Impact of inpatient educational programs on mortality after the start of dialysis therapy.

BACKGROUND: Although inpatient educational programs (IEPs) for non-dialysis-dependent chronic kidney disease (CKD) have been reported to slow disease progression, their legacy effect on prognosis after the start of dialysis therapy is unclear. METHODS: Consecutive patients who started dialysis therapy between January 1, 2011 and December 31, 2018 were included in a single-center, retrospective, observational study. The patients were divided into two groups according to whether or not they participated in IEPs before dialysis introduction, and their background characteristics were compared. The survival rate for each group was calculated using the Kaplan-Meier method and compared by the log-rank test. Furthermore, the hazard ratio (HR) of IEP participation adjusted for confounding factors associated with mortality was calculated using Cox regression analysis. RESULTS: Of the 490 subjects (median age 69 years, 71.0% male), 129 patients (26.3%) participated in the IEP. At the start of dialysis, the IEP group had higher serum albumin (3.5 vs. 3.3 g/dL, p < 0.001) and lower serum total cholesterol levels (151 vs. 166 mg/dL, p = 0.0076) and the proportion of patients with independence in their daily living activities was high (p = 0.034). The median observation period was 3.4 years, during which 153 patients (31.2%) died. The 5-year survival rates were 81.0 and 61.5% in the IEP and non-IEP groups, respectively (p = 0.0038). Cox regression analysis revealed a HR for IEP of 0.57 (95% Confidence interval 0.37-0.88, p = 0.011). CONCLUSION: IEPs for CKD patients are associated with a more favorable prognosis after the start of dialysis.

Fact-finding survey on health literacy among Japanese predialysis chronic kidney disease patients: a multi-institutional cross-sectional study.

BACKGROUND: Low health literacy (HL) has been associated with poor chronic disease management and adverse outcomes. However, reports on HL in predialysis chronic kidney disease (CKD) patients are limited in Japan. METHODS: From August 2019 to February 2020, the European Health Literacy Survey (Japanese version) and a patient background survey (highest level of education, income, social activities, and exercise habit) were conducted on adult predialysis CKD patients. We compared clinical parameters in two groups according to the average HL score of a healthy Japanese population. In addition, a median value of 42 items was used as a cutoff for extracting CKD patient background factors associated with HL since HLS-EU-Q47 included five items related to physical activity and exercise. RESULTS: Valid responses were received from 200 patients. Median general HL index was 25.2 points. The high-HL group (≥ 25.3 points) showed a low proportion of male (56.7% vs. 70.9%, p = 0.038), high social activities (69.1% vs. 48.5%, p = 0.003), and high exercise habit (36.1% vs. 13.6%, p < 0.001). In the multivariate analysis, social activity [OR (95% CI); 2.12 (1.16-3.89), p = 0.015] and exercise habit [OR (95% CI); 2.39 (1.16-4.90), p = 0.018] were extracted as the only significant variable. CONCLUSIONS: HL in Japanese predialysis CKD patients was associated with high social activity and exercise habit.

Fanconi syndrome with karyomegalic interstitial nephritis after ifosfamide treatment for osteosarcoma: a case report.

Patients with ifosfamide-induced renal damage present with Fanconi syndrome. Karyomegalic nephropathy/interstitial nephritis (KNIN) is a rare form of chronic tubulo-interstitial nephritis that was initially considered a type of familial nephropathy. However, several reports of drug-induced KNIN, i.e., KNIN-like nephropathy, have been reported in recent years. We present the case of an 18-year-old man who presented with Fanconi syndrome and progressive renal dysfunction after receiving chemotherapy including ifosfamide and cisplatin for right femoral osteosarcoma. Renal biopsy revealed numerous atrophied tubular epithelial cells with large, polymorphic nuclei, and the definitive diagnosis was KNIN. Most patients with KNIN-like nephropathy who receive ifosfamide are concomitantly treated with cisplatin, indicating that ifosfamide and cisplatin might act synergistically to increase the risk for KNIN-like nephropathy. Further investigation in case series is warranted to reveal potential treatment approaches and to evaluate prognosis.

