PD makes use of the peritoneal membrane as the dialysis membrane because it is thin, vascularized and has a large surface area. ^[1]

The peritoneum has a surface area roughly equal to body surface area (~1.7 m²). Its rich capillary network allows efficient diffusion of solutes and osmotic ultrafiltration. Over years, however, this membrane deteriorates (see PD failure below).

The PD catheter (commonly known as the Tenckhoff catheter) is a specially designed plastic tube with many side-holes in one end and two fibrous cuffs in the other end. ^[1]

• Side holes at the intraperitoneal end allow PD fluid to flow in and out freely.
• Two Dacron cuffs anchor the catheter: one sits in the rectus muscle, the other subcutaneously near the exit site. Tissue ingrowth into the cuffs creates a seal that prevents migration and serves as a barrier against bacterial tracking along the catheter.
• Exit site is where the catheter emerges through the skin.
• Insertion: via a paramedian incision.

Ideally, the tip of the PD catheter should be located inside the pelvis pointing downwards. ^[1]

Why pointing downwards in the pelvis? The pelvic cavity is the most dependent part of the abdomen when the patient is upright, so fluid pools here. If the catheter tip is directed downward into the pelvis, drainage is most efficient.

Commonly used PDFs are balanced salt solutions, with glucose as the osmotic agent and lactate as the buffer. They do not contain potassium. ^[1]

Key points to understand:

• No potassium in PD fluid: ESKD patients are typically hyperkalemic. By having zero K⁺ in the dialysate, potassium diffuses from blood into the PD fluid down its concentration gradient. This is how PD removes excess potassium. However, some patients on PD may develop hypokalemia if they have good residual renal function or poor oral intake—they may need potassium supplementation.

• Glucose as osmotic agent: Higher glucose concentration → greater osmotic gradient → more ultrafiltration (fluid removal). The 4.25% ("hypertonic") bag is used for fluid-overloaded patients. However, chronic exposure to high glucose concentrations damages the peritoneal membrane over time (→ PD failure).

• Lactate as buffer: Lactate is converted to bicarbonate by the liver. This corrects the metabolic acidosis of ESKD. (Note: icodextrin-based fluids use glucose polymer instead of dextrose as the osmotic agent for long dwells, but this is beyond the core lecture content.)

• Patient manually performs 3–4 exchanges per day (each exchange: drain out old fluid → infuse new fluid → dwell for 4–6 hours).
• Performed throughout the day — exchanges at breakfast, lunch, dinner, and bedtime is typical.
• No machine needed — gravity-driven.
• The peritoneal cavity always has fluid dwelling in it → "continuous."

APD makes use of an APD machine to help the patient to perform the PD exchanges, usually at night when the patient goes to bed. ^[1]

• A machine performs multiple short exchanges overnight while the patient sleeps.
• Two subtypes:
  • NIPD (Nocturnal Intermittent PD): exchanges only at night; abdomen is dry during the day.
  • CCPD (Continuous Cyclic PD): machine does exchanges at night, but a long daytime dwell is left in the abdomen as well (for additional clearance).

Why is QoL better in APD? The patient's daytime is free—they can work, attend school, or travel without worrying about exchanges. This is particularly important for younger, active patients.

Usually presents as redness and tenderness at the PD catheter exit site, sometimes associated with purulent discharge. PD catheter exit site infection may predispose to PD peritonitis. ^[1]

Why does exit site infection lead to peritonitis? Bacteria colonize the exit site → track along the catheter tunnel → enter the peritoneal cavity. This is why meticulous exit site care (daily cleaning, keeping it dry) is a critical part of PD patient education.

Why does constipation/diarrhea predispose to PD peritonitis? Bowel disturbance increases intestinal permeability and can promote transmural migration ("translocation") of gut bacteria into the peritoneal cavity. Always ask about bowel habits in a PD patient with peritonitis.

