hepatitis B/C serology, adequacy testing, transplant reassessment

	CRRT (CVVHD/CVVHDF)	Intermittent HD
Use when	Haemodynamically unstable - vasopressor-dependent, ICU	Rapid correction needed - severe hyperkalaemia, toxin removal, pulmonary oedema
Rate	Slow, continuous over 24 h	Fast, 3-5 h
Advantage	Less intradialytic hypotension, gradual fluid removal, avoids cerebral oedema	Efficient, less anticoagulation exposure, patient mobility
Anticoagulation	Regional citrate (preferred) or heparin	Heparin or none

*No mortality difference between CRRT and IHD in AKI* - the choice is haemodynamic tolerance and logistics
SLED (sustained low-efficiency dialysis) - a hybrid; increasingly used
Avoid rapid urea clearance in a first dialysis - dialysis disequilibrium syndrome (cerebral oedema, headache, seizures); prescribe short, low-efficiency sessions initially

Unfractionated heparin standard; regional citrate for high bleeding risk or in CRRT (complications: metabolic alkalosis, hypocalcaemia, citrate accumulation in liver failure)
Heparin-free with saline flushes if active bleeding or HIT

Lithium, salicylate, methanol, ethylene glycol, metformin-associated lactic acidosis, theophylline, valproate
Haemoperfusion (charcoal) for a few highly protein-bound agents; largely superseded

AV fistula > AV graft >> tunnelled catheter - fistula has the lowest infection and best patency
*Catheter-related bloodstream infection is the leading infectious cause of death on dialysis*
Plan the fistula ~6 months before need; preserve veins from the moment CKD is diagnosed

Cardiovascular disease - the leading cause of death; LVH, sudden cardiac death (highest on the long interdialytic interval - Monday/Tuesday)
Infection - catheter bacteraemia, PD peritonitis, exit-site infection
Dialysis-related amyloidosis - beta-2 microglobulin; carpal tunnel, shoulder pain, cystic bone lesions. Seen after years on low-flux dialysis
CKD-MBD, anaemia, protein-energy wasting
Intradialytic hypotension, cramps, arrhythmia
Disequilibrium syndrome, first-use/anaphylactoid reactions (avoid ACEi with AN69 membranes - bradykinin accumulation)
Depression, fatigue, restless legs, uraemic pruritus
Acquired cystic kidney disease -> renal cell carcinoma

Dialysis is a treatment, not a cure - median survival on dialysis is shorter than for many cancers
- Age 20-24: ~20 yrs; age >75: ~2-3 yrs
Transplantation gives better survival and quality of life for those who are candidates - assess everyone
Conservative kidney management is a legitimate alternative in the frail elderly with multimorbidity
- Survival difference is small over 75 with high comorbidity, and hospital-free days are often better
Residual renal function declines faster on HD than on PD - a reason to consider PD-first
Withdrawal from dialysis is a common and appropriate mode of death (~10-15%) - plan for it in advance

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