Nephron Clinical Practice最新文献

Background/aims: There is disagreement regarding the performance of conventional optical microscopy to assess the origin of hematuria. The aim of this study was to determine the optimal cutoff point for dysmorphic cells in order to detect glomerular hematuria by optical and phase-contrast microscopy.

Methods: In total, 131 urine samples (66 from patients with glomerulopathies and 65 from nephrolithiasis patients) were evaluated in a blinded fashion. The percentages of doughnut cells and acanthocytes were verified by optical and phase-contrast microscopy. A total of 131 patients were randomly allocated to the derivation (n = 73) and validation (n = 58) groups. Receiver-operating characteristic (ROC) curves were plotted to check the discriminatory power of each group and the best cutoff points were determined by the Youden index in the derivation group and subsequently tested in the validation group.

Results: All areas under the ROC curve (AUCs) were statistically significant using both methods (conventional optical and phase-contrast microscopy) and both groups (derivation and validation). AUCs did not differ between different glomerulopathies. The best cutoff point to determine the glomerular origin of hematuria by total dysmorphic cells was 22% using an optical conventional microscope and 40% by phase-contrast microscopy.

Conclusion: We determined the best cutoff points to interpret erythrocyte dysmorphism and demonstrated that it is possible to discriminate the origin of hematuria by evaluating erythrocyte dysmorphism in urinalysis using either an optical or a phase-contrast microscope.

Due to improvements in socioeconomic development and increased life expectancy, the proportion of older people in the general population is increasing worldwide. While this trend is something to celebrate, it also brings with it challenges for health care systems. One particular challenge is an increase in chronic kidney disease, the prevalence of which is higher in older people. This article reviews the key links between kidney function, age, health and illness, and discusses the implications of the ageing population for the care of people with chronic kidney disease.

Aims: Increased pulse pressure (PP) is associated with increased cardiovascular mortality in haemodialysis (HD) patients. Autonomic imbalance is common in HD patients and predisposes to sudden cardiac death, but its relationship to PP is unknown. We investigated the relationship between cardiac autonomic modulation assessed by heart rate variability (HRV) and PP in HD patients.

Methods: Continuous electrocardiograms recorded during HD sessions were repeated 5 times at 2-week intervals in stable HD patients. The high-frequency (HF) and low-frequency (LF) components and the LF/HF ratio of HRV were calculated during the first and last hour of the recordings. These values and the corresponding systolic blood pressure (SBP), diastolic blood pressure (DBP) and PP measurements were averaged in repeated recordings of each patient.

Results: Seventy-six patients were included in the final analysis (aged 61 ± 15 years, 32% females, 37% diabetics). In male patients, LF/HF correlated inversely with pre- and post-HD PP (r = -0.369, p = 0.007 and r = -0.546, p = 0.000, respectively), positively with pre- and post-HD DBP (r = 0.358, p = 0.009 and r = 0.306, p = 0.028, respectively) and inversely with post-HD SBP (r = -0.350, p = 0.011). In female patients, LF/HF correlated positively with post-HD SBP (r = 0.422, p = 0.040).

Conclusion: We observed an association between PP and HRV in male HD patients. Sex differences may be important for cardiac risk assessment.

Background/aims: An acid-base imbalance precedes renal disease progression in patients with chronic kidney disease (CKD). Little is known about the effects of a low-salt diet (LSD) on net endogenous acid production (NEAP) levels in CKD patients using angiotensin receptor blockade.

Methods: We enrolled a total of 202 nondiabetic CKD patients who underwent an 8-week treatment with olmesartan from the original trial [Effects of Low Sodium Intake on the Antiproteinuric Efficacy of Olmesartan in Hypertensive Patients with Albuminuria (ESPECIAL) trial: NCT01552954]. The patients were divided into good- and poor-LSD-compliance groups.

Results: During the interventional 8 weeks, the NEAP in the good-compliance group increased compared to the control group (12.9 ± 32.0 vs. -2.0 ± 35.0 mmol/day, p = 0.002). NEAP was positively associated with the good-LSD-compliance group in the fully adjusted analyses (r = 0.135, p = 0.016). The additional reduction of 2.39 g/day of protein intake with a reduction of 1 g/day of salt intake did not increase the NEAP under angiotensin II receptor blockade (ARB) treatment with an LSD (r = 0.546, p < 0.001).

