Dialysis and kidney transplantation

• Dialysis replaces the filtering and homeostatic work of failed kidneys; kidney transplantation replaces the organ itself. In chronic kidney failure they are complementary options in one pathway, discussed together with the patient.
• Dialysis is started on clinical grounds: symptoms of uraemia, uncontrolled fluid overload or dangerous biochemistry, or when the eGFR falls to about 5 to 7 ml/min per 1.73 m2 even without symptoms. ^[1][2]
• Haemodialysis filters blood across an artificial membrane, usually three times a week; peritoneal dialysis uses the patient's own peritoneum as the membrane and is done at home. Access (a fistula, graft, catheter or peritoneal catheter) is the single most important practical problem in long-term dialysis. ^[7]
• Kidney transplantation is the best kidney replacement therapy for suitable candidates, but suitability depends on overall risk, not on one isolated condition. ^[4][7]
• After transplantation, maintenance immunosuppression (induction plus a long-term combination of drug classes) prevents rejection; kidney transplant rejection is classified by Banff criteria as hyperacute, acute T cell-mediated, acute antibody-mediated or chronic, and needs biopsy for diagnosis. ^[3][9][10]

By the end of this page you should be able to:

1. State the indications for starting dialysis and for conservative management, and name the guidelines that frame them.
2. Compare haemodialysis with peritoneal dialysis on mechanism, setting, access, complications and effect on residual kidney function.
3. Plan dialysis access: type, timing, imaging, maturation checks and cannulation.
4. Describe the complications of haemodialysis, of peritoneal dialysis and of vascular access, and how to manage or refer them.
5. Assess transplant eligibility using risk factors rather than single exclusions, and explain why pre-emptive transplantation is preferred.
6. Outline standard immunosuppressive regimens and how induction differs from maintenance.
7. Classify kidney transplant rejection and describe its mechanisms, presentation, investigation and treatment.
8. Adapt the pathway when resources are limited.

Kidney failure is common and increasing. When chronic kidney disease (CKD) progresses to stage 5, the native kidneys cannot keep the body in biochemical and fluid balance. Renal replacement therapy (RRT) then means dialysis or transplantation. Dialysis is not a cure: it is a chronic, usually lifelong, support that removes solutes and water and corrects acid-base and electrolyte abnormalities. Transplantation is the better option when it is possible, because survival and quality of life are better and overall cost is lower than long-term dialysis. ^{[7] [4]}

This procedure page therefore covers both modalities of dialysis and kidney transplantation together, as they form one pathway: preparation and choice of modality, access creation, conduct of treatment, aftercare and complications. The newest guidelines used here are the Kidney Disease: Improving Global Outcomes (KDIGO) 2024 Clinical Practice Guideline for the Evaluation and Management of CKD; the KDIGO 2020 Clinical Practice Guideline on the Evaluation and Management of Candidates for Kidney Transplantation; the KDIGO 2009 Clinical Practice Guideline for the Care of Kidney Transplant Recipients; the National Institute for Health and Care Excellence (NICE) NG107 Renal replacement therapy and conservative management (published 2018, last reviewed 2023); and the Kidney Disease Outcomes Quality Initiative (KDOQI) Clinical Practice Guideline for Vascular Access, 2019 update. ^{[1][2][3][4][5]} Peritoneal dialysis outcome definitions are taken from the International Society for Peritoneal Dialysis (ISPD) standardised peritonitis definition, quoted in the 2022 review of global peritoneal dialysis outcomes. ^[8]

A practical principle runs through every section: decisions should be made with the patient, around predicted quality of life, prognosis and preference, rather than around a single laboratory result. ^[1]

Dialysis is indicated by danger, not by a number alone. NICE NG107 and the KDIGO 2024 CKD guideline agree on a composite assessment. ^[1][2]

• Impact of uraemic symptoms on daily living, such as anorexia, nausea, lethargy, pruritus, sleep disturbance or cognitive change that are attributable to kidney failure and not to other conditions.
• Biochemical indications, for example severe electrolyte disturbance, acidosis or hyperkalaemia that is not controlled medically.
• Uncontrolled fluid overload, pulmonary oedema or hypertension that does not respond to treatment.
• In the absence of symptoms, an eGFR around 5 to 7 ml/min per 1.73 m2. ^[1] This often but not invariably happens in the GFR range between 5 and 10 ml/min per 1.73 m2. ^[2]
• In children, poor growth that persists despite optimised nutrition, growth hormone and medical management. ^[2]

