Indications for dialysis

After reading this note you will be able to list the clinical situations that mandate initiation of renal replacement therapy, explain why each arises, and outline the immediate steps required while recognising that exact drug choices and local protocols must be verified against the Kenya Ministry of Health guidelines and your hospital formulary.

Definition

Dialysis is the extracorporeal or peritoneal removal of excess fluid, electrolytes, and metabolic waste when the kidneys can no longer perform these functions adequately. In the acute setting it is termed renal replacement therapy (RRT); in chronic disease it is called maintenance dialysis.

Anatomy and physiology you need

Understanding that the kidney normally balances fluid, electrolytes, acid‑base and clears nitrogenous waste underpins why dialysis is required when these processes fail.

Causes and risk factors

In Kenya the spectrum of renal injury reflects infectious, haemolytic, and chronic non‑communicable disease burdens.

Risk factors include late presentation to health facilities, limited access to early laboratory monitoring, and co‑existing malnutrition which can worsen renal reserve.

Pathophysiology

1. Initial renal insult → ↓ glomerular filtration rate (GFR)
2. Accumulation of nitrogenous waste (urea, creatinine) → uremic toxins → neuro‑cognitive changes, pericarditis
3. Impaired tubular secretion → hyperkalaemia, metabolic acidosis
4. Loss of tubular reabsorption → fluid overload, pulmonary oedema, hypertension
5. Endothelial dysfunction & inflammation → further nephron loss (vicious cycle)

When the combined effect of steps 2‑4 reaches thresholds that threaten life (e.g., refractory hyperkalaemia, severe acidosis, fluid overload unresponsive to diuretics, uremic encephalopathy), dialysis is indicated.

End of Part 1.

Clinical features

Examination findings

• Blood pressure – Hypertension suggests fluid overload; hypotension may indicate sepsis or adrenal insufficiency.
• Peripheral oedema – Pitting oedema of lower limbs, sacral area indicates volume excess.
• Jugular venous distension – Reflects raised central venous pressure from fluid overload.
• Lung auscultation – Bibasal crackles = pulmonary oedema, a dialysis indication when refractory.
• Heart – Tachycardia, muffled heart sounds, pericardial rub = uremic pericarditis.
• Neurological – Disorientation, asterixis, seizures = uremic encephalopathy.
• Skin – Pruritus, pallor, petechiae = uremic platelet dysfunction.
• Abdomen – Ascites may accompany severe hypo‑albuminaemia from nephrotic syndrome.

Each sign reflects the underlying accumulation of fluid, electrolytes, acid, or toxins that dialysis is designed to remove.

Differential diagnosis

Investigations

Diagnosis and severity

1. Confirm renal dysfunction – eGFR < 15 ml/min/1.73 m² (CKD‑5) or acute rise in serum creatinine ≥ 0.3 mg/dl within 48 h (AKI).

1. Identify life‑threatening complications that constitute absolute indications for dialysis:
   • Refractory hyperkalaemia (K⁺ > 6 mmol/L despite medical therapy)
   • Severe metabolic acidosis (pH < 7.1, HCO₃⁻ < 15 mmol/L)
   • Fluid overload unresponsive to diuretics, causing pulmonary oedema or refractory hypertension
   • Uremic syndrome (pericarditis, encephalopathy, severe pruritus, bleeding diathesis)

1. Relative indications – consider when any of the following are present and the patient is otherwise stable:
   • Persistent BUN > 100 mg/dl with symptoms
   • Progressive CKD with declining eGFR and worsening quality of life
   • Anticipated need for rapid clearance of toxins (e.g., severe malaria, drug overdose)

1. Severity grading (adapted from KDIGO):
   • Stage 1 – eGFR 15‑29 ml/min/1.73 m², no absolute indications, monitor closely.
   • Stage 2 – eGFR < 15 ml/min/1.73 m², one or more relative indications, plan for early dialysis access.
   • Stage 3 – Any absolute indication present; dialysis should be initiated promptly (emergent or urgent).

1. Decision pathway – If an absolute indication is present, arrange emergent haemodialysis (or peritoneal dialysis where haemodialysis unavailable). If only relative indications, discuss with patient, consider comorbidities, and schedule dialysis within days to weeks, while optimizing medical management (diuretics, potassium binders, bicarbonate, antihypertensives).

Key points for the Kenyan clinical setting

• High prevalence of infectious triggers (malaria, TB, HIV) means a low threshold for checking electrolytes and acid‑base status.
• Limited haemodialysis slots favour early identification of patients who can be managed with acute peritoneal dialysis, especially in rural hospitals.
• Socio‑economic constraints require clear documentation of absolute indications to justify resource allocation.

End of Part 2.

