Dialysis clears solute (diffusion, convection) and solvent (ultrafiltration) through extracorporeal or peritoneal circuits. HD 3x/week is standard for ESKD; CRRT for haemodynamically unstable ICU patients; PD for home-based therapy. Access is the lifeline — protect veins early.

principles

Two jobs, handled separately:

Solvent (water) clearance — ultrafiltration via pressure gradient: barometric (HD) or osmotic (PD)
Solute clearance — diffusion (concentration gradient across membrane) + convection (solute dragged with water movement)

access

Type	Details	Notes
Temporary catheter	Non-tunnelled, internal jugular or femoral	Short-term only; reassess daily
Tunnelled catheter (PermCath)	Subcutaneous cuff, internal jugular	Bridge to permanent access or when AVF/AVG not feasible
AVF	Native arteriovenous fistula	Lowest infection/thrombosis; needs 2–3 months to mature
AVG	Synthetic graft	Usable in ~2–4 weeks; higher thrombosis/infection than AVF

Current KDOQI framing favours “right access, right patient, right time” (ESKD Life-Plan) over a blanket “fistula first” approach — access choice should be individualised.

protect the veins

Avoid CVL/PICC lines in CKD patients whenever possible — venous stenosis/thrombosis destroys future access sites. Minimise venipuncture in dialysis patients; draw labs from the dialysis circuit 3x/week.

haemodialysis prescription

Standard chronic HD:

Parameter	Default
Frequency	3x/week (MWF or TuThSa)
Duration	4 h
Blood flow (Qb)	400 mL/min
Dialysate flow (Qd)	500 mL/min
Dialysate Na	140 mmol/L (should not exceed serum Na by >10)
Dialysate K	Rule of 7 minus pre-dialysis K (options: 1, 1.5, 3, 4 mmol/L)
Dialysate HCO3	30–40 mmol/L
Dialysate Ca	1.25 or 1.50 mmol/L
UF rate	Minimise; observational data associate >13 mL/kg/hr with increased mortality (some guidelines suggest ≤10 mL/kg/hr) — no absolute threshold is guideline-endorsed
Anticoagulation	Typically dalteparin 2500 units (tight) — agent and dose are unit-dependent; UFH used in many centres

Anticoagulation contraindications: HIT, pericarditis, new HD starts, recent major bleeding or surgery.

new HD start

Gradual ramp to avoid dialysis disequilibrium syndrome (cerebral oedema from rapid osmolality shifts). The schedule below is a typical institutional protocol — no specific DDS-prevention regimen is strongly evidence-based:

	Day 1	Day 2	Day 3
Duration	2 h	3 h	4 h
Qb	200 mL/min	300 mL/min	400 mL/min
Qd	300 mL/min	400 mL/min	500 mL/min
Anticoagulation	None	None	Start as appropriate

emergent indications

Mnemonic AEIOU: Acidosis (refractory to medical management — note that most lactic acidosis responds poorly to RRT as extracorporeal clearance is far below endogenous lactate turnover; metformin-associated lactic acidosis is the key exception), Electrolytes (refractory hyperkalaemia), Ingestion (dialysable toxin), Overload (refractory pulmonary oedema), Uraemia (encephalopathy, pericarditis, bleeding diathesis).

dialysable toxins

A drug is dialysable if it has low molecular weight, low Vd, low protein binding, and high water solubility. IHD is preferred over CRRT for most poisonings — faster clearance matters when the toxin is causing end-organ damage.