Some patients should also be considered for conservative management without dialysis. NICE NG107 covers renal replacement therapy (dialysis and transplantation) and conservative management for people with chronic kidney disease stages 4 and 5. ^[1] A KDIGO controversies conference quoted in the "Ten tips for the first haemodialysis sessions" review suggested delaying dialysis until eGFR is under 6 ml/min per 1.73 m2 in older patients without other indications, with careful advance care planning. ^[7]

Planning is as important as starting. ^[1][2]

• Start formal assessment for RRT or conservative management at least one year before it is likely to be needed, including in patients with a failing transplant. ^[1]
• Consider planning for pre-emptive kidney transplantation or dialysis access in adults when eGFR is under 15 to 20 ml/min per 1.73 m2 or the two-year risk of kidney replacement therapy is above 40 percent. ^[2]
• A two-year kidney failure risk above 40 percent also triggers modality education, vascular access planning and referral for transplantation in addition to eGFR-based criteria. ^[2]
• In children, pre-emptive living or deceased donor kidney transplantation is the treatment of choice when progressive irreversible CKD is present; it is often undertaken at eGFR 5 to 15 ml/min per 1.73 m2 depending on age, size and progression. ^[2]

Kidney transplantation is the treatment of choice for suitable patients with kidney failure, with better survival, quality of life and lower cost than dialysis. ^[4][7] NICE NG107 asks that individual risks and benefits be discussed, that living donor transplantation be included in the discussion, and that pre-emptive transplantation (living donor, or deceased donor listing) be offered to eligible patients. ^[1] It also says patients should not be excluded from transplantation on body mass index alone. ^[1]

There is no absolute list that applies to every patient. Suitability is decided by the total risk of transplantation set against the risk of staying on dialysis. ^[4]

• Absolute contraindications (unresectable malignancy, active uncontrolled infection, severe uncorrectable cardiac disease and similar) are present in only about 10 to 15 percent of incident patients in one cohort. ^[7]
• Longer dialysis vintage before transplantation is associated with higher post-transplant mortality, so early identification of potential candidates matters. ^[7]
• Only about one in five dialysis patients in a 2019 Canadian cohort was referred for transplantation within the first dialysis year, so late or inconsistent referral is a bigger barrier than medical unsuitability. ^[7]
• For very frail or multimorbid patients, conservative management without dialysis may be the better option, and its availability should always be discussed alongside dialysis modalities. ^[1]

Haemodialysis needs reliable blood flow. Peritoneal dialysis needs an indwelling catheter in the peritoneal cavity. Transplantation needs multiple anastomoses. The relevant anatomy is:

• Upper limb veins for an arteriovenous fistula (AVF): the cephalic and basilic veins of the forearm and upper arm, the median cubital perforator in the antecubital fossa, and the radial and brachial arteries. Subclavian and brachiocephalic veins are avoided for peripheral access because central stenosis limits future options.
• Central veins for a catheter: the right internal jugular vein, whose straight course leads to the upper right atrium and gives the highest blood flows and the least stenosis. ^[6]
• Peritoneal cavity: the dialysate must contact a large surface area of peritoneum; leaks occur at fascial defects or postoperative wounds.
• Transplant graft: the donor renal artery and vein are joined to the recipient external iliac artery and vein, and the ureter is implanted into the bladder. The patient's own kidneys are usually left in place.
• Heart and vessels for haemodialysis complications: the fistula arm must be spared from blood pressure cuffs, phlebotomy, injections, watches and contact sport. ^[6]

• For haemodialysis: a machine with a dialyser, blood pump, dialysate delivery system, water treatment plant, and vascular access (needles for fistula/graft or a central catheter). Electronic bed scales, blood pressure monitoring and a heparin syringe driver are part of the set-up. High-convection haemodiafiltration needs ultrafiltration-rate control that can reach high volumes.
• For peritoneal dialysis: a soft double-cuffed silicone catheter, sterile dialysate bags, CAPD tubing or an overnight cycler, and a trained patient or assistant. In low-resource settings the same catheter and locally prepared sterile solution can be used for acute kidney injury. ^[8]
• For transplantation: tissue typing laboratory (HLA and ABO), crossmatch facility, immunosuppression supply and biopsy capability.

