| 1. |
|
|
| 2. |
- Al-Hwiesh, AK, et al.
(författare)
-
Metformin in peritoneal dialysis: a pilot experience
- 2014
-
Ingår i: Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. - : SAGE Publications. - 1718-4304 .- 0896-8608. ; 34:4, s. 368-375
-
Tidskriftsartikel (refereegranskat)abstract
- In a number of patients, the antidiabetic drug metformin has been associated with lactic acidosis. Despite the fact that diabetes mellitus is the most common cause of end-stage renal disease (ESRD) and that peritoneal dialysis (PD) is an expanding modality of treatment, little is known about optimal treatment strategies in the large group of PD patients with diabetes. In patients with ESRD, the use of metformin has been limited because of the perceived risk of lactic acidosis or severe hypoglycemia. However, metformin use is likely to be beneficial, and PD might itself be a safeguard against the alleged complications. Methods Our study involved 35 patients with insulin-dependent type 2 diabetes [median age: 54 years; interquartile range (IQR): 47–59 years] on automated PD (APD) therapy. Patients with additional risk factors for lactic acidosis were excluded. Metformin was introduced at a daily dose in the range 0.5 – 1.0 g. All patients were monitored for glycemic control by blood sugar levels and HbA1c. Plasma lactic acid levels were measured weekly for 4 weeks and then monthly to the end of the study. Plasma and effluent metformin and plasma lactate levels were measured simultaneously. Results In this cohort, the median duration of diabetes was 18 years (IQR: 14 – 21 years), median time on PD was 31 months (IQR: 27 – 36 months), and median HbA1c was 6.8% (IQR: 5.9% – 6.9%). At metformin introduction and at the end of the study, the median anion gap was 11 mmol/L (IQR: 9 – 16 mmol/L) and 12 mmol/L (IQR: 9 – 16 mmol/L; p > 0.05) respectively, median pH was 7.33 (IQR: 7.32 – 7.36) and 7.34 (IQR: 7.32 – 7.36, p > 0.05) respectively, and mean metformin concentration in plasma and peritoneal fluid was 2.57 ± 1.49 mg/L and 2.83 ± 1.7 mg/L respectively. In the group overall, mean lactate was 1.39 ± 0.61 mmol/L, and hyperlactemia (>2 mmol/L to 5 mmol/L) was found in 4 of 525 plasma samples (0.76%), but the patients presented no symptoms. None of the patients registered a plasma lactate level above 5 mmol/L. We observed no correlation between plasma metformin and plasma lactate ( r = 0.27). Conclusions Metformin may be used with caution in APD patients with insulin-dependent type 2 diabetes. Although our study demonstrated the feasibility of metformin use in APD, it was not large enough to demonstrate safety; a large-scale study is needed.
|
|
| 3. |
- Al-Hwiesh, AK, et al.
(författare)
-
Prevention of peritoneal dialysis catheter infections in Saudi peritoneal dialysis patients: the emergence of high-level mupirocin resistance
- 2013
-
Ingår i: The International journal of artificial organs. - : SAGE Publications. - 1724-6040 .- 0391-3988. ; 36:7, s. 473-483
-
Tidskriftsartikel (refereegranskat)abstract
- Exit-site infection (ESI) and peritonitis remain the major causes of morbidity and mortality in peritoneal dialysis (PD) patients. This study compared the effectiveness of local mupirocin ointment and gentamicin cream in preventing both gram-positive and gram-negative bacterial infections in PD patients. Methods Patients from two centers (n = 203) were assigned to daily mupirocin ointment or gentamicin cream application. Infections were tracked prospectively by organisms and expressed as episodes per patient-year for both ESI and peritonitis. Results The rate of gram-positive ESI was 0.31/episode/patient-year and 0.22 episodes/patient-year (p<0.05), whereas the rate of gram-negative ESI was 0.28 episode/patient-year and 0.11 episode/patient-year (p<0.01) in the mupirocin group and gentamicin group, respectively. Gram-positive ESI occurred in 17.1% vs 10.2% of patients (p<0.05), whereas 20% of and 5.1% of patients (p<0.001) had gram-negative ESI in the 2 groups respectively. S.aureus was cultured at exit-site in the mupirocin group in 27.8% patients, 60% (16.7% of the total Gram-positive isolates) of them being with high-level mupirocin-resistance. Pseudomonas aeruginosa was cultured in 21.8% of ESI in the mupirocin group, and in only 6.7% in the gentamicin group (p<0.01). Peritonitis rates were lower using gentamicin cream, 0.17 episode/patient-year compared with mupirocin, 0.39 episode/patient-year (p<0.01). With multivariate analysis, only gentamicin exit-site use was a significant predictor for lower catheter infection rate. Conclusion Prolonged use of mupirocin for ESI-prophylaxis is associated with the emergence of mupirocin-resistant S. aureus. Gentamicin cream is superior to mupirocin ointment in the prevention of PD catheter infections.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Bonomini, M, et al.
