Ultrafiltration Failure Is a Reflection of Peritoneal Alterations in Patients Treated With Peritoneal Dialysis

Ultrafiltration (UF) failure is a common and important complication of peritoneal dialysis (PD), especially in long-term patients without residual urine production, because it often causes overhydration, which is an important cause of death in this population. The current review provides an overview of the pathways of peritoneal fluid transport, followed by the mechanisms and causes of UF failure. The egression of circulating fluid to the tissue compartment and its subsequent re-uptake by the colloid osmotic pressure are markedly influenced by PD, because the dialysis solutions contain glucose as a low molecular weight agent causing removal of fluid from the circulation by crystalloid osmosis. Pores involved in transcapillary UF consist of inter-endothelial small pores and the intra-endothelial water channel aquaporin-1. The former allows transport of plasma fluid with dissolved low molecular weight solutes and accounts for 60% of the filtered volume, the latter transports 40% as pure water. This free water transport (FWT) is driven by the crystalloid pressure gradient, while small pore fluid transport (SPFT) is dependent on both hydrostatic and crystalloid osmotic pressure. The number of perfused peritoneal microvessels as assessed by small solute transport parameters, is differently associated with UF: a positive relationship is present with SPFT, but a negative one with FWT, because the effect of more vessels is counteracted by a faster disappearance rate of glucose. Ultrafiltration failure can be present shortly after the start of PD, for instance due to mesothelial-to-mesenchymal transition. Late UF failure develops in 21% of long-term patients. Both FWT and SPFT can be affected. Patients with encapsulating peritoneal sclerosis have severely impaired FWT, probably due to interference of interstitial collagen-1 with the crystalloid osmotic gradient. This mechanism may also apply to other patients with reduced FWT. Those with mainly impaired SPFT likely have a reduced hydrostatic filtration pressure due to vasculopathy. Deposition of advanced glycosylation end products is probably important in the development of this vasculopathy. It can be concluded that long-term UF failure may affect both SPFT and FWT. Vasculopathy is important in the former, interstitial fibrosis in the latter. Measurements of peritoneal transport function should include separate assessments of small pore-and FWT

Quantification of free water transport in peritoneal dialysis

Quantification of free water transport in peritoneal dialysis.BackgroundIn peritoneal dialysis (PD) total net ultrafiltration (NUF) is dependent on transport through small pores and through water channels in the peritoneum. These channels are impermeable to solutes, and therefore, crystalloid osmotic-induced free water transport occurs through them. Several indirect methods to assess free water transport have been suggested. The difference in NUF between a 3.86% and a 1.36% solution gives a rough indication, but is very time consuming. The magnitude of the dip in dialysate/plasma (D/P) sodium in the initial phase of a 3.86% exchange is another way to estimate free water transport. In the present study, a method was applied to calculate free water transport by calculating sodium-associated water transport in one single 3.86% glucose dwell.MethodsForty PD patients underwent one standard peritoneal permeability analysis (SPA) with a 1.36% glucose solution, and another with a 3.86% glucose solution. At different time points intraperitoneal volume and sodium concentration were assessed. This made it possible to calculate total sodium transport. By subtracting this transport (which must have occurred through the small pores) from the total fluid transport, free water transport remained. These results were compared with the other methods to estimate free water transport.ResultsFor the 1.36% glucose dwell, total transcapillary ultrafiltration in the first hour (TCUF0-60) was 164 mL, transport through the small pores was 129 mL, and free water transport was 35 mL (21%). For the 3.86% glucose solution, total TCUF0-60 was 404 mL, transport through the small pores was 269 mL, and free water transport was 135 mL (34%). The contribution of free water transport in the first minute (TCUF0-1) was 39% of the total fluid transport. From the 40 patients, 11 patients had ultrafiltration failure (NUF <400 mL after 4 hours). For these patients the contribution of free water to TCUF0-1 was significantly lower than for those with normal ultrafiltration (20% vs. 48%, P < 0.05). A strong correlation was present between free water transport as a percentage of total fluid transport and the maximum dip in D/P sodium (r = 0.84). The correlation was not significant with the difference in net ultrafiltration of 3.86% and 1.36% solutions (r = 0.24, P = 0.3).ConclusionThe method applied here is the first direct quantification of free water transport, calculated from a single standard peritoneal function test. It offers a quick possibility to evaluate patients suffering from ultrafiltration failure. In these patients free water transport was impaired, but the origin of this impairment is still to be determined