Diagnosis:

PD fluid microscopy shows elevated WBC count with neutrophil predominance. PD fluid culture identifies the causative organism. ^[1]

The diagnostic threshold is WBC > 100/μL with > 50% neutrophils in the PD effluent (this is a standard ISPD criterion—worth knowing). Compare this to the clear-cut presentation in the 2020 minicase where a PD patient presented with fever and abdominal pain with turbid output. ^[3]

Treatment:

Empirical intraperitoneal antibiotics that cover common gram-positive and gram-negative bacteria (e.g., Cefazolin + Amikacin). Choice of antibiotics should be adjusted according to PD fluid culture results. ^[1]

Why intraperitoneal (IP) rather than IV? IP administration delivers antibiotics directly to the site of infection at high local concentrations. Systemic (IV) antibiotics poorly penetrate the peritoneal cavity. The IP route is the standard of care per ISPD guidelines.

Patients with refractory peritonitis might need to have their PD catheter removed and be put on temporary hemodialysis. ^[1]

When is peritonitis "refractory"? If there is no clinical improvement after 5 days of appropriate antibiotics, or if there is fungal peritonitis (almost always requires catheter removal), or if there is relapsing/repeat peritonitis from the same organism.

Complication of repeated peritonitis:

Frequent PD-related peritonitis will damage the peritoneal membrane and eventually lead to peritoneal dialysis failure. ^[1]

Chronic exposure to dextrose-containing PD fluids and repeated peritonitis will cause fibrosis of the peritoneal membrane, eventually leading to PD failure. ^[1]

Mechanism from first principles: High-glucose PD fluid generates glucose degradation products (GDPs) and advanced glycosylation end-products (AGEs). These trigger chronic inflammation, neovascularization, and fibrosis of the peritoneal membrane. The membrane becomes thick and leathery. Result:

• Loss of ultrafiltration capacity (can't remove fluid effectively)
• Loss of solute clearance (can't remove uremic toxins effectively)

The lecture slide shows a dramatic comparison: normal thin peritoneum vs. markedly thickened peritoneum after 10 years on PD. Eventually, the patient must switch to HD.

A severe form is encapsulating peritoneal sclerosis (EPS) — a cocoon-like thickening that encases the bowel, causing obstruction. This is a dreaded complication of long-term PD.

Occasionally, the tip of the PD catheter may migrate out of the pelvis, leading to poor drainage of the PD fluid. ^[1]

Clinical clue: The patient notices slow or incomplete drainage during exchanges. An abdominal X-ray (KUB) will show the catheter tip displaced superiorly or laterally instead of pointing downward in the pelvis. Management may involve laxatives (constipation can displace the catheter), repositioning under fluoroscopy, or surgical revision.

Occasionally, the PD fluid may leak out of the peritoneal cavity into the pleural cavity, the anterior abdominal wall, the perineum or the retro-peritoneal space. ^[1]

• Pleural leakage (hydrothorax): PD fluid enters the pleural space through a diaphragmatic defect (pleuro-peritoneal communication). Presents as unilateral (usually right-sided) pleural effusion that worsens with PD exchanges. Diagnosed by high glucose content in the pleural fluid. May require thoracoscopic repair or switching to HD.
• Abdominal wall leakage: Fluid tracks along the catheter tunnel or through a hernia. Presents as swelling around the catheter or inguinal region.
• Genital edema: Fluid tracks into the scrotum/labia via a patent processus vaginalis.

In HD, a vascular access is required to allow sufficiently high flow of blood from the patient to pass through the hemodialysis machine and then return to the patient. ^[1]

Blood flow rates of 200–400 mL/min are needed for effective HD. Normal peripheral veins cannot provide this flow. Hence, specialized vascular access is mandatory.

Three main types of vascular access: (1) Arteriovenous fistula (AVF), (2) Arteriovenous graft (AVG), (3) Tunneled cuffed double-lumen central venous catheter. ^[1]

Why is AVF best? It uses the patient's own tissue—no foreign material for bacteria to adhere to. The "arterialized" vein has thick walls that tolerate repeated needling. AVF has the lowest rates of infection, thrombosis, and hospitalization.

Why does a catheter have the highest infection risk? The catheter is a foreign body that directly communicates with the central venous system. Bacteria from the skin can track along the catheter or colonize the lumen, causing exit site infection → tunnel infection → bacteremia/septicemia.