(författare)
-
How to Improve the Biocompatibility of Peritoneal Dialysis Solutions (without Jeopardizing the Patient's Health)
- 2021
-
Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 22:15
-
Tidskriftsartikel (refereegranskat)abstract
- Peritoneal dialysis (PD) is an important, if underprescribed, modality for the treatment of patients with end-stage kidney disease. Among the barriers to its wider use are the deleterious effects of currently commercially available glucose-based PD solutions on the morphological integrity and function of the peritoneal membrane due to fibrosis. This is primarily driven by hyperglycaemia due to its effects, through multiple cytokine and transcription factor signalling—and their metabolic sequelae—on the synthesis of collagen and other extracellular membrane components. In this review, we outline these interactions and explore how novel PD solution formulations are aimed at utilizing this knowledge to minimise the complications associated with fibrosis, while maintaining adequate rates of ultrafiltration across the peritoneal membrane and preservation of patient urinary volumes. We discuss the development of a new generation of reduced-glucose PD solutions that employ a variety of osmotically active constituents and highlight the biochemical rationale underlying optimization of oxidative metabolism within the peritoneal membrane. They are aimed at achieving optimal clinical outcomes and improving the whole-body metabolic profile of patients, particularly those who are glucose-intolerant, insulin-resistant, or diabetic, and for whom daily exposure to high doses of glucose is contraindicated.
|
|
| 8. |
- Bonomini, M, et al.
(författare)
-
The osmo-metabolic approach: a novel and tantalizing glucose-sparing strategy in peritoneal dialysis
- 2021
-
Ingår i: Journal of nephrology. - : Springer Science and Business Media LLC. - 1724-6059 .- 1121-8428. ; 34:2, s. 503-519
-
Tidskriftsartikel (refereegranskat)abstract
- Peritoneal dialysis (PD) is a viable but under-prescribed treatment for uremic patients. Concerns about its use include the bio-incompatibility of PD fluids, due to their potential for altering the functional and anatomical integrity of the peritoneal membrane. Many of these effects are thought to be due to the high glucose content of these solutions, with attendant issues of products generated during heat treatment of glucose-containing solutions. Moreover, excessive intraperitoneal absorption of glucose from the dialysate has many potential systemic metabolic effects. This article reviews the efforts to develop alternative PD solutions that obviate some of these side effects, through the replacement of part of their glucose content with other osmolytes which are at least as efficient in removing fluids as glucose, but less impactful on patient metabolism. In particular, we will summarize clinical studies on the use of alternative osmotic ingredients that are commercially available (icodextrin and amino acids) and preclinical studies on alternative solutions under development (taurine, polyglycerol, carnitine and xylitol). In addition to the expected benefit of a glucose-sparing approach, we describe an ‘osmo-metabolic’ approach in formulating novel PD solutions, in which there is the possibility of exploiting the pharmaco-metabolic properties of some of the osmolytes to attenuate the systemic side effects due to glucose. This approach has the potential to ameliorate pre-existing co-morbidities, including insulin resistance and type-2 diabetes, which have a high prevalence in the dialysis population, including in PD patients.
|
|
| 9. |
|
|
| 10. |
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
|
|
| 15. |
- Davies, SJ, et al.
