Diabetes mellitus (DM) is a leading cause of End-Stage Kidney Disease (ESKD) globally, requiring many patients to undergo dialysis. Peritoneal Dialysis (PD) is a continuous, home-based treatment using the body’s own peritoneal membrane as a filter. This combination of DM and the specific mechanics of PD creates elevated medical risks that require specialized management. The characteristics of the dialysis fluid and the compromised health status of diabetic patients introduce complications not faced by non-diabetic PD patients.
Impact of Dialysate Glucose on Blood Sugar Management
The mechanism of fluid removal in PD relies on osmosis, achieved by instilling a high-concentration glucose solution, or dextrose, into the abdominal cavity. This dialysate draws excess water and toxins from the bloodstream across the peritoneal membrane. A significant portion of this dextrose is absorbed directly into the patient’s circulation throughout the dwell time.
The amount of glucose absorbed can range from 60 to 80% of the instilled dextrose over a typical four-hour exchange. This absorption translates to a substantial caloric intake, often equivalent to 100 to 300 grams of glucose daily. This continuous influx of sugar creates a persistent metabolic burden that makes achieving stable blood sugar control extremely challenging.
The result is chronic hyperglycemia, which necessitates a marked increase in the patient’s insulin requirements to manage the excessive glucose load. This increased insulin demand raises the long-term risk of diabetic complications. The continuous caloric absorption also contributes to weight gain and the development of obesity, further complicating insulin resistance and overall metabolic health.
Increased Susceptibility to Infection
Patients living with DM often have a compromised immune system, characterized by impaired function of infection-fighting cells, such as neutrophils. This vulnerability makes them more susceptible to all types of infections. For those on PD, this heightened risk is directed at peritonitis, an infection of the peritoneal cavity and the primary complication of the therapy.
Diabetes is associated with neuropathy, which can dull the sensation of abdominal pain, potentially delaying the diagnosis of peritonitis. A delayed diagnosis allows the infection to progress, leading to more severe outcomes and potentially requiring the patient to switch dialysis methods. High glucose concentrations in the peritoneal fluid also impair the local immune defenses within the abdominal cavity.
When infections occur, diabetic patients may face a higher risk of peritonitis caused by more aggressive pathogens, such as fungi or certain Gram-negative bacteria. Furthermore, the diabetic condition can impede the healing of exit site infections around the PD catheter. Poor healing allows bacteria to travel along the catheter tunnel, increasing the likelihood of recurrent infections.
Accelerated Peritoneal Membrane Damage
The prolonged and continuous exposure of the peritoneal membrane to the glucose-based dialysate solutions causes structural and functional damage over time. This damage is exacerbated by the underlying diabetic condition, which accelerates the formation of Advanced Glycation End products (AGEs). AGEs are harmful compounds formed when excess sugar molecules attach to proteins or lipids without the aid of an enzyme.
The combination of AGE formation and the presence of glucose breakdown products (GDPs) in the dialysate triggers chronic inflammation and morphological changes in the peritoneal tissue. Over years, this process leads to peritoneal fibrosis, a scarring of the membrane, and neoangiogenesis, which is the formation of new, leaky blood vessels. These changes ultimately impair the membrane’s efficiency.
The most severe consequence is Ultrafiltration Failure (UFF), where the membrane loses its ability to effectively draw water out of the body. When UFF occurs, the patient can no longer effectively manage fluid balance with PD. This loss of technique efficacy is a major reason why diabetic patients may be forced to discontinue PD and transition to hemodialysis.
Exacerbation of Existing Cardiovascular Risk
Cardiovascular disease is the leading cause of death in patients with both DM and ESKD. The PD modality adds elements that worsen this risk. The continuous absorption of dialysate glucose contributes to chronic hyperinsulinemia and insulin resistance.
This metabolic stress promotes an unfavorable shift in the patient’s lipid profile, known as dyslipidemia, characterized by abnormal levels of cholesterol and triglycerides. This worsening metabolic environment accelerates the development of atherosclerosis, which is the hardening and narrowing of the arteries.
Challenges of glycemic control and compromised ultrafiltration capacity contribute to a risk of chronic volume overload. Excess fluid volume places strain on the heart, raising blood pressure and accelerating heart failure and hypertension.
The cumulative effect of increased insulin resistance, dyslipidemia, and difficulty in managing fluid balance creates an environment where cardiovascular events are more likely. The PD-specific metabolic changes layer onto the pre-existing risks from diabetes, creating a cycle of accelerated vascular damage that poses a serious threat to long-term survival.