Management

Immediate Stabilisation

• Airway and Breathing: Position sitting upright if pulmonary oedema is present. Administer high-flow oxygen via a non-rebreather mask. Provide non-invasive positive pressure ventilation (CPAP/BiPAP) if severe respiratory distress or flash pulmonary oedema persists.
• Circulation (Temporising Measures while preparing Dialysis):
  • Hyperkalaemia: Intravenous calcium gluconate to stabilise the cardiac membrane (does not lower potassium). Intravenous soluble insulin combined with dextrose to drive potassium intracellularly. Nebulised salbutamol provides an additive intracellular shift. Intravenous sodium bicarbonate is indicated if severe metabolic acidosis co-exists. Oral or rectal potassium binders (e.g., calcium polystyrene sulfonate) facilitate gastrointestinal elimination but act too slowly for emergency stabilisation.
  • Fluid Overload: Intravenous loop diuretics (e.g., furosemide) at high doses if the patient has residual urine output; discontinue immediately if the patient is anuric. Intravenous nitrates (e.g., glyceryl trinitrate infusion) reduce preload and afterload in pulmonary oedema if systolic blood pressure permits.
  • Severe Metabolic Acidosis: Intravenous sodium bicarbonate infusion can be used cautiously as a temporising bridge to dialysis, monitoring carefully for volume overload and hypocalcaemia.

Definitive Treatment (Renal Replacement Therapy)

• Emergent Indications ("AEIOU"):
  • Acidosis: Refractory metabolic acidosis ($pH < 7.15$ or severe base deficit) unresponsive to medical therapy.
  • Electrolytes: Severe, refractory, or rapidly rising hyperkalaemia (
    gt; 6.5\text{ mmol/L}$) with or without ECG changes.
  • Ingestions: Toxic alcohols (methanol, ethylene glycol), lithium, salicylates, theophylline.
  • Overload: Diuretic-refractory pulmonary oedema.
  • Uraemia: Clinical complications of uraemia—encephalopathy, pericarditis, uraemic pleuritis, or uraemic bleeding/platelet dysfunction.
• Modality Selection:
  • Intermittent Haemodialysis (IHD): First choice for rapid clearance of potassium, small toxins, and fluid in hemodynamically stable patients.
  • Continuous Renal Replacement Therapy (CRRT): Preferred in hemodynamically unstable patients (e.g., septic shock on inotropes) or acute brain injury/cerebral oedema.
  • Peritoneal Dialysis (PD): Used in acute settings when vascular access or haemodialysis machines are unavailable, or for chronic maintenance.
• Vascular Access: Temporary non-tunnelled double-lumen central venous catheter (internal jugular vein preferred; femoral vein acceptable for emergency bed-bound patients; avoid subclavian vein to preserve future arteriovenous fistula sites).

Monitoring and Safety

• Continuous ECG monitoring until hyperkalaemia resolves.
• Strict intake-output charting (fluid balance).
• Serial serum electrolytes, urea, creatinine, and blood gas analysis every 2 to 4 hours during acute stabilisation.
• Monitor blood pressure during dialysis; rapid fluid removal precipitates intradialytic hypotension and further ischaemic renal injury.

Contraindications and Safety Precautions

• Relative contraindications to Haemodialysis: Severe hemodynamic instability (use CRRT instead), lack of vascular access, severe coagulopathy (unless performed without heparin).
• Relative contraindications to Peritoneal Dialysis: Recent abdominal surgery, severe abdominal adhesions, active peritonitis, diaphragmatic defects.

Complications and Prognosis

Prognosis: AKI requiring dialysis carries an in-hospital mortality of 30–50%, rising significantly in multi-organ failure. Surviving patients require close follow-up; up to 20% progress to chronic kidney disease (CKD) within 1 year.

High-Yield Exam Points

• The Absolute Non-Indication: Elevated serum urea or creatinine alone is never an absolute indication for emergency dialysis without a clinical or physiological complication (AEIOU).
• Uraemic Pericarditis is a Dialysis Indication, not Anticoagulation: Pericardial friction rub in renal failure indicates urgent dialysis. Avoid systemic heparinisation during dialysis to prevent converting a serofibrinous effusion into cardiac tamponade.
• Subclavian Access Trap: Examiners will fail students who suggest placing a temporary subclavian catheter in a patient who may later need an AV fistula, due to the high risk of subclavian vein stenosis. The right internal jugular is the correct primary site.
• Calcium Gluconate misconception: Examiners frequently ask: "Does calcium gluconate lower serum potassium?" The answer is strictly no; it only raises the cardiac threshold potential to prevent fatal arrhythmias.
• Look-alike conditions: Severe hyperkalaemia can present as ascending muscle flaccidity mimicking Guillain-Barré syndrome, or heart block mimicking primary conduction disease.

Clinical Case

A 28-year-old male with known HIV infection on tenofovir-based ART presents with 3 days of severe generalized weakness, vomiting, and reduced urine output. Clinical examination reveals tachypnoea (respiratory rate 32/min), blood pressure 150/95 mmHg, elevated jugular venous pressure, bilateral basal lung crackles, and absent deep tendon reflexes.

Bedside point-of-care results:

• Serum Potassium: $7.8\text{ mmol/L}$
• Venous Blood Gas: $pH\ 7.08,\ HCO_3^-\ 8\text{ mmol/L}$
• ECG: Wide QRS complexes blending into tall, tented T waves (sine-wave appearance).

