Renal replacement therapy
Renal replacement therapy (RRT), intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), prolonged intermittent renal replacement therapy (PIRRT), or peritoneal dialysis (PD), substitutes for lost kidney function when acute kidney injury or end-stage kidney disease causes refractory acidosis, hyperkalemia, volume overload, or uremia. Modality is chosen mainly by hemodynamic stability: CRRT or PIRRT for the unstable patient, IHD for rapid clearance of severe hyperkalemia or a dialyzable toxin.
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What this article covers
- Overview
Definition: renal replacement therapy (RRT), intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), prolonged intermittent renal replacement therapy (PIRRT), peritoneal…
- Epidemiology
AKI population: severe acute kidney injury from sepsis, acute tubular necrosis, nephrotoxin exposure, or obstruction accounts for most in-hospital RRT starts, usually in the intensive care unit.
- Risk factors
CKD progression: hypertension, diabetes, cardiovascular disease, tobacco use, obesity, and family history raise the likelihood of reaching the RRT threshold.
- Pathophysiology
Diffusive clearance (IHD): blood and dialysate flow countercurrent across a dialyzer membrane; potassium, urea, and creatinine move down their gradient into dialysate, and ultrafiltration removes plasma water.
- Clinical features
Acidosis: tachypnea compensates for severe metabolic acidosis; if respiratory drive fatigues, confusion worsens and respiratory failure threatens, most often in sepsis, diabetic ketoacidosis, or a toxic ingestion.
- Differential diagnosis
CRRT versus IHD: CRRT avoids IHD's rapid shifts and suits the unstable patient, but trials show no survival difference, and IHD is favored instead for rapid clearance, as in severe hyperkalemia or a toxin.
- Diagnosis
The decision to start RRT is established by: an Acidosis, Electrolyte imbalance, Intoxication, Overload, or Uremia (AEIOU) indication refractory to medical management, or a persistently low…
- Management
First, choose the modality by hemodynamic status: CRRT or PIRRT for the unstable patient or cerebral edema; IHD for the stable patient needing rapid clearance, as for severe hyperkalemia or a toxin.
- Complications
Intradialytic hypotension: rapid removal on IHD causes hypotension and, with repeated episodes, organ hypoperfusion injury; less frequent with slower CRRT or PIRRT clearance.
- Prognosis
No survival benefit between modalities: trials show no mortality difference between CRRT and IHD or PIRRT in critically ill AKI; choice affects tolerance, not survival.
- Prevention
Preserve vascular access: avoid PICC lines and subclavian catheters once eGFR is below 60 mL/min/1.73m2, and refer for AVF evaluation months ahead.
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Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Chronic kidney disease
Chronic kidney disease is abnormal kidney structure or function present for more than 3 months, staged by the Kidney Disease: Improving Global Outcomes (KDIGO) system using estimated glomerular filtration rate and albuminuria, and managed with blood pressure control, renin-angiotensin blockade, an SGLT2 inhibitor, and correction of its metabolic complications.
- Hyperkalemia
Hyperkalemia is a serum potassium level above 5.0 mEq/L, most often from decreased kidney excretion, transcellular shifts, or excess intake, with levels above 6.0-6.5 mEq/L or any ECG change constituting a medical emergency from the risk of fatal arrhythmia. Treatment sequences cardiac membrane stabilization with calcium, transcellular potassium shifting with insulin/dextrose and albuterol, then definitive potassium removal with binders, diuretics, or dialysis.
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- Metabolic acidosis
Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.
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Chronic kidney disease-mineral and bone disorder (CKD-MBD) is the syndrome of disturbed calcium, phosphorus, PTH, vitamin D, and FGF-23 homeostasis, abnormal bone mineralization (renal osteodystrophy), and vascular calcification that develops as kidney function declines. Management centers on serial phosphorus/calcium/PTH monitoring, dietary phosphorus restriction plus phosphate binders (noncalcium-based preferred) to normalize phosphorus, avoiding hypercalcemia and unnecessary calcitriol before dialysis, and calcimimetics or activated vitamin D for uncontrolled secondary hyperparathyroidism on dialysis, reserving parathyroidectomy for tertiary disease.