Lucan · Conditions

Dialysis indications and complications

Australian guidance: CARI Dialysis Guidelines

1. Definition and epidemiology

Dialysis is a renal replacement therapy (RRT) that removes uraemic toxins, excess fluid, and electrolytes when the kidneys can no longer perform these functions adequately. In Australia, more than 31,000 people live with kidney failure requiring dialysis or transplantation, and approximately 2,300 individuals commence RRT annually. The burden of kidney failure is disproportionately high among First Nations Australians, who are also more likely to commence dialysis at a younger age and in remote locations where home dialysis support is limited.

2. Pathophysiology

End-stage kidney disease (ESKD) is the final common pathway of progressive chronic kidney disease (CKD), representing CKD stage 5 with an estimated glomerular filtration rate (eGFR) below 15 mL/min/1.73 m2 or current dialysis dependence. As nephron mass falls, the remaining nephrons undergo compensatory hyperfiltration and hypertrophy; this adaptive response accelerates glomerulosclerosis and tubulointerstitial fibrosis, creating a self-perpetuating cycle of nephron loss (Robbins Ch 20). Retained uraemic solutes include urea, creatinine, middle-molecule toxins such as beta-2-microglobulin, and protein-bound toxins such as indoxyl sulphate. These accumulate across multiple organ systems, causing the uraemic syndrome. Concurrently, loss of renal endocrine function produces erythropoietin deficiency (normochromic normocytic anaemia), impaired 1-alpha-hydroxylation of 25-hydroxyvitamin D (secondary hyperparathyroidism, renal osteodystrophy), and failure of renin-angiotensin regulation. When the residual kidney function can no longer maintain acceptable homeostasis, dialysis removes solutes and water by diffusion across a semipermeable membrane (haemodialysis, HD) or by diffusion and convection across the peritoneal membrane (peritoneal dialysis, PD).

3. Clinical presentation and diagnostic criteria

Uraemia becomes clinically apparent in stage 4 or 5 CKD and produces a syndrome of anorexia, nausea, vomiting, lethargy, pruritus, restless legs, and pericarditis. Advanced encephalopathy presents as confusion, asterixis, muscle twitching, seizures, or coma. Fluid overload causes dyspnoea, peripheral oedema, and hypertension refractory to multiple agents. Examination may reveal a pericardial rub, crackles at the lung bases, and features of the underlying aetiology such as diabetic retinopathy or signs of vasculitis. The standard indication for commencing dialysis is symptomatic uraemia, not a specific eGFR value; the KHA CKD Management in Primary Care Handbook (5th edition) explicitly states that dialysis should be commenced based on assessment of uraemic symptoms rather than eGFR or biochemistry alone. Emergency dialysis indications include hyperkalaemia refractory to medical management, severe metabolic acidosis unresponsive to bicarbonate, and pulmonary oedema unresponsive to diuretics.

4. Investigations and AU-specific cutoffs

Initial workup in the pre-dialysis period should include a full blood count, serum urea, electrolytes, creatinine, and eGFR; urine albumin to creatinine ratio (uACR); calcium, phosphate, parathyroid hormone (PTH), and 25-hydroxyvitamin D; fasting lipids; haemoglobin A1c if diabetes is present; and kidneys, ureters, and bladder (KUB) ultrasound scan. Nephrologist referral is indicated for eGFR below 30 mL/min/1.73 m2, a sustained fall in eGFR of 25% or more within 12 months, a sustained fall exceeding 10 mL/min/1.73 m2 per year, or a persistent uACR at or above 30 mg/mmol. An eGFR that falls more than 15 mL/min/1.73 m2 over three months or signs of acute nephritis (oliguria, haematuria, acute hypertension, oedema) constitute a medical emergency requiring referral without delay. In patients commencing haemodialysis, the CARI guidelines recommend baseline serological screening for hepatitis B (HBsAg, anti-HBc, anti-HBs), hepatitis C (anti-HCV), and HIV status prior to the first dialysis session, with repeat anti-HCV testing every six months in seronegative patients.

