scholarly journals Effects of sucroferric oxyhydroxide and sevelamer carbonate on chronic kidney disease–mineral bone disorder parameters in dialysis patients

2018 ◽  
Vol 34 (7) ◽  
pp. 1163-1170 ◽  
Author(s):  
Markus Ketteler ◽  
Stuart M Sprague ◽  
Adrian C Covic ◽  
Anjay Rastogi ◽  
Bruce Spinowitz ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Formation ◽  
Phosphate Binders ◽  
Dialysis Patients ◽  
Post Hoc Analysis ◽  
Sevelamer Carbonate ◽  
Bone Disorder ◽  
Fgf 23 ◽  
Post Hoc

Abstract Background Treatment of hyperphosphataemia is the primary goal of chronic kidney disease–mineral and bone disorder (CKD-MBD) management. This post hoc analysis of a randomized, Phase 3 study evaluated the effects of 1-year treatment with the phosphate binders sucroferric oxyhydroxide or sevelamer carbonate (‘sevelamer’) on CKD-MBD indices among dialysis patients with hyperphosphataemia. Methods After a 2- to 4-week washout from previous phosphate binders, 1059 patients were randomized 2:1 to sucroferric oxyhydroxide 1.0–3.0 g/day (n = 710) or sevelamer 2.4–14.4 g/day (n = 349) for up to 24 weeks. Eligible patients enrolled in a 28-week extension. This post hoc analysis was performed for patients who completed ≥1 year of continuous treatment (n = 549). As the treatment groups showed similar CKD-MBD outcomes, the data were pooled for this analysis. Results Phosphate-binder therapy was associated with significant and sustained 30% reductions in serum phosphorus (P < 0.001). Median intact fibroblast growth factor-23 (FGF-23) also significantly decreased (P < 0.001) by 64% over 1 year. Intact parathyroid hormone decreased significantly after 24 weeks (P < 0.001), but levels returned to near baseline values by Week 52; minimal changes in serum calcium were observed. Of the bone resorption markers evaluated, tartrate-resistant acid phosphatase 5b (TRAP5b) decreased significantly (P < 0.001), whereas CTx increased transiently but returned to baseline levels by Week 52. The bone formation markers bone-specific alkaline phosphatase and osteocalcin both increased over 1 year of treatment. Conclusions Overall, 1 year of sucroferric oxyhydroxide or sevelamer treatment significantly reduced serum FGF-23, which has been associated with clinical benefit in patients with CKD. The trend towards increased bone formation marker levels indicates a beneficial effect on bone metabolism.

P0889TO WHAT EXTENT CAN WE ACHIEVE MINERAL BONE METABOLISM TREATMENT TARGETS AS SUGGESTED BY UPDATED 2017 KDIGO GUIDELINES IN PATIENTS WITH PREDIALYSIS CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mevlut Tamer Dincer ◽  
Şeyda Gül Özcan ◽  
Selma Alagoz ◽  
Cebrail Karaca ◽  
Sibel Gulcicek ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Phosphate Binders ◽  
Time Points ◽  
Therapeutic Inertia ◽  
Mineral Bone Disorder ◽  
Bone Disorder ◽  
Kdigo Guidelines ◽  
Data Point

Abstract Background and Aims The mineral bone disorder is an essential problem in chronic kidney disease (CKD). It is an independent modifiable risk factor for renal damage progression and CKD related mortality. Therefore, it is important to treat chronic kidney disease mineral bone disorder (CKD-MBD) according to international guidelines. Data on the management of mineral bone disorders in predialysis patients is scarce. We aimed to investigate the proportion of CKD-MBD patients reaching targets suggested by the updated 2017 KDIGO guidelines. Method We performed a multicenter cross-sectional study. We recruited consecutive adult (&gt;18 years of age) CKD 3-5 patients who were on regular nephrology outpatient clinic follow up. Patients who have GFR loss over 30% in the last six months, patients with malignancy, and decreased life expectancy due to severe comorbid disease and patients on renal replacement therapy were excluded. Data were collected in two-time points: one during the recruitment (second data point) and one, three to six months prior to the current visit (first data point). Persistent laboratory abnormalities were defined by out of normal range values in both time points. Therapeutic inertia was calculated for hyperphosphatemia. It was defined as a lack of using phosphate binders despite hyperphosphatemia. Results We examined a total of 213 patients for 3 different nephrology outpatient clinics. Of these patients, 49.5 % were male, with a mean age of 64,9 ± 12,0 years. 51.7 % of the patients were diabetic, 78 % were hypertensive, and 20.1 % had a history of coronary artery disease. Laboratory values related to MBD are shown in Table 1. KDIGO guideline targets were not reached in 14.8%, 18.4%, 59.0%, 71.0% patients regarding Ca, P, PTH, and vitamin D in the first visit. The targets were not reached in 15.0%, 19,2%, 61,2%, 81% patients regarding Ca, P, PTH, and vitamin D in the second visit. Persistence of out of target values were observed in 5.8%, 9.9%, 49.2% and 65.4% of the patients for Ca,P, PTH and Vitamin D respectively. The prevalence of therapeutic inertia for hyperphosphatemia was 34,4 % in the second visit Conclusion Regarding KDIGO guidelines, MBD is not optimally managed in predialysis CKD patients. Clinicians should have an active attitude regarding the correction of MBD even at the earlier stages of CKD.