(författare)
-
Icodextrin improves the fluid status of peritoneal dialysis patients: Results of a double-blind randomized controlled trial
- 2003
-
Ingår i: Journal of the American Society of Nephrology. - 1046-6673. ; 14:9, s. 2338-2344
-
Tidskriftsartikel (refereegranskat)abstract
- Worsening fluid balance results in reduced technique and patient survival in peritoneal dialysis. Under these conditions, the glucose polymer icodextrin is known to enhance ultrafiltration in the long dwell. A multicenter, randomized, double-blind, controlled trial was undertaken to compare icodextrin versus 2.27% glucose to establish whether icodextrin improves fluid status. Fifty patients with urine output <750 ml/d, high solute transport, and either treated hypertension or untreated BP >140/90 mmHg, or a requirement for the equivalent of all 2.27% glucose exchanges, were randomized 1: 1 and evaluated at 1, 3, and 6 mo. Members of the icodextrin group lost weight, whereas the control group gained weight. Similar differences in total body water were observed, largely explained by reduced extracellular fluid volume in those receiving icodextrin, who also achieved better ultrafiltration and total sodium losses at 3 mo (P < 0.05) and had better maintenance of urine volume at 6 mo (P = 0.039). In patients fulfilling the study's inclusion criteria, the use of icodextrin, when compared with 2.27% glucose, in the long exchange improves fluid removal and status in peritoneal dialysis. This effect is apparent within I mo of commencement and was sustained for 6 mo without harmful effects on residual renal function.
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
|
|
| 20. |
|
|
| 21. |
|
|
| 22. |
|
|
| 23. |
|
|
| 24. |
|
|
| 25. |
- Divino, JC, et al.
(författare)
-
Glutamate concentration in plasma, erythrocyte and muscle in relation to plasma levels of insulin-like growth factor (IGF)-I, IGF binding protein-1 and insulin in patients on haemodialysis
- 1998
-
Ingår i: The Journal of endocrinology. - : Bioscientifica. - 0022-0795 .- 1479-6805. ; 156:3, s. 519-527
-
Tidskriftsartikel (refereegranskat)abstract
- Elevated insulin-like growth factor binding protein (IGFBP) levels, including IGFBP-1, occur in renal failure, and may contribute towards reduced IGF bioactivity in uraemia. The reduced IGF bioactivity may, in turn, contribute towards the disturbances in protein metabolism present in renal failure. In this study, the relationships between intra- and extracellular amino acid (AA) levels and IGF-I and/or IGFBP-1 levels were studied in 30 adult patients (aged 24-70 years) on haemodialysis who had no clinical signs of malnutrition. Blood samples (n = 30) and muscle biopsies (n = 13) were collected for determination of free AA in erythrocytes (RBC), plasma and muscle by reverse-phase HPLC while IGFBP-1, IGF-I and insulin plasma levels were determined by radioimmunoassay The patients on haemodialysis had elevated glutamate concentrations in RBC and plasma compared with healthy controls (524 +/- 26 vs 448 +/- 17 mumol/l, P < 0.05 and 45 +/- 4 vs 32 +/- 4 mumol/l, P < 0.01 respectively), although glutamate levels in muscle were within the normal range. The mean IGF-I level was slightly increased (s.d. score +0.74 +/- 0.30) but insulin levels were within the normal range. IGFBP-1 levels, which were inversely correlated to insulin (r = -0.40, P < 0.02), were elevated threefold compared with controls. No plasma AA level displayed a significant correlation with IGF-I, IGFBP-1 or insulin levels. However, glutamate concentrations in RBC were positively correlated to IGFBP-1 (r = 0.51, P < 0.01) and inversely correlated to IGF-I (r = -0.46. P < 0.01), although unrelated to insulin. Muscle glutamate, which was inversely related to RBC glutamate, displayed an opposite pattern with an inverse relation to IGFBP-1 levels (r = - 0.73, P < 0.01) and a positive correlation to IGF-I levels (r = 0.64, P < 0.02). Glutamate was the only AA to display an inverse correlation between RBC and muscle (r = -0.65, P < 0.02, n = 12). These findings lead us to propose that, in uraemia, the elevated IGFBP-I levels, which reduce the bioavailability of IGFs, are linked to glutamate uptake in muscle, resulting in accumulation of RBC glutamate. Whether there is a causal relationship or the correlation is due to some common regulator is not clarified in the present study.
|
|