Toxin	When to dialyse	Notes
methanol	level >15.6 mmol/L (>21.8 if fomepizole on board), visual symptoms, refractory acidosis, AKI	give fomepizole while arranging HD; cofactor: folinic acid; avoid systemic anticoagulation (intracerebral haemorrhage risk)
ethylene glycol	level >50 mmol/L or osmolal gap >50; glycolate >12 mmol/L or AG >27 (recommend) / glycolate 8–12 or AG 23–27 (suggest); coma, seizures, AKI	with early fomepizole and preserved renal function, many patients no longer need HD — acidosis, glycolate, and organ dysfunction drive the decision more than the EG level alone; cofactors: thiamine, pyridoxine
lithium	severe symptoms (decreased LOC, seizures, life-threatening dysrhythmias) irrespective of level; level >4 with AKI; level >5	rebound common — check level 6 h post-HD; may need repeat sessions
salicylates	level >7.2 mmol/L (100 mg/dL), altered mental status, refractory acidosis, pulmonary oedema, AKI	urine alkalinisation first-line; HD if failing or severe
metformin	lactic acidosis with lactate >20 mmol/L and pH ≤7.0, haemodynamic instability, failure to improve with supportive care	low Vd, no protein binding — clears well on HD
valproic acid	level >6900 µmol/L (1000 mg/L), cerebral oedema, haemodynamic instability	high protein binding at therapeutic levels but saturates in overdose → becomes dialysable
baclofen	refractory coma, seizures, or cardiovascular collapse not responding to supportive care	no antidote; low Vd, minimal protein binding — dialyses well
theophylline	acute: level >555 µmol/L (100 mg/L); chronic: >333 µmol/L (60 mg/L) with seizures or arrhythmia	low Vd; charcoal haemoperfusion historically used but HD is sufficient
carbamazepine	progressive clinical deterioration despite supportive care	rebound common — may need prolonged or repeat HD

not dialysable

Digoxin (very large Vd — use digoxin-specific antibody fragments), tricyclic antidepressants (large Vd, high protein binding), benzodiazepines, opioids, colchicine (large Vd, high tissue binding — no role for HD despite severe toxicity), calcium channel blockers, beta-blockers.

CRRT

ICU-only modality for haemodynamically unstable patients who cannot tolerate intermittent HD.

Default mode: CVVHD (continuous venovenous haemodialysis)
Filters changed every 72 h — natural reassessment point: still need CRRT or ready for intermittent HD?
Anticoagulation escalation: none (default) → regional citrate (if filter clotting) → systemic heparin
Substantially more resource-intensive than intermittent HD

CRRT vs intermittent HD

STARRT-AKI (2020) showed no mortality benefit from early RRT initiation. Modality choice (CRRT vs iHD) is driven by haemodynamic tolerance, not timing.

peritoneal dialysis

Home-based therapy using the peritoneal membrane as the dialysis surface. Dextrose-based dialysate creates an osmotic gradient for fluid removal.

solutions

Solution	Composition	Notes
Dianeal 1.5%	Dextrose ~8.3 mmol/L glucose	Standard
Dianeal 2.5%	Dextrose ~13.9 mmol/L glucose	More UF
Dianeal 4.25%	Dextrose ~23.6 mmol/L glucose	Maximum UF; significant glucose load
Extraneal (icodextrin)	Glucose polymer	Non-glucose osmotic agent — preferred for long dwells (colloid osmosis sustains UF); also useful for glycaemic control in diabetics

modalities

CAPD — continuous ambulatory PD: manual exchanges, typically 4x/day
APD/CCPD — automated/continuous cycling PD: machine performs overnight exchanges

Generally continue home PD prescription during hospital admission. Modify for volume overload (higher concentration) or hyperkalaemia.

PD and glucose

Dianeal dextrose loads can cause significant hyperglycaemia — adjust insulin accordingly. Extraneal (icodextrin) has minimal glucose effect but interferes with some glucometer readings (maltose cross-reactivity).

HD and PD have no significant mortality difference at initiation — modality choice is largely patient-preference and lifestyle-driven.

practical points

No need to repeat lytes post-HD unless concerned about dialysis adequacy or persistent hyperkalaemia — they will be transiently abnormal
Do not correct serum K in dialysis patients unless <2 mmol/L or symptomatic — risk of rebound hyperkalaemia
When unsure about access or prescription logistics, ask the dialysis nurses

dialysis overview