Renal Osteodystrophy in Peritoneal Dialysis: Special Considerations

2008 ◽  
Vol 28 (2_suppl) ◽  
pp. 11-19 ◽  
Author(s):  
Ronen Levy ◽  
Anca Gal-Moscovici
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Peritoneal Dialysis ◽  
Kidney Disease ◽  
Renal Osteodystrophy ◽  
Bone Disease ◽  
Bone Lesion ◽  
Phosphate Binders ◽  
Vitamin D Metabolites ◽  
Bone Disorder

Bone disease is one of the most challenging complications in patients with chronic kidney disease. Today, it is considered to be part of a complex systemic disorder manifested by disturbances of mineral metabolism and vascular calcifications called chronic kidney disease – mineral bone disorder (CKD-MBD). The term renal osteodystrophy is reserved to define the specific bone lesion in CKD-MBD, whose spectrum ranges from high turnover to low turnover disease. Phosphate retention, decreased serum calcium, and 1,25-dihydroxy vitamin D synthesis are involved in the pathogenesis of high bone turnover. However, the various therapeutic approaches (calcium supplements, phosphate binders, and vitamin D metabolites, among others), the renal replacement modality (hemodialysis or continuous ambulatory peritoneal dialysis), and the types of patients to whom dialysis is offered (more patients who are diabetic or older, or both) may influence the evolution of the bone disorder. As a result, recent studies have reported a greater prevalence of adynamic forms of renal osteodystrophy, especially in diabetic and peritoneal dialysis patients. The present article reviews, for patients treated with peritoneal dialysis, the pathophysiologic mechanisms involved in the evolution and perpetuation of this bone disease and the therapeutic modalities for treating and preventing adynamic bone.

scholarly journals Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD)

2018 ◽  
Author(s):  
Marinella Ruospo ◽  
Suetonia C Palmer ◽  
Patrizia Natale ◽  
Jonathan C Craig ◽  
Mariacristina Vecchio ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Phosphate Binders ◽  
Mineral And Bone Disorder ◽  
Bone Disorder

scholarly journals FP152EFFECT OF BARDOXOLONE METHYL TREATMENT ON URINARY ALBUMIN IN PATIENTS WITH TYPE 2 DIABETES AND CHRONIC KIDNEY DISEASE - POST-HOC ANALYSIS FROM BEAM AND BEACON

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i27-i27
Author(s):  
Peter Rossing ◽  
Geoffrey Block ◽  
Glenn Chertow ◽  
Melanie Chin ◽  
Angie Goldsberry ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Urinary Albumin ◽  
Post Hoc Analysis ◽  
Post Hoc

scholarly journals Effects of canagliflozin on hyperkalaemia and serum potassium in people with diabetes and chronic kidney disease: insights from the CREDENCE trial

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
B L Neuen ◽  
M Oshima ◽  
V Perkovic ◽  
C Arnott ◽  
G Bakris ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Potassium ◽  
Sglt2 Inhibitor ◽  
Renin Angiotensin System ◽  
Renin Angiotensin ◽  
Post Hoc Analysis ◽  
Intention To Treat ◽  
Potassium Binders ◽  
Post Hoc