Conclusion: We found that an LSD may increase the NEAP in nondiabetic CKD patients using ARB, which suggests that additional acid producing-protein restriction should be required to prevent the NEAP from rising.

Background/aims: The assessment of myocardial fatty acid metabolism impairment by single-photon emission computed tomography (SPECT) using (123)I-β-methyliodophenyl-pentadecanoic acid (BMIPP) might predict the risk of cardiac death in hemodialysis patients. We investigated the potential of oral nicorandil to improve myocardial fatty acid metabolism after percutaneous coronary intervention (PCI) in this population.

Methods: We evaluated 128 hemodialysis patients who had obtained coronary revascularization by PCI (90 men and 38 women, 66 ± 9 years). Participants for the analysis were randomly assigned to either the nicorandil (n = 63) or control group (n = 65). BMIPP SPECT was performed every year after coronary revascularization by PCI. Uptake on SPECT was graded in 17 segments on a 5-point scale (0, normal; 4, absent) and assessed as BMIPP summed scores (SS).

Results: The incidence of cardiac death was lower (p = 0.004) in the nicorandil group (7/63, 11.1%) than in the control group (21/65, 32.3%) during a mean follow-up of 2.7 ± 1.4 years. BMIPP SS reduction rates improved in the nicorandil group compared with the control group from 3 years of administration. In Kaplan-Meier analyses, free survival rate of cardiac death was higher in patients with a ≥20% BMIPP SS reduction rate as compared with those with a <20% BMIPP SS reduction rate (p = 0.0001). In multiple logistic analysis, oral administration of nicorandil was associated with ≥20% reduction rates of BMIPP SS (odds ratio 2.823, p = 0.011).

Conclusion: Long-term oral administration of nicorandil may improve impaired myocardial fatty acid metabolism after coronary revascularization by PCI in hemodialysis patients.

Background/aim: End-stage renal disease patients require resources for emergent and inpatient care in addition to ambulatory dialysis. There are two dialysis modalities and settings which patients switch between. Our aim was to characterize the patterns and reasons for switching, as well as the emergent and inpatient utilization of these patients at the University Health Network.

Methods: Patients who received chronic dialysis between March 1, 2006, and April 30, 2011, were identified. Utilization was measured by emergency department (ED) visits, inpatient hospitalizations, and bed-days occupied per year.

Results: Out of 576 patients identified, 18.6% switched modality and/or setting. The majority of switches occurred during the first year of dialysis. Patients who switched had increased utilization compared to those on a continuous modality/setting. Overall, patients had a median rate of 0.91 ED visits per patient-year, compared to 1.56 for patients who switched modality and setting. Median inpatient bed resource requirement was 4.46 bed-days/patient-year overall, compared to 8.91 for patients who switched modality and setting.

Conclusions: Emergent and inpatient utilization is related to the setting and modality of dialysis, although differences are partly explained by comorbidities. Patients who switch modalities use more resources and may be a prime population for interventions.

Background: Recent studies have shown that hyperuricemia is an independent risk factor for cardiovascular disease. However, few studies have examined whether hyperuricemia is a risk factor for chronic kidney disease (CKD), so to investigate the significance of hyperuricemia as a risk factor for CKD, we analyzed data collected in annual health check-ups.

Methods: The data of 11,048 subjects who underwent an annual health check-up were analyzed in cross-sectional and longitudinal studies.

Results: After adjustment for covariate factors, a multivariate logistic regression analysis showed that age, systolic blood pressure, diastolic blood pressure, LDL-cholesterol, triglyceride, HbA1c, and uric acid (hazard ratio: 1.66) were independently and significantly associated with CKD. We also analyzed the data of 1,652 subjects who underwent annual health check-ups for 5 consecutive years. Over that 5-year period, 93 subjects developed CKD. We compared the baseline data of the subjects who developed CKD with the data of those who did not, and we found significant between-group differences in gender, age, HDL-cholesterol, the estimated glomerular filtration rate, and uric acid. After adjustment for several covariate factors, a multivariate Cox regression analysis showed that only age and hyperuricemia (hazard ratio: 1.36) were independent risk factors for the development of CKD.

Conclusions: We found that hyperuricemia is an independent risk factor for the development of CKD.

Background/aims: JTT-751 (ferric citrate hydrate) is a novel iron-based phosphate approved in Japan for the treatment of hyperphosphatemia in dialysis and nondialysis patients with chronic kidney disease.