Preparation takes months and should begin at least one year before RRT is likely to be needed. ^[1] Shared decision-making is the standard of care.

• Take a medical history including diabetes, vascular disease, previous central lines, pacemakers, anticoagulant or antiplatelet use and oncological history, because each changes access strategy and listing. ^[6]
• Offer a full dietary assessment by a renal dietitian and psychological or psychiatric review for adults at risk and for all children being considered for transplantation. ^[1]
• Discuss how each modality affects life: time, travel, home modification, body image, work, fertility and social activity, in line with NICE's recommended list of topics. ^[1]
• Refer for vascular ultrasound. For an arteriovenous fistula, aim for arterial diameter about 2 mm, venous diameter about 2 to 2.5 mm, and for a graft at least 4 mm; the right internal jugular vein is used for catheters. ^[6]
• Consent includes the benefit of extending life alongside infection, malignancy, drug toxicity, and the possibility that the first access fails.
• Identify candidates for transplantation early: in one cohort only 10 to 15 percent of incident patients had an absolute contraindication. ^[7]

The aim is repeated removal of solutes and controlled ultrafiltration. Standard care is three sessions a week, but incremental (once or twice weekly) regimens can be used while residual kidney function is present. ^[7]

• Vascular access is cannulated; a standard session lasts several hours and is tailored to the patient's size and tolerance.
• Solute clearance is monitored by Kt/V or urea reduction ratio, with a minimum goal rather than a fixed number.
• Ultrafiltration is set against an estimated dry weight; volume control is the harder of the two goals. ^[7]
• First sessions should be shortened and dialyser flow down-scaled to avoid dialysis disequilibrium syndrome. A default dialysate sodium of 140 mmol/L is reasonable when it is not individualised. ^[7]
• Anticoagulation: unfractionated heparin is used worldwide to prevent circuit clotting; many patients do not need it in short first sessions, and patients already anticoagulated for another indication may need little or none. ^[7]
• Haemodiafiltration (HDF) added to high-flux dialysis can give a survival benefit when a convection volume above 23 litres per session is reliably achieved, usually through a well-functioning fistula rather than a catheter. ^[7] NICE NG107 prefers HDF to HD in centre-based programmes and allows HDF or HD at home. ^[1]
• NICE NG107 also suggests HDF over HD in centre even though the statistics are fragile and the benefit depends on patient health. ^[1][7]

The peritoneum is the membrane. Hypertonic (or icodextrin) dialysate drawn into the peritoneal cavity draws water and solutes down osmotic and concentration gradients.

• Continuous ambulatory peritoneal dialysis (CAPD) uses several manual exchanges each day with at least one overnight dwell; automated peritoneal dialysis (APD) uses a cycler at night. NICE NG107 offers both to anyone choosing PD, if medically appropriate. ^[1]
• PD is the first choice for children under two years, preserves residual kidney function, and has lower rates of blood-borne virus infection than haemodialysis. ^[1][8]
• A pre-emptive or early peritoneal catheter should be inserted by an open technique about two weeks before dialysis starts. ^[1]
• Dose is described as small-solute clearance and ultrafiltration rather than a single numeric target; volume and residual function often matter more to the patient.
• NICE NG107 recommends not switching a patient off PD in anticipation of future complications such as encapsulating peritoneal sclerosis, but monitoring risk factors such as loss of ultrafiltration. ^[1]

Access is the critical pathway. Three types exist, used in a patient-specific plan. ^[5][6]

• Ultrasound scanning is offered to determine arteriovenous fistula sites. ^[1]
• Save the veins: in CKD avoid cannulation above the wrist and avoid PICC lines; avoid subclavian vein catheters to protect central veins. ^[6]
• Maturation checks: the rule of 6s (about 6 weeks, 6 mm diameter, under 6 mm deep, 600 ml/min flow) or the more lenient UAB criteria (down to 4 mm, at least 500 ml/min), together with the pragmatic test that two needles can be inserted reliably. ^[6]
• Cannulation uses rope-ladder rotation for fistulae; buttonhole is reserved; area cannulation is avoided. ^[6]
• Patient education on thrill monitoring and warning signs (infection, aneurysmal thinning, absent thrill, altered sensation) is the first layer of surveillance. ^[6]

The operation itself is not done by most trainees, but the pathway must be understood.