Duration of last depressive episode may influence serum BDNF levels in remitted patients with major depression.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) may have an important role in the pathophysiology of depression. Previous studies indicate that serum BDNF levels were lower in patients with depression and increased after treatment with antidepressants. However, results of studies on serum BDNF levels in remitted patients with depression have been inconsistent. The purpose of the present study was to determine which factors influence the alteration of serum BDNF levels in depression in the remitted state. METHODS: Serum BDNF levels were evaluated in 75 remitted inpatients with major depressive disorder (MDD) and 108 controls. Multiple regression analyses were conducted using serum BDNF levels as the dependent variable; and the number of episodes, Hamilton Rating Scale for Depression score at admission, or duration of last depressive episode as independent variables. RESULTS: Serum BDNF levels were lower in remitted patients with MDD than in controls (P < .001). Multiple regression analysis showed a significant effect between the duration of the last depressive episode and serum BDNF levels (P < .022). CONCLUSIONS: Serum BDNF levels in remitted patients with MDD did not recover to the level of healthy controls, and lower serum BDNF levels were influenced by a longer duration of last depressive episode. It is possible that persistent hippocampal reduction in remitted depression may be caused by lower BDNF levels associated with a longer duration of the last depressive episode.

Serum amyloid beta protein in young and elderly depression: a pilot study.

BACKGROUND: Depression may increase the risk of developing Alzheimer's disease (AD). Recent large cohort studies have also shown that a low plasma amyloid beta (Abeta)-42 level combined with a high Abeta40 level increases the risk of developing AD, suggesting plasma Abeta42/40 ratio as useful for identifying risk of developing mild cognitive impairment and AD. Although several studies have examined Abeta levels in the peripheral blood of elderly individuals with depression, results have been inconsistent. Furthermore, no results have been described for younger depression. METHODS: Serum Abeta40, Abeta42 level and Abeta40/42 ratio were evaluated using enzyme-linked immunosorbent assay in 60 patients with major depressive disorder (MDD) and 60 healthy controls. The results were analyzed in two age groups (young, <60 years; elderly, >or=60 years). RESULTS: Serum Abeta40 level was significantly higher in young MDD patients compared to young controls (P < 0.001), but it was not significantly deferent in the elderly group. Serum Abeta42 level did not differ significantly in both young and elderly groups. Abeta40/42 ratio was significantly higher in both young (P < 0.001) and elderly (P < 0.001) patients with MDD compared to controls. CONCLUSIONS: Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. This may suggest that even young subjects with MDD undergo pathological changes in the very early stage of amyloid deposition.

Proton-pump Inhibitor-induced Severe Hypomagnesemia and Hypocalcemia are Clinically Masked by Thiazide Diuretic.

Hypomagnesemia, a side effect of proton-pump inhibitors (PPIs), can be asymptomatic. The presence of hypocalcemia or hypokalemia is indicative of hypomagnesemia; however, the concomitant use of PPIs and thiazide may mask hypocalcemia. A 79-year-old woman with a history of chronic heart failure and chronic kidney disease developed symptomatic hypocalcemia and hypomagnesemia. Five weeks earlier, she had developed thiazide-induced hyponatremia, so thiazide had been discontinued. Reviewing the patient's charts revealed that three discontinued thiazide administrations in the clinical course had unmasked hypocalcemia. Our case demonstrates that thiazide-induced hypercalcemia can be so prominent as to mask PPI-induced hypocalcemia and hypomagnesemia.

Metabolism of amyloid-ß protein may be affected in depression.

OBJECTIVE: Epidemiologic studies have demonstrated that a history of depression increases the risk of developing Alzheimer's disease, particularly among individuals with early-onset depression. On the other hand, recent studies have suggested that a higher amyloid-ß protein (Aß)40 to Aß42 ratio may be associated with the future onset of Alzheimer's disease. Our objective was to assess whether the pathophysiology of early-onset depression may involve or affect Aß metabolism. METHOD: In this extension of a case-control pilot study, 193 inpatients with DSM-IV major depressive disorder (MDD) (mean age = 55.9 years) from the Juntendo Koshigaya Hospital, Saitama, Japan, and 413 healthy controls from the community (mean age = 56.6 years) were recruited between May 2004 and April 2009. Serum Aß40 and Aß42 levels, Aß40/Aß42 ratio, and other clinical and biological factors were compared between controls and patients in 3 age groups: young (< 40 years), middle-aged (≥ 40 to < 65 years), and elderly (≥ 65 years). Depressive symptoms were assessed with the Hamilton Depression Rating Scale. All patients were receiving antidepressant medication at the time of the study, and doses of current antidepressants were converted to an equivalent imipramine dose. RESULTS: The serum Aß40/Aß42 ratio was significantly higher in MDD patients than controls in all age groups (young: P = .003; middle-aged: P < .001; elderly: P = .006). These differences were also observed in noncarriers of the apolipoprotein E ε4 allele. CONCLUSIONS: Our findings suggest that Aß metabolism may be affected in depression; these findings also possibly answer the question of why even early-onset depression is a risk factor for developing Alzheimer's disease.