Dialysis Modalities & Uremic Complications
Uremic emergencies, access, and the complications of each modality
When to dialyze: the uremic syndrome
Indications. Urgent dialysis is needed for problems that medical therapy cannot control (AEIOU):
- Acidosis
- Electrolytes, above all hyperkalemia
- Intoxications with dialyzable agents (methanol, ethylene glycol, lithium, salicylates, metformin), which are small, water-soluble, and poorly protein-bound
- volume Overload
- Uremia: pericarditis, encephalopathy, or bleeding
In progressive CKD, the timing depends on symptoms and complications rather than a GFR threshold. Most patients start around an eGFR of 5–10, when they develop fatigue, anorexia, nausea, weight loss, pruritus, or volume and potassium problems that no longer respond to medication.
Uremic pericarditis. Patients with a very high BUN develop pleuritic chest pain, a friction rub, and often an effusion. Because the inflammation does not extend into the myocardium, the ECG often lacks the diffuse ST elevation and PR depression of viral pericarditis. Dialysis is the treatment, usually daily at first, with little or no heparin to limit bleeding into the pericardium. Pericarditis that develops in a patient already on dialysis calls for more intensive dialysis. Tamponade requires pericardiocentesis.
Uremic encephalopathy and other symptoms. Early features are fatigue, poor concentration, and reversed sleep. These progress to asterixis, myoclonus, seizures, and coma, and dialysis reverses the process. Uremia also causes stocking-glove peripheral neuropathy, restless legs, pruritus, nausea, anorexia, and a metallic taste.
Uremic bleeding. Uremic toxins impair platelet adhesion and aggregation. The platelet count, PT, and PTT are normal, but the bleeding time is prolonged, and anemia worsens the defect by letting platelets drift away from the vessel wall. Treatment for active bleeding or before a procedure:
- Desmopressin releases von Willebrand factor and factor VIII from endothelium. It works within about an hour and lasts hours, but repeated doses lose effect.
- Dialysis removes the toxins responsible.
- Conjugated estrogens act more slowly but last up to about 2 weeks, which suits recurrent bleeding.
- Correcting anemia with ESA and iron, or transfusion, improves platelet contact with the vessel wall.
Choosing a modality
| Feature | Hemodialysis | Peritoneal dialysis | CRRT |
|---|---|---|---|
| Schedule | In-center, 3×/week for 3–4 h | Daily at home (manual exchanges or overnight cycler) | Continuous, in the ICU |
| Access | Fistula, graft, or catheter | Peritoneal catheter | Temporary venous catheter |
| Strengths | Efficient, staff-delivered | Independence; preserves residual kidney function | Gentle fluid removal in unstable patients |
| Typical problems | Hypotension, disequilibrium, access infection and thrombosis | Peritonitis, hyperglycemia, hypokalemia, hernias | Anticoagulation of the circuit, immobility |
| Needs | Vascular access | Intact abdomen, able patient or caregiver | Hemodynamic instability |
Vascular access
Fistula first. A native arteriovenous fistula has the longest patency and the fewest infections and thromboses. It needs 6 weeks to several months to mature, so it must be created well before dialysis is needed. From an eGFR below 30, discuss modalities and protect the veins of the nondominant arm: no venipuncture or IVs there, and no PICCs in either arm, because PICCs cause central vein stenosis and thrombosis that can ruin future access.
| Feature | AV fistula | AV graft | Tunneled catheter |
|---|---|---|---|
| Ready to use | After maturation (weeks to months) | 2–3 weeks | Immediately |
| Patency | Best | Frequent stenosis and thrombosis | Poor; central vein stenosis |
| Infection | Lowest | Intermediate | Highest; S. aureus bacteremia |
| Role | Preferred | When veins are unsuitable | Bridge only; linked to the highest mortality |
Catheter-related bacteremia. Fever or rigors at the start of a session in a patient with a tunneled catheter is catheter infection until proven otherwise. Coagulase-negative staphylococci and S. aureus (including MRSA) predominate. Draw blood cultures and start empiric vancomycin, dosed after dialysis, plus gram-negative coverage. S. aureus bacteremia requires catheter removal, echocardiography to look for endocarditis, and a prolonged course of antibiotics.
Thrombosis and stenosis. A healthy fistula has a continuous thrill and bruit. Loss of both means thrombosis, usually on top of a venous outflow stenosis, and needs urgent thrombectomy with angioplasty (endovascular or surgical) to salvage the access. A temporary catheter is placed only if dialysis cannot wait. Stenosis announces itself earlier with prolonged bleeding after needle removal, arm or facial swelling (central stenosis), falling access flow, and inadequate dialysis.
Steal syndrome. The access diverts arterial flow away from the hand, causing coolness, pallor, pain, numbness, or weakness that worsens during dialysis. Risk is highest with brachial artery–based access, diabetes, and peripheral artery disease. Mild symptoms are observed. Rest pain, motor weakness, or tissue loss needs urgent surgical revision: distal revascularization–interval ligation (DRIL), banding, or ligation.
