Care of the hospitalised patient receiving peritoneal dialysis: Your questions answered.

Peritoneal dialysis (PD) patients have higher hospitalisation rates than the general population. The hospitalisations are not always related to dialysis issues, and physicians with little or no experience with PD may be responsible for the care of these hospitalised patients. Furthermore, the hospital may not be familiar with or equipped to manage these patients. This review highlights barriers, knowledge gaps and management strategies to guide the care of hospitalised PD patients.

Klebsiella pneumoniae Renal Abscess and Peritonitis in a Peritoneal Dialysis Patient: A Novel Route of Infection.

We present a peritoneal dialysis (PD) patient who had a renal biopsy performed during an episode of urosepsis and subsequently presented with a renal abscess at the biopsy site along with concurrent peritonitis. Microbiology from the PD effluent and from the renal abscess were both positive for Klebsiella pneumoniae We propose that the PD peritonitis was the result of seeding of the peritoneal cavity with bacteria from the renal abscess. Successful treatment was achieved through drainage of the abscess and intraperitoneal antibiotics.

Myths in peritoneal dialysis.

PURPOSE OF REVIEW: To clarify misconceptions about the feasibility and risks of peritoneal dialysis that unnecessarily limit peritoneal dialysis uptake or continuation in patients for whom peritoneal dialysis is the preferred dialysis modality. The inappropriate choice of haemodialysis as a result of these misconceptions contributes to low peritoneal dialysis penetrance, increases transfer from peritoneal dialysis to haemodialysis, increases expenditure on haemodialysis and compromises quality of life for these patients. RECENT FINDINGS: Peritoneal dialysis is an excellent renal replacement modality that is simple, cost-effective and provides comparable clinical outcomes to conventional in-centre haemodialysis. Unfortunately, many patients are deemed unsuitable to start or continue peritoneal dialysis because of false or inaccurate beliefs about peritoneal dialysis. Here, we examine some of these 'myths' and critically review the evidence for and against each of them. We review the feasibility and risk of peritoneal dialysis in patients with prior surgery, ostomies, obesity and mesh hernia repairs. We examine the fear of mediastinitis with peritoneal dialysis after coronary artery bypass graft surgery and the belief that the use of hypertonic glucose dialysate causes peritoneal membrane failure. SUMMARY: By clarifying common myths about peritoneal dialysis, we hope to reduce overly cautious practices surrounding this therapy.

The Enigmatic Fallopian Tube: A More Common Cause of Catheter Malfunction than Previously Recognized.

Successful performance of peritoneal dialysis (PD) depends on a properly functioning PD catheter. Catheter malfunction remains a significant cause of technique failure, especially early in the course of therapy. Common causes of catheter malfunction include catheter displacement, omental or bowel wrapping, and fibrin clots. Less commonly, various intraperitoneal structures have been reported to lead to obstruction, including appendices epiploicae of sigmoid colon and the fallopian tube. Peritoneal dialysis catheter blockage due to fimbriae of the fallopian tube is being recognized as an important cause of catheter malfunction in females due to the increasing availability of diagnostic laparoscopy. We report 5 episodes of catheter malfunction in 4 patients on PD from a single center as a result of obstruction by the fallopian tube.

The outcome of nephrectomy in peritoneal dialysis patients.

Data regarding the outcomes of peritoneal dialysis (PD) patients undergoing nephrectomy are limited. In the 20-year retrospective study reported here, we included patients who underwent nephrectomy and then subsequently started PD within 1 year (group A) and those who underwent nephrectomy while already on PD (group B). We examined mechanical complications including incisional hernia, peritoneal leak, and wound infection or dehiscence. Among biochemical outcomes (group B only), we analyzed serum creatinine, albumin, potassium, and phosphate for 1 year pre- and post-nephrectomy. Among the 8 patients identified (4 in group A, 4 in group B), 7 underwent unilateral nephrectomy, and 1, bilateral nephrectomy. Surgery was laparoscopic in 1 patient and open in 7 patients. The approach was transperitoneal in 5 patients, and retroperitoneal in 3 patients. Incisional hernia occurred in 4 patients (2 in each group), and retroperitoneal leak was seen in 1 patient in group B after 2 months. No wound dehiscence or other complications occurred. In group B, 2 patients required hybrid therapy in the form of once-weekly hemodialysis with continuous ambulatory PD. Among the biochemical complications, we noted that serum creatinine increased (as expected), and serum albumin significantly declined and remained lower post-nephrectomy. Our data show that, post-nephrectomy, PD patients have a high incidence of incisional hernia. They also experience a significant decline in serum albumin and a substantial loss in residual kidney function potentially requiring intensified dialysis. The retroperitoneal approach may on occasion predispose to retroperitoneal leak of dialysate.

Cancer antigen 125 as a biomarker in peritoneal dialysis: mesothelial cell health or death?

The concentration or appearance rate of cancer antigen 125 (CA125) in peritoneal dialysis (PD) effluent has been used for many years as a biomarker for mesothelial cell mass in patients on PD. However, this marker has limitations, and emerging evidence has raised doubts as to its significance. This review explores our current understanding of CA125, its prominent role in studies of "biocompatible" PD solutions, and the ongoing uncertainty concerning its interpretation as a measure of mesothelial cell health.