Methods: In this phase 3, multicenter, open-label, dose-adjusted study, we investigated the efficacy and safety of JTT-751 in peritoneal dialysis patients. A total of 56 patients with serum phosphate ≥5.6 and <10.0 mg/dl were enrolled in the study. The dose of JTT-751 was adjusted to between 1.5 and 6.0 g/day, according to the target range of serum phosphate (3.5-5.5 mg/dl), for 12 weeks. The primary endpoint was change in serum phosphate from baseline to end of treatment. Secondary endpoints included the percentage of patients achieving target serum phosphate levels and changes in intact parathyroid hormone.

Results: Serum phosphate was significantly reduced by 2.26 mg/dl (p < 0.001). The percentage of patients achieving target serum phosphate levels was 76.8%. Intact parathyroid hormone decreased significantly (p < 0.001). The most common adverse drug reactions were diarrhea and constipation. Most of the events were considered to be mild. Treatment with JTT-751 resulted in significant increases in serum ferritin and transferrin saturation (p < 0.001).

Conclusion: In peritoneal dialysis patients with hyperphosphatemia, 12-week treatment with JTT-751 resulted in significant reductions in serum phosphate while simultaneously increasing serum iron parameters. JTT-751 was well tolerated.

Introduction: Simple peritoneal fibrosis and encapsulating peritoneal sclerosis (EPS) are important lesions in the peritoneum of patients on peritoneal dialysis (PD). We have previously described a population of podoplanin-positive myofibroblasts in peritoneal biopsies from patients with EPS. Platelet-derived growth factor receptor-β (PDGFRβ) is a marker of pericytes, and PDGFs might be involved in the fibrotic response of the peritoneum. This study aimed to describe PDGFRβ in the human peritoneum.

Methods: In this retrospective analysis, we localized PDGFRβ in peritoneal biopsies from patients with EPS (n = 6) and patients on PD without signs of EPS (n = 5), and compared them with normal peritoneum (n = 4) and peritoneum from uremic patients (n = 5). Consecutive sections were stained for smooth-muscle actin (SMA) and podoplanin. Slides were scored semiquantitatively by 2 observers blinded to the diagnosis.

Results: PDGFRβ was expressed by cells of arterial walls in all biopsies. A prominent population of PDGFRβ-positive cells was present in the normal peritoneum, which were SMA negative on consecutive sections. In patients on PD, a high number of PDGFRβ were also positive for SMA. In EPS, the majority of podoplanin-positive cells were positive for PDGFRβ. In peritoneal biopsies from normal and uremic patients, the expression of SMA was mainly restricted to cells of arterial walls. Podoplanin expression was restricted to lymphatic vessels in normal peritoneum, in uremic patients, and in patients on PD without EPS.

Conclusions: As podoplanin-positive myofibroblasts express PDGFRβ, these cells might be related to pericytes (rather than other sources of fibroblasts). PDGFRβ might turn out to be a therapeutic target in EPS.

Background: Sclerostin is a potent inhibitor of bone formation, but the meaning of its serum levels remains undetermined. We evaluated the association between sclerostin levels and clinical or biological data in hemodialyzed patients (HD), notably parathormone (PTH), biomarkers of bone turnover, vascular calcifications and mortality after 2 years.

Methods: 164 HD patients were included in this observational study. The calcification score was assessed with the Kauppila method. Patients were followed for 2 years.

Results: Median sclerostin levels were significantly (p < 0.0001) higher in HD versus healthy subjects (n = 94) (1,375 vs. 565 pg/ml, respectively). In univariate analysis a significant association (p < 0.05) was found between sclerostin and age, height, dialysis vintage, albumin, troponin, homocysteine, PTH, C-terminal telopeptide of collagen type I, bone-specific alkaline phosphatase and osteoprotegerin, but not with the calcification score. In a multivariate model, the association remained with age, height, dialysis vintage, troponin, homocysteine, phosphate, PTH, but also with vascular calcifications. Association was positive for all variables, except PTH and vascular calcifications. The baseline sclerostin concentration was not different in survivors and non-survivors.

Conclusions: We confirm a higher concentration of sclerostin in HD patients, a positive association with age and a negative association with PTH. A positive association with phosphate, homocysteine and troponin calls for additional research. The clinical interest of sclerostin to assess vascular calcifications in HD is limited and no association was found between sclerostin and mortality.