Questions and Model Answers

1. What is the immediate sequence of medical steps while the nephrology team prepares for dialysis? Answer: Immediately administer intravenous calcium gluconate to stabilise the myocardium against fatal arrhythmias. Follow this with rapid-acting intracellular shift agents: intravenous soluble insulin with dextrose, nebulised salbutamol, and cautious intravenous sodium bicarbonate for the severe metabolic acidosis.

2. State the definitive indications for urgent dialysis present in this patient. Answer: (1) Life-threatening hyperkalaemia refractory to immediate medical therapy with ECG sine-wave changes. (2) Severe, refractory metabolic acidosis ($pH < 7.15$). (3) Fluid overload with pulmonary congestion.

3. Which temporary vascular access site should be chosen, and which site must be avoided? Answer: The right internal jugular vein should be chosen because it provides a straight anatomical path to the right atrium and lowest complication rates. The subclavian vein must be avoided to prevent central vein stenosis, which would ruin the ipsilateral limb for future arteriovenous fistula creation.

Practice Questions

Question 1

A 54-year-old female with long-standing poorly controlled diabetes presents with lethargy and nausea. Serum potassium is $6.8\text{ mmol/L}$. Her ECG shows tall peaked T waves. Intravenous calcium gluconate, insulin with dextrose, and nebulised salbutamol are administered. Repeat potassium 2 hours later is $6.6\text{ mmol/L}$, and she develops dyspnoea and bilateral pulmonary crackles. What is the most appropriate next step?

A. Repeat the dose of intravenous calcium gluconate B. Administer oral calcium polystyrene sulfonate C. Place a temporary dialysis catheter and initiate urgent haemodialysis D. Administer high-dose intravenous spironolactone

Answer: C. Place a temporary dialysis catheter and initiate urgent haemodialysis Explanation: The patient has severe hyperkalaemia refractory to medical temporising measures combined with acute pulmonary fluid overload, which constitutes an absolute indication for emergency dialysis. Calcium polystyrene sulfonate has a delayed onset of action and is inappropriate for acute, life-threatening hyperkalaemia.

Question 2

An examiner at the bedside asks you to examine the chest of a 42-year-old man with end-stage kidney disease who missed three dialysis sessions. You detect a rough, scratchy, superficial sound best heard at the left lower sternal border with the patient leaning forward. What is the definitive management for this finding?

A. Immediate pericardiocentesis B. High-dose oral NSAIDs C. Systemic anticoagulation with low-molecular-weight heparin D. Urgent haemodialysis, avoiding systemic heparin

Answer: D. Urgent haemodialysis, avoiding systemic heparin Explanation: The finding is a pericardial friction rub indicating uraemic pericarditis, which is an absolute indication for urgent dialysis. Heparin must be avoided or minimised during dialysis to prevent intrapericardial haemorrhage and cardiac tamponade.

Question 3

A 35-year-old male with severe falciparum malaria develops anuria, jaundice, and a rising serum creatinine. Arterial blood gas shows a pH of 7.10 with standard bicarbonate of $10\text{ mmol/L}$. He is hemodynamically stable. Which vascular access route should be prioritised for emergent intermittent haemodialysis?

A. Left subclavian vein B. Right internal jugular vein C. Right radial arteriovenous graft D. Left femoral artery

Answer: B. Right internal jugular vein Explanation: The right internal jugular vein is the site of choice for temporary non-tunnelled haemodialysis catheters because of its straight anatomical course and lowest risk of venous thrombosis or stenosis. Subclavian access is strictly avoided to preserve upper-extremity veins for permanent access.

Question 4

A 60-year-old male undergoing his first session of acute intermittent haemodialysis for severe uraemia (urea

A. Intracerebral haemorrhage secondary to systemic heparinisation B. Rapid clearance of intravascular urea causing water movement into brain tissue C. Hypocalcaemia induced by rapid correction of metabolic acidosis D. Acute air embolism through the central venous catheter

Answer: B. Rapid clearance of intravascular urea causing water movement into brain tissue Explanation: This presentation is characteristic of Dialysis Disequilibrium Syndrome (DDS). Rapid extracorporeal removal of urea lowers plasma osmolality faster than urea can exit brain cells, creating a transient osmotic gradient that drives water into brain parenchyma, resulting in cerebral oedema.

Question 5

A 68-year-old female with severe septic shock on two vasopressors develops anuric acute kidney injury with refractory metabolic acidosis and volume overload. What is the most appropriate modality of renal replacement therapy?

A. Intermittent haemodialysis with aggressive ultrafiltration B. Continuous renal replacement therapy (CRRT) C. Acute manual peritoneal dialysis D. Conservative medical management until vasopressors are stopped

Answer: B. Continuous renal replacement therapy (CRRT) Explanation: Continuous renal replacement therapy (CRRT) is the treatment of choice in patients with marked hemodynamic instability (e.g., septic shock requiring vasopressors) because slow, continuous fluid and solute removal avoids the rapid hemodynamic shifts and hypotension induced by intermittent haemodialysis. Delaying treatment in refractory acidosis is life-threatening.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.