1. Donor identification and matching: living (related, unrelated, paired exchange) or deceased (donation after brain death, or after circulatory death). ABO compatibility and HLA type are checked; crossmatch detects donor-specific antibodies. The degree of HLA mismatch is the strongest predictor of long-term graft survival. ^[10]
2. Donor evaluation: in living donation, the donor's kidney function, anatomy and long-term risk are assessed; KDIGO's living donor guideline is usually applied alongside the candidate guideline. ^[4]
3. Surgical anastomoses: renal artery to external iliac artery, renal vein to external iliac vein, ureter to bladder; the native kidneys stay in place.
4. Induction immunosuppression: a biologic agent is given before, at, or immediately after transplantation, most commonly an interleukin-2 receptor antagonist or, for high immunological risk, a lymphocyte-depleting agent. ^[3]
5. Initial care: a double-J ureteric stent is often used, with surveillance (ultrasound, creatinine, urine output) and prophylaxis against infection.
6. Long-term regimen: triple therapy is tapered to the lowest effective dose, with regular review.

Aftercare is where outcomes are won or lost. Three parallel streams run.

• Haemodialysis care: adjustment of dry weight, potassium, calcium, phosphate, anaemia and bone-mineral management; regular fistula checks; assessment of adequacy. The CONVINCE trial and subsequent meta-analysis showed that HDF can reduce mortality compared with high-flux HD, through convection volumes above 23 litres per session; the effect depends on the patient and on access. ^[7]
• Peritoneal dialysis care: monitor peritonitis, exit-site infection, leaks, ultrafiltration loss and nutrition. The ISPD 2022 definition of PD peritonitis requires two of: abdominal pain or cloudy effluent; dialysate white cell count above 100 per microlitre with over 50 percent neutrophils after a two-hour dwell; positive dialysate culture. ^[8]
• Transplant care: graft function by creatinine trend, drug levels, biopsy when function deteriorates, infection prophylaxis, malignancy screening, cardiovascular risk and vaccination review. The transition from dialysis to transplant improves outcome when the candidate is optimised early. ^[7]

• Intradialytic hypotension is the commonest acute complication: excessive ultrafiltration rate, missed dry weight or cardiac dysfunction. It shortens dialysis and is associated with loss of residual function. ^[7]
• Dialysis disequilibrium syndrome: cerebral oedema from rapid osmolar shifts, presenting with headache, restlessness, seizures; prevented by short first sessions. ^[7]
• Bleeding: from anticoagulation or access puncture sites; in anticoagulated surgery planning, extra care is needed. ^[7]
• Haemolysis, air embolism and dialyser reactions are rare but lethal and need immediate recognition. ^[7]
• In the first year, mortality is high: a German dataset reported 33.8 percent average first-year mortality after haemodialysis initiation, highest early on. ^[7]
• Medication burden is substantial: over two thirds of a 3,094-patient Canadian haemodialysis cohort took nine or more medications. Simplify and reconcile at the first session. ^[7]

• Thrombosis: treat AVF/AVG thrombosis within 24 to 48 hours with mechanical thrombectomy plus correction of downstream stenosis; CVC dysfunction is managed by flushing, repositioning, line reversal and, if needed, thrombolytics. ^[6]
• Stenosis: non-urgent stenoses are corrected surgically or by angioplasty; pre-emptive angioplasty of asymptomatic stenosis without clinical indicators is not recommended. ^[11]
• Steal (haemodialysis access-induced distal ischaemia) and high-flow access: managed with ligation, distal revascularisation or revision, depending on severity. ^[6]
• Aneurysm and infection: overlying skin infection or necrosis needs excision; prosthetic graft infection needs removal; AVF infection is usually lower risk but must be taken seriously. ^[6]
• Central vein stenosis: follows subclavian or left jugular catheters; leads to arm swelling and threatens all future access on that side. ^[6]
• Primary failure occurs in about 24.7 percent of fistulae in a recent meta-analysis; hence plan A and plan B at the time of surgery. ^[6]