5. Management

The three treatment modalities for kidney failure in Australia are dialysis (either HD performed in-centre or at home, or automated or continuous ambulatory PD performed at home), kidney transplantation, and comprehensive conservative care without dialysis. Patients and their families should receive comprehensive education well before dialysis is required so that an informed, shared decision can be reached. Timely nephrology referral improves outcomes by allowing adequate time for vascular access creation, peritoneal catheter insertion, and transplant workup before the need arises. For HD, an arteriovenous (AV) fistula is the preferred access; creation should be planned at least three to six months before anticipated commencement. For PD, a Tenckhoff catheter is placed laparoscopically several weeks in advance. When uraemia becomes symptomatic and conservative measures are insufficient, dialysis is commenced at an individualised rate determined by symptoms, residual kidney function, and patient preference rather than a fixed eGFR threshold. Blood pressure management, dietary protein modification (target 0.8 g/kg/day for non-dialysis CKD), salt restriction to below 5 g/day, and pharmacological CKD progression retardation with renin-angiotensin system blockade, sodium-glucose linked transporter-2 (SGLT-2) inhibitors (where indicated), and non-steroidal mineralocorticoid receptor antagonists should be continued up to and during dialysis where applicable.

6. Pharmacology and AU PBS notes

Erythropoiesis stimulating agents (ESAs) such as darbepoetin alfa and epoetin alfa are used in dialysis-dependent anaemia and are PBS-funded with authority prescription for dialysis patients with haemoglobin below 100 g/L. Iron supplementation (intravenous iron polymaltose or ferric carboxymaltose preferred in HD patients) is required alongside ESAs; transferrin saturation below 20% and serum ferritin below 200 micrograms/L indicate iron deficiency. Phosphate binders are required in most HD patients due to dietary phosphate load; calcium carbonate is the first-line agent (PBS unrestricted) with sevelamer carbonate available for patients with persistent hypercalcaemia or vascular calcification risk (PBS streamlined authority). Cinacalcet is used for secondary hyperparathyroidism refractory to phosphate binders and vitamin D analogues, available on PBS authority (streamlined) when PTH exceeds 32 pmol/L in dialysis patients. Calcitriol (1-alpha-calcidol) or paricalcitol address vitamin D receptor activation and are PBS available for CKD-related mineral bone disorder in dialysis. Antihypertensive regimens continue throughout dialysis, targeting blood pressure below 130/80 mmHg; agents removed by dialysis (e.g. water-soluble beta-blockers such as atenolol) require post-dialysis dosing.

7. Complications and monitoring

Haemodialysis complications include hypotension during dialysis (the most common acute complication), dialysis disequilibrium syndrome (cerebral oedema in rapid urea shifts, typically at first sessions), access-related infections, and air embolism. All HD patients should be monitored with six-monthly anti-HCV serology if seronegative, and HBsAg every six months if anti-HBs titre is below 10 mIU/mL. Hepatitis B non-immune HD patients must receive a full hepatitis B vaccination course per the National Immunisation Program schedule. HBsAg-positive patients should be dialysed in a dedicated machine in a separate area. Screening for methicillin-resistant Staphylococcus aureus (MRSA) is recommended in inpatient HD patients at centres with MRSA-related infections or high colonisation rates; decolonisation should be considered for colonised patients with central venous catheters as dialysis access.

Peritoneal dialysis complications centre on peritonitis, which remains the leading cause of PD technique failure. The diagnosis of PD-associated peritonitis requires at least two of: abdominal pain, cloudy effluent, and peritoneal dialysate white cell count exceeding 100 cells/mm3 with over 50% polymorphonuclear neutrophils (PMN); in automated PD, greater than 50% PMN alone is a strong indicator. Empiric intraperitoneal (IP) antibiotic therapy covering Gram-positive organisms (vancomycin or first-generation cephalosporin) and Gram-negative organisms (third-generation cephalosporin or aminoglycoside) should commence promptly. Catheter removal is indicated for relapsing peritonitis, refractory peritonitis, fungal peritonitis, and refractory exit-site or tunnel infection. The ANZDATA Registry reports an overall Australian peritonitis rate of 0.60 episodes per patient-year, which is higher than rates reported from the USA, Canada, and Shanghai.

Long-term monitoring for all dialysis patients includes monthly pre-dialysis urea, creatinine, electrolytes, and bicarbonate; three-monthly full blood count, PTH, and iron studies; six-monthly lipids, hepatitis serology, and assessment of dialysis adequacy (Kt/V targeting at or above 1.2 per session for HD). Cardiovascular disease remains the leading cause of death in dialysis patients, and ongoing cardiovascular risk factor management is paramount.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.