Ischemic monomelic neuropathy causes acute pain, weakness, and numbness of the hand right after brachial access creation, often with a warm hand and a palpable pulse. It needs immediate access ligation.
Hemodialysis complications
Intradialytic hypotension. This is the most common acute complication. Ultrafiltration removes fluid faster than the plasma refills from the tissues, and antihypertensives taken before the session, autonomic neuropathy, and heart disease make it worse. Cramps often come with it.
- Treat the episodePause or slow ultrafiltration, Trendelenburg position, small saline bolus
- Limit fluid to removeSalt restriction to reduce interdialytic weight gain; reassess dry weight
- Adjust drugs and prescriptionHold antihypertensives before sessions; cooler dialysate; longer or more frequent sessions
- Refractory casesMidodrine before dialysis
Dialysis disequilibrium syndrome. This occurs during or soon after the first sessions in a patient with a very high BUN. Rapid urea removal lowers plasma osmolality faster than brain osmolality, and water moves into brain cells. The result is headache, nausea, restlessness, confusion, seizures, and occasionally coma. Prevent it with short, slow initial treatments (low blood flow, modest urea reduction) repeated on consecutive days.
β2-microglobulin amyloidosis. β2-microglobulin (part of MHC class I) is normally filtered and catabolized by the kidney, and older dialysis membranes clear it poorly. After years on dialysis it deposits as amyloid in synovium, tendons, and bone. The result is bilateral carpal tunnel syndrome, shoulder arthropathy, bone cysts, and destructive spondyloarthropathy. High-flux membranes slow it, and kidney transplant halts it.
Mortality. Cardiovascular disease is the leading cause of death on dialysis, with sudden cardiac death or arrhythmia the largest category and infection second. Hyperkalemia, volume overload, and cardiac deaths cluster after the long 2-day weekend interval, so attendance at every session and dietary potassium and salt limits matter.
Peritoneal dialysis complications
Metabolic. PD solutions use dextrose to pull water across the peritoneum. The absorbed glucose causes hyperglycemia, weight gain, and hypertriglyceridemia. Potassium-free dialysate, continuous removal, and insulin-driven shift of potassium into cells cause hypokalemia, unlike hemodialysis patients, who trend toward hyperkalemia. Protein lost into the effluent lowers albumin.
Mechanical. Fluid in the abdomen raises intra-abdominal pressure. The consequences are hernias (umbilical, inguinal, incisional), dialysate leaks, and hydrothorax when fluid crosses a diaphragmatic defect.
Peritonitis. PD peritonitis presents with cloudy effluent, abdominal pain, and fever. The diagnosis is an effluent WBC >100/μL with >50% neutrophils after a dwell of at least 2 hours, supported by Gram stain and culture. Most cases come from touch contamination with skin flora (coagulase-negative staphylococci, S. aureus), followed by gram-negative rods.
- Culture the effluentCell count, Gram stain, culture in blood-culture bottles
- Empiric intraperitoneal antibioticsVancomycin or a first-generation cephalosporin plus ceftazidime or an aminoglycoside; the IP route is preferred over IV
- Tailor to cultureNarrow therapy once the organism is known
- Remove the catheterRefractory infection (effluent not clear after 5 days), fungal or relapsing peritonitis, or a tunnel infection with the same organism
Several enteric organisms, especially with anaerobes, suggest secondary peritonitis from bowel perforation, which needs surgical evaluation rather than antibiotics alone.
Anemia and calciphylaxis
Anemia of CKD. The failing kidney makes too little erythropoietin, and iron deficiency (blood loss in the dialysis circuit, phlebotomy) and inflammation contribute. Check transferrin saturation and ferritin and replete iron first. HD patients usually receive IV iron, which is given when TSAT is ≤30% and ferritin ≤500 ng/mL. Start an ESA when Hgb is below 10 g/dL and aim for about 10–11.5 g/dL, never above 13. Higher targets increase stroke, thrombosis (including access thrombosis), hypertension, and death. Poor ESA response most often reflects iron deficiency, inflammation or infection, severe hyperparathyroidism, or inadequate dialysis. Oral HIF prolyl-hydroxylase inhibitors (daprodustat, vadadustat) are an alternative for dialysis patients.
Calciphylaxis (calcific uremic arteriolopathy). Small arterioles of the skin and fat calcify and thrombose. Patients develop exquisitely painful violaceous, livedo-like plaques that ulcerate into black eschars, usually over fatty areas such as the thighs and abdomen. Mortality is high, mainly from wound sepsis. Risk factors include warfarin, female sex, obesity, diabetes, high calcium-phosphate product, hyperparathyroidism, and calcium-based binders or active vitamin D.
Treat calciphylaxis with IV sodium thiosulfate and intensified dialysis. Stop warfarin, calcium, and vitamin D, control PTH (cinacalcet or parathyroidectomy), and provide careful wound care and pain control.