Gynecologic issues in peritoneal dialysis.

This paper reviews the issues associated with the reproductive system in the special population of female patients with end-stage renal disease on peritoneal dialysis (PD). We summarize current knowledge concerning cancer screening tests, elective and urgent gynecologic procedures, and the issues of menstruation, contraception, pregnancy, and delivery in these patients. Finally, we present the potential effects of gynecologic problems on PD and the complications of PD that can present with symptoms of the female genitalia.

The biocompatibility of neutral pH, low-GDP peritoneal dialysis solutions: benefit at bench, bedside, or both?

For patients on peritoneal dialysis (PD), the development of peritonitis, the decline of residual kidney function, and the loss of peritoneal membrane function are central events that affect both patient and technique survival. The use of glucose as the osmotic agent in conventional PD solutions may increase the susceptibility to each of these events. However, its use may also be associated with systemic metabolic perturbations and, in turn, an increase in cardiovascular morbidity. Both in vitro and in vivo evidence suggest that both the local peritoneal and systemic toxicity induced by the use of glucose may be in part mediated by the presence of glucose degradation products (GDPs) coupled with the hyperosmolarity, reduced pH, and use of lactate as the buffer in conventional PD solutions. Therefore, the use of neutral pH, low-GDP (NpHL(GDP)), bicarbonate-buffered PD solutions may represent a promising strategy to attenuate some of these adverse effects. However, the impact of these novel solutions on clinical outcomes remains largely unknown. In this review, we will highlight evidence regarding the biocompatibility of NpHL(GDP) PD solutions, review the utility of current biomarkers in the evaluation of biocompatibility, and discuss the clinical outcome data with these solutions.

Persistent proteinuria and dyslipidemia increase the risk of progressive chronic kidney disease in lupus erythematosus.

Advances in immunotherapy have improved survival of patients with systemic lupus erythematosus who now face an increasing burden of chronic diseases including that of the kidney. As systemic inflammation is also thought to contribute directly to the progression of chronic kidney disease (CKD), we assessed this risk in patients with lupus, with and without a diagnosis of nephritis, and also identified modifiable risk factors. Accordingly, we enrolled 631 patients (predominantly Caucasian), of whom 504 were diagnosed with lupus within the first year and followed them an average of 11 years. Despite the presence of a chronic inflammatory disease, the rate of decline in renal function of 238 patients without nephritis was similar to that described for non-lupus patient cohorts. Progressive loss of kidney function developed exclusively in patients with lupus nephritis who had persistent proteinuria and dyslipidemia, although only six required dialysis or transplantation. The mortality rate was 16% with half of the deaths attributable to sepsis or cancer. Thus, despite the presence of a systemic inflammatory disease, the risk of progressive CKD in this lupus cohort was relatively low in the absence of nephritis. Hence, as in idiopathic glomerular disease, persistent proteinuria and dyslipidemia (modifiable risks) are the major factors for CKD progression in lupus patients with renal involvement.

Encapsulating peritoneal sclerosis: a single-center experience and review of the literature.

Encapsulating peritoneal sclerosis (EPS) is a serious and often fatal complication of long-term PD with severe malnutrition and poor prognosis. It causes progressive obstruction and encapsulation of the bowel. This retrospective study reviews our experience and that reviewed in the literature concerning EPS. It refers to a total of 1966 patients treated with chronic PD between 1974 and 2008. Twenty one of them (1.1%) developed EPS, with the incidence increasing with the duration of PD. Mean age of our patients with EPS was 43, ranging from 18 to 71 years, 8 were men and 13 women with a mean body mass index (BMI) of 21.6 kg/m(2). Only one patient had Type II diabetes, 15 patients had glomerular disease, and six of these 15 had an autoimmune disease such as Wegener's granulomatosis and SLE. Thirteen patients developed EPS while on PD, 7 within 2 years after transfer to HD, and only one after renal transplantation. However, 7 patients had a previous renal transplant before returning to PD and subsequently developing EPS. Interestingly, we did not observe more episodes of EPS after transplantation. In the patients who developed EPS, the peritonitis rate over the period of observation was 1/15.6 pt-months and was due to Staphylococcus aureus, coagulase-negative staphylococcus, Pseudomonas and fungi. A history of peritonitis was not a prerequisite for developing EPS, since one patient had no episodes of peritonitis and 4 had just one previous episode. Fifteen patients presented with peritonitis within 4 months before the diagnosis of EPS with particularly virulent micro-organisms such as S. aureus, Candida, Pseudomonas, Corynebacterium, and Peptostreptococcus. Eleven patients were treated with hypertonic dextrose solutions (4.25 g/dl of dextrose) and seven with icodextrin, indirectly suggesting problems with ultrafiltration. Nine of 21 patients were on beta-blockers. The diagnosis of EPS was made either surgically or radiologically with signs of small bowel obstruction in combination with severe malnutrition. Eleven of our patients (52%) had evidence of small bowel obstruction and 14 patients required total parenteral nutrition (TPN). Tamoxifen (10-20 mg daily) was started in 6 patients, 4 of whom are alive and 2 deceased 3 and 5 years after EPS was diagnosed. Of the 12 patients who were not given tamoxifen, 2 are alive and 10 died. No side effects of tamoxifen were reported. Only 7 of our patients (33%) died during the first year after the diagnosis of EPS. Currently, 4 patients are on HD and 3 have had a renal transplant. Six patients of the fourteen who underwent surgery (42.8%) died within the first 6 months after operation and five died after an average of 6.6 years, mostly due to cardiovascular causes, three are still alive. As EPS becomes more prevalent with longer duration of PD, large multicenter prospective studies are needed to establish its incidence and identify risk factors, therapeutic approach, and prognosis.