• Peritonitis: global mean rates fell from 0.6 to 0.3 episodes per patient-year between 1992 and 2019, but rates are higher in some regions (for example, parts of Asia and Africa). Gram-positive organisms predominate in many countries; culture-negative rates often exceed the ISPD target of under 15 percent. Peritonitis led 60 percent of transfers from PD to HD in one systematic review. Medical cure occurs in 69 to 80.7 percent of episodes, catheter removal in 10.8 to 20.4 percent, and mortality in 1.8 to 6.0 percent. ^[8]
• Exit-site and tunnel infection: important causes of peritonitis and technique failure; 8.5 to 20.8 percent of peritonitis episodes had concomitant exit-site or tunnel infection in one multicountry study. ^[8]
• Encapsulating peritoneal sclerosis (EPS): rare but lethal; incidence 0.7 to 13.6 per 1,000 patient-years; risk is low in the first 3 to 5 years; risk factors include PD vintage, recurrent peritonitis, high-glucose or acetate-buffered solutions, and anti-rejection drugs after transplantation. ^[8]
• Mechanical complications (leaks, catheter malfunction, pleuroperitoneal leaks at 1.6 to 10 percent) affect about 40 percent of PD patients overall. ^[8]
• Technique survival: three-year PD technique survival ranges from 29 to 91 percent worldwide, driven by centre experience, case mix and definition; larger centres do better. ^[8]
• Cognitive function is better preserved in PD than in haemodialysis in the first few years, with dialysis-dependent uraemia and inflammation impairing cognition three- to five-fold more than in the general population. ^[8]

• Hyperacute rejection: antibody-mediated, within minutes to hours, now rare because of ABO/HLA compatibility testing; catastrophic when it occurs. ^[10]
• Acute rejection: mostly within the first year; occurs in about 10 to 20 percent of recipients despite immunosuppression; driven by T-cell-mediated or antibody-mediated mechanisms, detected by rising creatinine and confirmed by biopsy. ^[10] Prompt treatment usually restores function.
• Chronic rejection: months to years later; presents as progressive fibrosis and vasculopathy. In the kidney this is interstitial fibrosis and tubular atrophy (IFTA); graft survival is about 95 percent at one year, 90 percent at three years and 80 percent at five years in the review cited. ^[10]
• Immunosuppression toxicity: nephrotoxicity, neurotoxicity, diabetes, hypertension, osteoporosis, cytopenias and gastrointestinal disturbance; increased infection (from common pathogens to opportunistic organisms and viruses) and malignancy (lymphoma, skin cancer). ^[10]
• Adherence is a safety issue: non-adherence is reported in 20 to 70 percent of transplant recipients, and it is a major cause of acute and antibody-mediated rejection and graft loss. ^[10]
• Recurrent disease, delayed graft function, surgical complications and drug interactions all contribute to graft loss and must be considered in aftercare.

Transplant eligibility is not a single yes-or-no rule; it is the synthesis of a risk profile. ^[4]

• Medical evaluation covers cardiovascular risk (which is the leading cause of early death after transplantation), diabetes status, obesity (but BMI alone is not an exclusion), infection history, malignancy and its remission, substance use, immunological sensitisation and adherence capacity. ^[1][4][10]
• Pre-existing donor-specific antibodies from transfusion, pregnancy or a previous transplant raise cPRA and rejection risk; advanced matching (eplet or PIRCHE-based) improves prediction. ^[10]
• Living donor transplantation should be included in every discussion, and every eligible candidate should be offered pre-emptive transplantation. ^[1]
• Older age and multimorbidity are not automatic exclusions; with good selection the benefit persists. ^[7]
• KDIGO 2009 deliberately excludes pre-transplant care; it covers post-transplant management. For candidate evaluation the KDIGO 2020 guideline is the relevant edition. ^[3][4]
• Psychological assessment and support improve selection and outcome; children always, adults where risk of poor outcomes is identified. ^[1]