Contains a blood pump (drives blood through the circuit at the required flow rate) and connects to the hemodialyzer where actual dialysis occurs.

Hemodialyzer in a HD machine is where the hemodialysis actually occurs. ^[1]

This is essentially a cylinder containing thousands of hollow fibres (the semi-permeable membrane). Blood flows through the inside of the fibres; dialysate flows on the outside in the opposite direction (counter-current flow maximizes the concentration gradient and therefore diffusion efficiency).

Vascular access stenosis, vascular access thrombosis, upper limb ischemia. ^[1]

• Stenosis: Neointimal hyperplasia (especially at the venous outflow of AVF or at the venous anastomosis of AVG) narrows the vessel. Detected by reduced thrill/bruit, elevated venous pressures during dialysis, or poor clearance. Diagnosed by fistulogram (angiography). Treated by angioplasty or surgical revision.

• Thrombosis: Often a consequence of underlying stenosis. The fistula loses its thrill and bruit. Urgent thrombectomy or thrombolysis is needed.

• Upper limb ischemia (steal syndrome):

Elderly and diabetic patients with severe atherosclerosis are prone to develop ischemia in the limb bearing the AV fistula. ^[1]

Why? The AV fistula diverts arterial blood directly into the vein (low resistance pathway), "stealing" blood from the distal arterial bed. In patients with pre-existing peripheral vascular disease, the residual flow to the hand is insufficient → cold, painful, pale fingers → digital gangrene in severe cases. Management: may require ligation or banding of the fistula.

Catheter exit site infection, catheter-associated bacteremia, catheter malfunction. ^[1]

• Exit site infection:

Usually localized to the skin and soft tissue around the catheter exit site. Uncontrolled exit site infection may spread along the subcutaneous tunnel into the systemic circulation, causing bacteremia or septicemia. ^[1]

The pathway: Exit site infection → Tunnel infection → Bacteremia → Septicemia (including metastatic infections like infective endocarditis, osteomyelitis, epidural abscess).

• Catheter-associated bacteremia (CLAB): A feared complication. Most commonly caused by S. aureus and coagulase-negative staphylococci. Management: blood cultures, empirical IV vancomycin + gentamicin, and often catheter removal/exchange if the infection is not rapidly controlled.

• Catheter malfunction:

Blood clot can occlude the catheter lumen. ^[1]

Managed with thrombolytic lock (e.g., alteplase instilled into the catheter lumen) or catheter exchange.

Cardiovascular: Hypotension, Cardiac arrhythmia. Neuromuscular: Muscle cramps. Technical malfunctions: Air embolism, Blood loss. ^[1]

• Intradialytic hypotension: The most common acute complication. Caused by rapid ultrafiltration (fluid removal) exceeding plasma refilling rate. Manifests as lightheadedness, nausea, cramps. Managed by reducing UF rate, giving saline bolus, Trendelenburg position.
• Arrhythmia: Electrolyte shifts (especially potassium) during dialysis can trigger arrhythmias. Patients with pre-existing cardiac disease are most vulnerable.
• Muscle cramps: Due to rapid fluid/electrolyte shifts.
• Air embolism: Rare but potentially fatal. Modern HD machines have air detectors as safety mechanisms.
• Blood loss: Circuit disconnection, membrane rupture, or post-needle removal bleeding.

In Hong Kong, the living donors are usually first-degree relatives or spouse of the patients. The living donors should be healthy and have normal renal function and structure. ^[1]

• Why first-degree relatives? Better HLA matching (parent shares at least one haplotype with child; siblings have a 25% chance of being fully matched). Better outcomes with better matching. Also, HK law restricts living donation to close relatives or spouses to prevent organ trafficking.
• Donor nephrectomy: Performed via laparoscopic nephrectomy (minimally invasive, faster recovery for the donor).

Deceased kidney donors have irreversible brain damage leading to brain stem death. They should have no known history of kidney diseases, long-standing HT or DM and have normal renal function. ^[1]

• Donor nephrectomy: Open nephrectomy (the operation occurs in the context of multi-organ retrieval).
• Brain stem death is the prerequisite: the diagnosis is made by clinical testing of brainstem reflexes. Two independent assessments by senior doctors are required in HK.

