13.4 Chronic Kidney Disease and Haemodialysis
Key Takeaways
- Chronic kidney disease is staged by eGFR, with stage 5 or end-stage renal disease below 15 mL/min/1.73 m2.
- Loss of renal 1-alpha-hydroxylase and phosphate retention cause hypocalcaemia, secondary hyperparathyroidism and renal osteodystrophy.
- Radiographic features of renal osteodystrophy include loss of lamina dura, a ground-glass trabecular pattern and brown tumours.
- Haemodialysis patients are best treated the day after dialysis, once heparin with a half-life of one to two hours has cleared and fluid balance is stable.
- Nephrotoxic drugs, particularly NSAIDs, should be avoided and doses of renally excreted drugs reduced.
4. Chronic Kidney Disease: Staging, Renal Osteodystrophy, and Dialysis Protocol
Chronic Kidney Disease (CKD) is characterized by gradual, progressive loss of renal excretory, endocrine, and metabolic function.
Staging of Chronic Kidney Disease
Staging is categorized according to estimated Glomerular Filtration Rate (eGFR, in $\text{mL/min/1.73 m}^2$):
- Stage 1: $\text{eGFR} \ge 90$ (normal or increased eGFR, with proven structural kidney damage).
- Stage 2: $\text{eGFR } 60-89$ (mild reduction in GFR).
- Stage 3a: $\text{eGFR } 45-59$ and Stage 3b: $\text{eGFR } 30-44$ (moderate reduction).
- Stage 4: $\text{eGFR } 15-29$ (severe reduction; pre-dialysis stage).
- Stage 5: $\text{eGFR } < 15$ (End-Stage Renal Disease [ESRD]; requires chronic renal replacement therapy via haemodialysis, peritoneal dialysis, or renal transplantation).
Secondary Hyperparathyroidism and Renal Osteodystrophy
Failing kidneys lose the enzyme 1-alpha-hydroxylase, located in proximal tubular cells, which catalyses the final conversion of 25-hydroxyvitamin D into active 1,25-dihydroxyvitamin D (calcitriol). Concurrently, impaired glomerular filtration causes phosphate retention (hyperphosphataemia):
- Calcitriol deficiency severely reduces intestinal calcium absorption, producing persistent hypocalcaemia.
- Hyperphosphataemia and hypocalcaemia continuously stimulate the four parathyroid glands to hyper-secrete Parathyroid Hormone (PTH), establishing secondary hyperparathyroidism.
- Elevated PTH drives unremitting osteoclastic bone resorption to mobilize calcium into the plasma. This skeletal breakdown is termed renal osteodystrophy.
- Oral and Radiographic Manifestations:
- Loss of the lamina dura surrounding tooth roots.
- Diffuse demineralization of the mandible and maxilla, with a distinctive "ground-glass" trabecular bone pattern resembling fibrous dysplasia.
- Development of Brown Tumours of Hyperparathyroidism (osteoclastomas): destructive intraosseous osteolytic lesions filled with vascular fibrous tissue, osteoclast-like multinucleated giant cells, and extensive haemosiderin pigment deposits (which impart a brownish gross appearance). Brown tumours are histologically indistinguishable from central giant cell granulomas.
Drug Prescribing and Nephrotoxicity
- NSAIDs: Strictly contraindicated in CKD Stages 3, 4, and 5. Renal perfusion in compromised kidneys is dependent on vasodilatory prostaglandins ($PGE_2, PGI_2$) maintaining patency of the afferent glomerular arteriole. NSAIDs block cyclooxygenase, abolishing prostaglandins, causing profound afferent arteriolar vasoconstriction, sharp drops in glomerular filtration, fluid retention, and acute-on-chronic renal failure.
- Renally Excreted Antimicrobials: Amoxicillin, ampicillin, cephalosporins, and aciclovir are eliminated unchanged by the kidneys. In CKD Stages 4 and 5, reduce the dosage or extend the inter-dose administration interval to prevent toxic systemic accumulation.
- Analgesic of Choice: Paracetamol is primarily metabolized by hepatic glucuronidation and sulfation and is entirely safe to use at normal adult doses (1 g QDS) without dose adjustment in renal disease.
Dental Management of the Haemodialysis Patient
Patients with end-stage renal disease (Stage 5) undergo haemodialysis 3 times per week (typically Monday-Wednesday-Friday or Tuesday-Thursday-Saturday) for 4 to 5 hours per session. During dialysis, blood is circulated through an external dialyser, requiring systemic anticoagulation with unfractionated heparin or low-molecular-weight heparin (LMWH) to prevent clotting within the extracorporeal circuit.
| Clinical Consideration | Haemodialysis Management Protocol | Rationale |
|---|---|---|
| Appointment Timing | Schedule dental care on the DAY AFTER dialysis (non-dialysis day) | Allows systemic heparin to be completely cleared (half-life ~1–2 hours); patient is metabolically optimal, with normalized fluid and electrolyte balance. |
| Day of Dialysis | AVOID invasive dental surgery | High risk of uncontrolled haemorrhage due to active systemic heparinisation. |
| Arteriovenous (AV) Fistula | NEVER place a blood pressure cuff, tourniquet, or IV line on the fistula arm | External compression causes intraluminal turbulence, endothelial damage, and acute thrombosis, destroying life-sustaining vascular access. |
| Infection Risk | Universal aseptic precautions; screen for blood-borne viruses (HBV, HCV) | Chronic immunosuppression; frequent vascular access increases blood-borne viral transmission risk. |
Bleeding, Anaemia and Infection Risk
Chronic kidney disease affects dental care through four linked mechanisms. Uraemic platelet dysfunction causes a bleeding tendency despite a normal platelet count and normal clotting screen, so local haemostatic measures should be planned even when laboratory tests look reassuring. Anaemia is common because of reduced erythropoietin production and contributes to mucosal pallor and fatigue. Immunosuppression, whether from uraemia itself or from transplant medication, increases infection risk and alters healing. Renal osteodystrophy produces the radiographic changes of secondary hyperparathyroidism in the jaws, including loss of lamina dura and a ground-glass pattern.
Oral Findings and Transplant Patients
Oral signs are directly examinable: uraemic fetor with an ammoniacal odour, xerostomia, a metallic taste, mucosal pallor, uraemic stomatitis with grey pseudomembranes in advanced disease, and enamel hypoplasia when renal failure occurred during tooth development. Renal transplant recipients on ciclosporin and calcium channel blockers commonly develop drug-influenced gingival enlargement, managed first by meticulous plaque control and liaison with the physician about an alternative immunosuppressant, with surgical reduction reserved for persistent cases.
Before transplantation, patients undergo a dental clearance to eliminate potential sources of infection, because immunosuppression after transplantation makes odontogenic sepsis dangerous. After transplantation, elective dental care is deferred for the first few months while immunosuppression is heaviest, and lifelong mucosal surveillance is required because these patients have a markedly increased risk of lip and skin malignancy.
Timing Treatment Around Dialysis
Haemodialysis patients are usually dialysed three times a week and are systemically heparinised during each session. Elective dental treatment is therefore best provided on the day after dialysis, when the heparin effect has dissipated and uraemic toxins are at their lowest, rather than on a dialysis day. Blood pressure is measured and venous access is protected: never use the arm containing an arteriovenous fistula for a blood pressure cuff or venepuncture.