Abstract Background Hyperkalaemia is a common complication of type 2 diabetes mellitus (T2DM) and limits the optimal use of agents that block the renin-angiotensin aldosterone system (RAAS), particularly in patients with chronic kidney disease (CKD). In patients with CKD, sodium glucose cotransporter 2 (SGLT2) inhibitors provide cardiorenal protection, but whether they affect the risk of hyperkalaemia remains uncertain. Purpose We sought to assess the effect of canagliflozin on hyperkalaemia and other potassium-related outcomes in people with T2DM and CKD by conducting a post-hoc analysis of the CREDENCE trial. Methods The CREDENCE trial randomized 4401 participants with T2DM and CKD to the SGLT2 inhibitor canagliflozin or matching placebo. In this post-hoc analysis using an intention-to-treat approach, we assessed the effect of canagliflozin on a composite outcome of time to either investigator-reported hyperkalaemia or the initiation of potassium binders. We also analysed effects on central laboratory-determined hyper- and hypokalaemia (serum potassium ≥6.0 and &lt;3.5 mmol/L, respectively) and change in serum potassium. Results At baseline the mean serum potassium in canagliflozin and placebo arms was 4.5 mmol/L; 4395 (99.9%) participants were receiving renin angiotensin system blockade. Canagliflozin reduced the risk of investigator-reported hyperkalaemia or initiation of potassium binders (HR 0.78, 95% CI 0.64–0.95, p=0.014; Figure 1). The incidence of laboratory-determined hyperkalaemia was similarly reduced (HR 0.77, 95% CI 0.61–0.98, p=0.031; Figure 2); the risk of hypokalaemia (HR 0.92, 95% CI 0.71–1.20, p=0.53) was not increased. Mean serum potassium over time with canagliflozin was similar to that of placebo. Conclusion Among patients treated with RAAS inhibitors, SGLT2 inhibition with canagliflozin may reduce the risk of hyperkalaemia in people with T2DM and CKD without increasing the risk of hypokalaemia. FUNDunding Acknowledgement Type of funding sources: None. Figure 1 Figure 2

scholarly journals Ticagrelor monotherapy in patients with concomitant diabetes mellitus and chronic kidney disease: a post hoc analysis of the GLOBAL LEADERS trial

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Chao Gao ◽  
Mariusz Tomaniak ◽  
Kuniaki Takahashi ◽  
Hideyuki Kawashima ◽  
Rutao Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Primary Endpoint ◽  
Composite Endpoint ◽  
Bleeding Events ◽  
Post Hoc Analysis ◽  
Post Hoc ◽  
Type 3 ◽  
Q Wave

Abstract Background Patients with both diabetes mellitus (DM) and chronic kidney disease (CKD) are a subpopulation characterized by ultrahigh ischemic and bleeding risk after percutaneous coronary intervention. There are limited data on the impact of ticagrelor monotherapy among these patients. Methods In this post hoc analysis of the GLOBAL-LEADERS trial, the treatment effects of the experimental (one-month dual-antiplatelet therapy [DAPT] followed by 23-month ticagrelor monotherapy) versus the reference regimen (12-month DAPT followed by 12-month aspirin alone) were analyzed according to DM/CKD status. The primary endpoint was a composite endpoint of all-cause death or new Q-wave myocardial infarction at 2-years. The patient-oriented composite endpoint (POCE) was defined as the composite of all-cause death, any stroke, site-reported MI and any revascularization, whereas net adverse clinical events (NACE) combined POCE with BARC type 3 or 5 bleeding events. Results At 2 years, the DM + /CKD + patients had significantly higher incidences of the primary endpoint (9.5% versus 3.1%, adjusted HR 2.16; 95% CI [1.66–2.80], p < 0.001), BARC type 3 or 5 bleeding events, stroke, site-reported myocardial infraction, all revascularization, POCE, and NACE, compared with the DM-/CKD- patients. Among the DM + /CKD + patients, after adjustment, there were no significant differences in the primary endpoints between the experimental and reference regimen; however, the experimental regimen was associated with lower rates of POCE (20.6% versus 25.9%, HR 0.74; 95% CI [0.55–0.99], p = 0.043, pinteraction = 0.155) and NACE (22.7% versus 28.3%, HR 0.75; 95% CI [0.56–0.99], p = 0.044, pinteraction = 0.310), which was mainly driven by a lower rate of all revascularization, as compared with the reference regimen. The landmark analysis showed that while the experimental and reference regimen had similar rates of all the clinical endpoints during the first year, the experimental regimen was associated with significantly lower rates of POCE (5.8% versus 11.0%, HR 0.49; 95% CI [0.29–0.82], p = 0.007, pinteraction = 0.040) and NACE (5.8% versus 11.2%, HR 0.48; 95% CI [0.29–0.82], p = 0.007, pinteraction = 0.013) in the second year. Conclusion Among patients with both DM and CKD, ticagrelor monotherapy was not associated with lower rates of all-cause death or new Q-wave, or major bleeding complications; however, it was associated with lower rates of POCE and NACE. These findings should be interpreted as hypothesis-generating. Clinical Trial Registration: ClinicalTrials.gov (NCT01813435).

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