Renal transplant recipients are immunocompromised and prone to opportunistic infections. Causative organisms include CMV, Pneumocystis jiroveci, BK virus, and M. tuberculosis. ^[1]

Pneumocystis Pneumonia (PCP):

Usually presents with acute onset of fever, cough and shortness of breath, associated with severe type I respiratory failure. CXR shows diffuse, bilateral, interstitial infiltrates. Diagnosed by microscopy with staining of BAL fluid for Pneumocystis jiroveci. Treated with high-dose septrin (co-trimoxazole). Transplant recipients are usually given septrin prophylaxis. ^[1]

Why PCP prophylaxis? PCP has a very high mortality in immunosuppressed patients if untreated. Routine low-dose co-trimoxazole (480 mg daily or 960 mg 3×/week) is given for at least 6–12 months post-transplant (or lifelong if heavily immunosuppressed). It also provides prophylaxis against toxoplasmosis and common UTIs.

BK virus: A polyomavirus that reactivates under immunosuppression. Causes BK virus-associated nephropathy (BKVAN) which can mimic rejection on clinical grounds (rising creatinine). Diagnosed by BK viral load in blood and urine; confirmed by biopsy showing viral inclusions ("decoy cells" in urine). Treatment: reduce immunosuppression.

CMV: Causes fever, leukopenia, hepatitis, colitis, pneumonitis. Prophylaxis with valganciclovir is given for high-risk patients (D+/R−). Monitored by serial CMV viral loads.

Renal transplant recipients have increased risk of developing malignancies, including post-transplant lymphoproliferative disorders (PTLDs). ^[1]

Why? Chronic immunosuppression impairs immune surveillance against virally-driven cancers and allows unchecked cell proliferation. PTLDs are most commonly EBV-driven B-cell lymphomas. Also increased: skin cancers (SCC > BCC, reversed from the general population), Kaposi sarcoma (HHV-8), cervical/anogenital cancers (HPV).

PTLD management: Reduce immunosuppression, rituximab (anti-CD20), chemotherapy.

CVD is the most important cause of death with a functioning graft in renal transplant recipients. ^[1]

Transplant recipients have multiple cardiovascular risk factors such as diabetes, hypertension and hyperlipidemia (related to the underlying renal disease or the use of immunosuppressive drugs). ^[1]

Why so much CVD? Multiple compounding risk factors:

• Pre-existing CKD-associated vascular disease
• Steroids → hyperglycemia, hyperlipidemia, HTN
• CNIs → HTN, hyperlipidemia
• Tacrolimus → new-onset DM
• mTOR inhibitors → hyperlipidemia

Aggressive cardiovascular risk factor management is essential: statins, BP control, glycemic control, smoking cessation.

Classic clinical exam findings:

• Cushingoid features (prednisolone) — moon face, central obesity, striae, thin skin, buffalo hump
• Gum hypertrophy (cyclosporine) — also caused by phenytoin and nifedipine; exam loves to ask for the differential

A clinico-pathological syndrome characterized by slow progressive decline in renal graft function, proteinuria, hypertension, and histological features of interstitial fibrosis and tubular atrophy (IF/TA), caused by both immune and non-immune factors. It is the leading cause of late graft failure after renal transplantation. ^[1]

Immune factors: Subclinical rejection, non-adherence to immunosuppression, donor-specific antibodies. Non-immune factors: CNI nephrotoxicity, hypertension, recurrent disease, BK nephropathy.

The cause of the renal transplant recipient's original kidney disease may recur in the transplanted kidney. Recurrence of IgA nephropathy, membranous nephropathy and FSGS are not uncommon. ^[1]

This is conceptually important: transplantation replaces the organ but not the underlying pathogenic mechanism. IgA nephropathy recurrence on biopsy is very common (~50%) but only causes graft loss in ~10%. FSGS (especially if due to a circulating permeability factor) can recur within hours of transplantation and is more aggressive.