Augmenting solute clearance in peritoneal dialysis

Augmenting solute clearance in peritoneal dialysis.BackgroundThe removal of low molecular weight solutes by peritoneal dialysis is less than by hemodialysis. The targets for Kt/Vurea and creatinine clearance formulated in the Dialysis Outcome Quality Initiative are unlikely to be achieved in a substantial portion of peritoneal dialysis patients. Possibilities to increase small solute clearances have therefore been subject to many investigations.MethodsA review of the literature and of recent new data on determinants of solute removal, such as residual renal function, the role of drained dialysate volume and manipulation of the diffusive capacity of the peritoneum are presented.ResultsThe contribution of residual GFR is more important for the clearance of creatinine than for Kt/Vurea. It is even more important for the removal of organic acids that are removed from the body by tubular secretion. High dosages of furosemide increase the urinary volume and the fractional Na+ excretion, but have no effect on the magnitude of residual GFR, renal creatinine clearance, renal urea clearance, and peritoneal transport characteristics. The drained dialysate volume per day is the main determinant of the peritoneal removal of urea. Its effect decreases the higher the molecular weight of a solute. It can be augmented by using large instillation volumes, by the application of more exchanges, and by increasing peritoneal ultrafiltration. A large exchange volume is especially effective in patients with an average transport state, but in those with high solute transport rates, Kt/Vurea is especially influenced by the number of exchanges. Possibilities to increase ultrafiltration are discussed. The diffusive capacity of the peritoneum can be augmented by using low dosages of intraperitoneally administered nitroprusside. This increases solute transport most markedly when it is applied in combination with icodextrin as osmotic agent.ConclusionsSmall solutes clearances cannot be increased by furosemide. Increasing the instilled volume of dialysis fluid and the number of exchanges both affect solute clearance. Studies are necessary on long-term effects of manipulation of the peritoneal membrane with nitroprusside

Local Anaesthesia Suppressing Idiopathic Ventricular Tachycardia - A Cause of Non-inducible Arrhythmia During Electrophysiology Study

AbstractA 13year old boy having idiopathic ventricular tachycardia had non-inducible tachycardia twice on electrophysiology (EP) study due to suppression of arrhythmia by local anaesthetic agent, lignocaine. This case report demonstrates a cause of non-inducibility or arrhythmia during EP study and effect of lignocaine in suppression of idiopathic ventricular tachycardia

ACE I/D polymorphism is associated with mortality in a cohort study of patients starting with dialysis

ACE I/D polymorphism is associated with mortality in a cohort study of patients starting with dialysis.BackgroundIn dialysis patients, only a few follow-up studies have addressed the relationship between the insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene and mortality, but the available data are contradictory.MethodsA cohort of 453 consecutive patients starting dialysis between January 1999 and January 2002 and participating in a Dutch multicenter prospective study was examined. Patients who died within 3 months after the start of dialysis were excluded. Patients were followed until date of death or censoring in November 2003.ResultsThe ACE II, ID, and DD genotype frequencies were 24.3% (N = 110), 50.1% (N = 227), and 25.6% (N = 116). Besides a slightly higher number of Caucasians in the DD group, all other patient characteristics of the 3 ACE groups were similar at the start of dialysis. After adjustment for age, comorbidity, and ethnic background, patients with the ID and DD genotype showed an increased hazard ratio (HR) for all-cause mortality of 1.55 (95% CI 1.00-2.42) and 2.30 (95% CI 1.41-3.75), compared to patients with the II genotype. Slightly lower HRs were found for cardiovascular mortality. All groups of primary kidney disease showed a 2- to 3-fold increased adjusted HR for DD.ConclusionThe DD genotype identifies dialysis patients at an increased risk for mortality

Survival in dialysis patients is not different between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition

On dialysis, survival among patients with diabetes mellitus is inferior to survival of non-diabetic patients. We hypothesized that patients with diabetes as primary renal disease have worse survival compared to patients with diabetes as a co-morbid condition and aimed to compare all-cause mortality between these patient groups. Data were collected from the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD), a multicenter, prospective cohort study in which new patients with end stage renal disease (ESRD) were monitored until transplantation or death. Patients with diabetes as primary cause of ESRD were compared with patients with diabetes as co-morbid condition and both of these patient groups were compared to patients without diabetes. Analysis was performed using Kaplan-Meier and Cox regression. Fifteen % of the patients had diabetic nephropathy as primary renal disease (N = 281); 6% had diabetes as co-morbid condition (N = 107) and 79% had no diabetes (N = 1465). During follow-up 42% of patients (N = 787) died. Compared to non-diabetic patients, mortality risk was increased for both patients with diabetes as primary renal disease HR: 1.9 (95% CI 1.6, 2.3) and for patients with diabetes as co-morbid condition HR: 1.7 (95% CI 1.3, 2.2). Mortality was not significantly higher in patients with diabetes as primary renal disease compared to patients with diabetes as co-morbid condition (HR 1.06; 95% CI 0.79, 1.43). This study in patients with ESRD showed no survival difference between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition. Both conditions were associated with increased mortality risk compared to non-diabetic patient

30 years of peritoneal dialysis development: the past and the future

A review is given of 30 years of development in peritoneal dialysis (PD). After a short description of the first 20 years, the main emphasis is put on the last 10 years. Subjects discussed are the increasing use of PD in high-risk populations, peritonitis and other catheter-related problems, adequacy of dialysis and nutrition, patient outcomes in comparison with hemodialysis, and peritoneal membrane changes with time on PD. Topics that have emerged during the last decade and the challenges for the next decennium are discussed. The great importance of quality assurance in fast-growing PD populations and of prevention of long-term membrane alterations are emphasize

Dry Body Weight: Water and Sodium Removal Targets in PD

BACKGROUND/AIMS: Cardiovascular mortality is high in peritoneal dialysis patients. This may be due to the presence of hypertension and fluid overload. Dietary intake of water and sodium are likely to be important, especially in anuric patients. METHODS: A review of the literature on assessment of fluid status, and on peritoneal removal of water and sodium. RESULTS: MF-BIA added to clinical judgement is helpful for the assessment of fluid status. Natriuretic hormones in patients without heart failure are promising, but their value in clinical practice has not been established yet. Peritoneal ultrafiltration and sodium removal in anuric peritoneal dialysis patients are associated with survival. APD patients have lower sodium removal than CAPD, icodextrin increases it. The value of routine use of low sodium dialysis solutions has not been established. Definite targets on fluid and sodium removal have not been established, but the maintenance of euvalemia, while reducing the exposure to 3.86% glucose solutions at the same time, is largely facilitated by dietary salt and water restrictions. CONCLUSION: MF-BIA is a useful addition to clinical judgement of hydration status. The use of high dose loop diuretics facilitates water and salt removal in the presence of residual renal function. A dietary salt restriction of 4 g/day in anuric patients improves hypertension and is likely to reduce fluid intak

Corrigendum: Aging of the Peritoneal Dialysis Membrane(Front. Physiol., (2022), 13, (885802), 10.3389/fphys.2022.885802)

In the original article, there was an error. A remark at the end of Combinations of Osmotic Agents could be interpreted as an expression of criticism of the scientific content of specific cited papers, which was never the intention. A correction has been made to Prevention and Treatment, Combinations of Osmotic Agents, final sentence. The corrected sentence appears below: It should be appreciated, however, that ref (Bonomini et al., 2021; Masola et al., 2021; Rago et al., 2021) were not published in any of the 72-nephrology journals, but rather in journals owned by the same publisher of many online journals. This should not be regarded as disqualifying the scientific value of these cited papers, but it underlines the importance of the results of the multicenter clinical trial. The author apologizes for this error and states that this does not change the scientific conclusions of the article in any way. The original article has been updated