Hyponatraemia caused by LGI1-associated limbic encephalitis.

Limbic encephalitis (LE), once thought to be a rare paraneoplastic phenomenon, is increasingly diagnosed in patients without malignancy. Autoimmune LE has emerged as a distinct clinical entity. Autoantibodies to neuronal cell surface proteins have been described and may now be tested for. This has led to an exponential increase in the number of cases being reported. The most recently implicated autoantibody is to the leucine-rich anti-glioma 1 protein (LGI1). This protein is involved in synaptic transmission and inherited loss-of-function mutations cause autosomal dominant lateral temporal epilepsy. LGI1 is also expressed in specific tubules in the kidney. Anti-leucine-rich anti-glioma 1 protein (anti-LGI1) LE presents with sub acute onset of progressive neurological, cognitive and psychiatric disturbance. The condition is complicated in up to 60% of cases with severe and life threatening hyponatraemia. As well as causing significant morbidity, the co-existence of hyponatraemia may confuse the initial diagnosis. We present a case of anti-LGI1 which was complicated by hyponatraemia with a comprehensive review of the literature.

Glucoregulatory hormones and choice of osmotic agent in peritoneal dialysis.

OBJECTIVE: The present study was performed to explore the range of effects of amino acid-based peritoneal dialysis (PD) solutions on glucoregulatory hormones in comparison with an osmotically equivalent glucose-based solution. ♢ METHODS: 13 adult nondiabetic patients on PD underwent 2 peritoneal dwells of 2 hours' duration with either 1.5% dextrose solution or 1.1% amino acid solution. Serial sampling for glucoregulatory hormones was done throughout the duration of the dwell. ♢ RESULTS: Instillation of the 1.5% dextrose solution resulted in a modest change in plasma glucose, paralleled by a small increase in plasma insulin levels and plasma insulin-like growth factor (IGF-1). Plasma glucagon was not changed and plasma growth hormone level declined. Instillation of the 1.1% amino acid solution resulted in an increase in plasma glucose, plasma insulin, plasma glucagon, and plasma IGF-1. Plasma growth hormone level declined. Both solutions led to an increase in plasma norepinephrine but no changes were observed in epinephrine or dopamine. ♢ CONCLUSIONS: Our observations suggest that the mere replacement of glucose by amino acids in PD solutions does not necessarily imply "glucose sparing" from the perspective of induction of a glucoregulatory hormonal response because of the aminogenic stimulation of secretion of multiple hormones.

The renin-angiotensin-aldosterone system in peritoneal dialysis: is what is good for the kidney also good for the peritoneum?

Morphological changes of the peritoneal membrane that occur over time among patients on peritoneal dialysis include fibrosis and neoangiogenesis. While the pathophysiologic mechanisms underlying these changes are not fully understood, the activation of the renin-angiotensin-aldosterone system (RAAS) may have an important role. Components of the RAAS are constitutively expressed within peritoneal mesothelial cells, and are upregulated in the presence of acute inflammation and chronic exposure to peritoneal dialysate. The high glucose concentration, low pH, and the presence of glucose degradation products in peritoneal dialysis solutions have all been implicated in modulation of peritoneal RAAS. Furthermore, activation of the RAAS, as well as the downstream production of transforming growth factor-beta, contributes to epithelial-to-mesenchymal transformation of mesothelial cells, resulting in progressive fibrosis of the peritoneal membrane. This process also leads to increased vascular endothelial growth factor production, which promotes peritoneal neoangiogenesis. Functionally, these changes translate into reduced ultrafiltration capacity of the peritoneal membrane, which is an important cause of technique failure among patients on long-term peritoneal dialysis. This brief review will describe our current state of knowledge about the role of peritoneal RAAS in peritoneal membrane damage and potential strategies to protect the membrane.

Inflammatory pseudotumor of the kidney allograft.

Inflammatory myofibroblastic tumor, or inflammatory pseudotumor, usually is a benign lesion composed of mixed inflammatory and fibroblastic elements. It has rarely been reported in the posttransplantation setting and never in association with a renal allograft. Although the pathogenesis of this lesion is unclear, exposure to immunosuppressive agents and various infections have been implicated in its development. We report the first case of inflammatory myofibroblastic tumor infiltrating a renal allograft and highlight the role immunosuppression may have in the development of this lesion.