The goals are to prevent rejection with the least possible toxicity. ^[3][10]

• Induction: KDIGO 2009 recommends starting a combination of immunosuppressive drugs before or at transplantation and including a biologic induction agent. ^[3]
  • Interleukin-2 receptor antagonist (basiliximab) is the first-line induction agent. ^[3]
  • A lymphocyte-depleting agent (anti-thymocyte globulin) is preferred for immunologically high-risk recipients. ^[3]
• Maintenance ("triple therapy"): a calcineurin inhibitor (tacrolimus usually preferred over ciclosporin for potency and nephrotoxicity profile), an antimetabolite (mycophenolate mofetil preferred over azathioprine), plus corticosteroids, tapered to the lowest effective exposure. ^[10]
• Other agents: mTOR inhibitors (such as sirolimus), belatacept as a costimulation blocker with less nephrotoxicity but higher Epstein-Barr virus-associated post-transplant lymphoproliferative risk and no licence for liver transplantation, and rituximab for antibody-mediated rejection with high donor-specific antibodies. ^[10]
• MMF is contraindicated in pregnancy (FDA class D, teratogenic). Drug-specific pregnancy counselling should precede transplantation. ^[10]
• Monitoring: drug levels for calcineurin inhibitors, haematology for antimetabolites, infection and malignancy surveillance, adherence support and therapeutic drug education. Evidence for infection management often rests on clinical judgement rather than trial data. ^[10]
• Kidney transplantation is the treatment of choice for stage 5 CKD. The risk of death for kidney transplant recipients is less than half that for patients remaining on dialysis, so even a marginally inferior immunosuppressive regimen produces a better outcome than not transplanting. ^[3]

Rejection is the recipient immune system recognising the graft as foreign. ^[10]

• Hyperacute: minutes to hours, pre-existing antibodies, complement activation, thrombosis; prevented by modern crossmatching. ^[10]
• Acute T-cell-mediated (TCMR): recipient T cells recognise donor HLA directly or indirectly, releasing IL-2, interferon-gamma, TNF-alpha and IL-17; histology shows interstitial inflammation and tubulitis, and the clinical marker is rising creatinine. Banff 2019 reinstated borderline classification only when interstitial inflammation involves at least 10 percent of non-sclerotic cortex (i1) with at least mild tubulitis. ^[9][10]
• Acute antibody-mediated (AMR): donor-specific antibodies activate complement, causing microvascular inflammation and C4d deposition in peritubular capillaries; managed with plasma exchange, intravenous immunoglobulin, rituximab and, for refractory cases, proteasome inhibitors. ^[9][10]
• Chronic rejection: develops over months to years, driven by chronic low-grade immune injury plus ischaemia-reperfusion, drug toxicity and infection, producing interstitial fibrosis and tubular atrophy in the kidney and graft vasculopathy. Non-adherence is a common precipitant of the acute component. ^[10]
• Diagnosis in practice: any deterioration in graft function needs donor-specific antibody testing, ultrasound, and usually an allograft biopsy, read with the Banff classification (categories: normal, borderline TCMR, acute TCMR, AMR, chronic changes and other). ^[9][10]
• Treatment of acute rejection usually responds to high-dose corticosteroids; steroid-resistant rejection requires anti-thymocyte globulin or plasma exchange depending on type. Dose-based regimens beyond the class descriptions above should follow local transplant unit protocols and the clinical pharmacology lab. ^[10]

• Blood group and HLA laboratory access, biopsy processing and drug-level monitoring limit care in many settings. The guideline texts used here were developed with implementation in varied settings in mind, so the pathway (choice, access, immunosuppression, monitoring) still applies even when the tools do not. ^[2][4]
• Ultrasound skills and access-care education can be taught; they reduce primary fistula failure and infection more consistently than expensive hardware. ^[6]

Chronic kidney disease; acute kidney injury; glomerular diseases; hypertension and vascular disease; anaemia in CKD; CKD mineral and bone disorder; organ transplantation principles and complications; transplant rejection and graft-versus-host disease; urology and peritoneal access; vascular surgery.