The Long-Term Survival Outcome in Older Patients with Different Pathological Types of Chronic Kidney Disease.

INTRODUCTION: Chronic kidney diseases (CKDs) are prevalent in older people, and renal pathological manifestations are important for diagnosis, treatment, and prognosis. However, the long-term survival outcome and risk factors for older CKD patients with different pathological types are not fully understood and need to be further investigated. METHODS: Medical data were recorded and all-cause mortality was followed up in patients who underwent renal biopsy diagnosed in Guangdong Provincial People's Hospital from 2005 to 2015. Kaplan-Meier analysis was used to identify the incidence of survival outcomes. Multivariate Cox regression models and nomograms were applied to analyze pathological types and other factors for overall survival outcomes. RESULTS: 368 cases were included and the median follow-up was 85 (46.5, 111) months. Overall mortality was 35.6%. The highest mortality was in the mesangioproliferative glomerulonephritis (MPGN) group (88.9%), followed by amyloidosis (AMY) group (84.6%), and the lowest mortality was in the minimal change disease (MCD) group (21.9%). Moreover, multivariate Cox regression model showed that survival times of MPGN {hazard ratio (HR) = 8.215 (95% confidence interval [CI]: 2.735-24.674), p < 0.001} and AMY (HR = 6.130 [95% CI: 2.219-16.94], p < 0.001) were significantly shorter than MCD. In addition, age, lower baseline estimated glomerular filtration rate (eGFR), history of chronic obstructive pulmonary disease (COPD) and cerebrovascular accidents (CVA)/transient ischemic attack (TIA), MPGN, and AMY were independent risk factors for the mortality of older patients with CKD. CONCLUSION: The long-term survival outcome of older CKD patients showed differences among different pathological types, and MPGN, AMY, age, baseline eGFR, CVA/TIA, and COPD were independent predictors for mortality.

Hospital-Acquired Acute Kidney Injury in Older Patients: Clinical Characteristics and Drug Analysis.

BACKGROUND: Information on older patients with hospital-acquired acute kidney injury (HA-AKI) and use of drugs is limited. AIM: This study aimed to assess the clinical characteristics, drug uses, and in-hospital outcomes of hospitalized older patients with HA-AKI. METHODS: Patients aged ≥65 years who were hospitalized in medical wards were retrospectively analyzed. The study patients were divided into the HA-AKI and non-AKI groups based on the changes in serum creatinine. Disease incidence, risk factors, drug uses, and in-hospital outcomes were compared between the groups. RESULTS: Of 26,710 older patients in medical wards, 4,491 (16.8%) developed HA-AKI. Older patients with HA-AKI had higher rates of multiple comorbidities and Charlson Comorbidity Index score than those without AKI (p < 0.001). In the HA-AKI group, the proportion of patients with prior use of drugs with possible nephrotoxicity was higher than that of patients with prior use of drugs with identified nephrotoxicity (p < 0.05). The proportions of patients with critical illness, use of nephrotoxic drugs, and the requirements of intensive care unit treatment, cardiopulmonary resuscitation, and dialysis as well as in-hospital mortality and hospitalization duration and costs were higher in the HA-AKI than the non-AKI group; these increased with HA-AKI severity (all p for trend <0.001). With the increase in the number of patients with continued use of drugs with possible nephrotoxicity after HA-AKI, the clinical outcomes showed a tendency to worsen (p < 0.001). Moreover, HA-AKI incidence (adjusted odds ratio [OR], 10.26; 95% confidence interval (CI), 8.27-12.74; p < 0.001), and nephrotoxic drugs exposure (adjusted OR, 1.76; 95% CI, 1.63-1.91; p < 0.001) had an association with an increased in-hospital mortality risk. CONCLUSION: AKI incidence was high among hospitalized older patients. Older patients with HA-AKI had worse in-hospital outcomes and higher resource utilization. Nephrotoxic drug exposure and HA-AKI incidence were associated with an increased in-hospital mortality risk.

[The role of TGF-beta1/Smads in the development of peritoneal fibrosis induced by high glucose peritoneal dialysate and LPS].

OBJECTIVE: To investigate the expression and the potential role of TGF-beta/Smads in peritoneal fibrosis induced by high glucose dialysate and LPS in rats. METHODS: 24 male Sprague-Dawley rats were randomly allocated into four groups: control group, normal rats; LPS group: rats were treated with intraperitoneal injection of LPS (0.6 mg/kg body weight) on days 1, 3, 5, 7; dialysate Group: rats were treated with daily intraperitoneal injection of 4.25% peritoneal dialysate (100 ml/kg body weight) for 4 weeks; LPS + dialysate Group: daily intraperitoneal injection of 4.25% dialysate combined with four times injection of LPS (0.6 mg/kg body weight on days 1, 3, 5, 7) for 4 weeks. The parietal thickness was measured with masson stain. The expression of alpha-SMA, TGF-beta1, Smad 2/3, Smad 7 and ColI in peritoneal membrane was detected with confocal microscope by immuno-fluorescence, Western-blot and RT-PCR. RESULTS: Masson stain show the parietal thickness of the rats in all groups was significantly increased compared with control group and collagen deposition was evident in the thickened submesothelial compact zone. Parietal thickness of the rats in LPS + dialysate Group was most (vs LPS group: 41.5 +/- 3.3 microm vs 34.70 +/- 3.6 microm, P = 0.007, vs dialysate Group, 41.5 +/- 3.3 microm vs 20.2 +/- 3.6 microm, P = 0.000). The expression of alpha-SMA, Col I, TGF-beta1, Smad 3 was up-regulated in protein and mRNA level and the protein level of phosphorylated-Smad 2/3 was increased significantly. The most significant changes were found in LPS + dialysate Group. Compared with control group the mRNA and protein level of Smad7 was increased, but the protein ratio of phosphorylated Smad/Smad 7 in all groups was higher. Under electro-microscope, the mesothelial cells in LPS + dialysate Group had myofibroblast morphology with the presence of large bundles of actin microfilaments and dense bodies within the cytoplasm. CONCLUSIONS: High concentration glucose dialysate or LPS contributes to peritoneal fibrosis by stimulating TGF-beta/Smads signaling. 4.25% peritoneal dialysate can coordinate with LPS to activate TGF-beta/Smads signaling pathway and induce mesenchymal transdifferentiation and peritoneal fibrosis.