[Development of a High-School Students' Version of the Daily Conversation Scale with Classroom Teachers].

Objective　This study was intended to develop a "High-School Students' Version of the Daily Conversation Scale with Classroom Teachers" to measure the frequency of daily conversations between high-school students and their classroom teachers.Methods　The study consisted of Surveys I and II. Survey I was intended to validate the structural validity and reliability of the "High-School Students' Daily Conversation Scale with Classroom Teachers (Prototype Version).

VEGF-A Links Angiolymphoid Hyperplasia With Eosinophilia (ALHE) to THSD7A Membranous Nephropathy: A Report of 2 Cases.

Autoantibodies against thrombospondin type 1 domain-containing 7A (THSD7A) cause membranous nephropathy (MN); however, the mechanisms involved in THSD7A expression and immunization are uncertain. We present 2 cases of THSD7A-associated MN accompanied by angiolymphoid hyperplasia with eosinophilia (ALHE), a benign tumor characterized by proliferation of plump endothelial cells. Prednisolone therapy, but not surgical resection of ALHE tumors, successfully suppressed eosinophilia and proteinuria in both cases.

Difference in IgA1 O-glycosylation between IgA deposition donors and IgA nephropathy recipients.

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis, and disease recurrence often occurs after transplantation. On the other hands, Asymptomatic IgA deposition (IgAD) is occasionally observed in donated kidney. It is recognized that IgAD does not progress to IgAN, but the mechanism has not demonstrated yet.

Analysis of an ADTKD family with a novel frameshift mutation in MUC1 reveals characteristic features of mutant MUC1 protein.

Background: Medullary cystic kidney disease Type 1 is an autosomal dominant tubulointerstitial kidney disease (ADTKD). Recently, mucin 1 (MUC1) was identified as a causal gene of medullary cystic kidney disease (ADTKD-MUC1). However, the MUC1 mutation was found to be a single cytosine insertion in a single copy of the GC-rich variable number of tandem repeats (VNTRs), which are very difficult to analyze by next-generation sequencing.

Antioxidant role of autophagy in maintaining the integrity of glomerular capillaries.

Autophagy is a lysosomal degradation system by which cytosolic materials and damaged organelles are broken down into basic components. To explore the physiological role of autophagy in glomerular endothelial cells (GEnCs), we compared the autophagic flux among cells in the kidney under starvation. Inhibition of autophagy by chloroquine administration significantly increased the number of autophagosomes or autolysosomes in GEnCs and proximal tubular cells, but not in podocytes, suggesting that the GEnCs exhibit substantial autophagic activity.

Lipophagy maintains energy homeostasis in the kidney proximal tubule during prolonged starvation.

Macroautophagy/autophagy is a self-degradation process that combats starvation. Lipids are the main energy source in kidney proximal tubular cells (PTCs). During starvation, PTCs increase fatty acid (FA) uptake, form intracellular lipid droplets (LDs), and hydrolyze them for use.

Autophagy Inhibits the Accumulation of Advanced Glycation End Products by Promoting Lysosomal Biogenesis and Function in the Kidney Proximal Tubules.

Advanced glycation end products (AGEs) are involved in the progression of diabetic nephropathy. AGEs filtered by glomeruli or delivered from the circulation are endocytosed and degraded in the lysosomes of kidney proximal tubular epithelial cells (PTECs). Autophagy is a highly conserved degradation system that regulates intracellular homeostasis by engulfing cytoplasmic components.

High-Fat Diet-Induced Lysosomal Dysfunction and Impaired Autophagic Flux Contribute to Lipotoxicity in the Kidney.

Excessive fat intake contributes to the progression of metabolic diseases cellular injury and inflammation, a process termed lipotoxicity. Here, we investigated the role of lysosomal dysfunction and impaired autophagic flux in the pathogenesis of lipotoxicity in the kidney. In mice, a high-fat diet (HFD) resulted in an accumulation of phospholipids in enlarged lysosomes within kidney proximal tubular cells (PTCs).

Time-dependent dysregulation of autophagy: Implications in aging and mitochondrial homeostasis in the kidney proximal tubule.

Autophagy plays an essential role in cellular homeostasis through the quality control of proteins and organelles. Although a time-dependent decline in autophagic activity is believed to be involved in the aging process, the issue remains controversial. We previously demonstrated that autophagy maintains proximal tubular cell homeostasis and protects against kidney injury.

Autophagic clearance of mitochondria in the kidney copes with metabolic acidosis.

Metabolic acidosis, a common complication of CKD, causes mitochondrial stress by undefined mechanisms. Selective autophagy of impaired mitochondria, called mitophagy, contributes toward maintaining cellular homeostasis in various settings. We hypothesized that mitophagy is involved in proximal tubular cell adaptations to chronic metabolic acidosis.

Autophagy protects kidney proximal tubule epithelial cells from mitochondrial metabolic stress.

Chronic metabolic stress is related to diseases, whereas autophagy supplies nutrients by recycling the degradative products. Cyclosporin A (CsA), a frequently used immunosuppressant, induces metabolic stress via effects on mitochondrial respiration, and thereby, its chronic usage is often limited. Here we show that autophagy plays a protective role against CsA-induced metabolic stress in kidney proximal tubule epithelial cells.

Renal transplantations from parents to siblings with autosomal recessive Alport syndrome caused by a rearrangement in an intronic antisense Alu element in the COL4A3 gene led to different outcomes.

Two siblings with autosomal recessive Alport syndrome (ARAS) obtained renal transplants from their consanguineous parents. Their COL4A3 mRNA transcripts were disrupted by a 139 bp intronic sequence between exon 48 and 49, which was derived from an antisense Alu element in this intron. The new amino acid sequence from the cryptic exon was terminated by a stop codon at the 1511th codon, resulting in the loss of 76 % α3(IV)NC1.

[Clinical characteristics of adult-onset minimal change nephrotic syndrome in our hospital].

Objective: Few findings are available regarding adult-onset minimal change nephrotic syndrome (MCNS) with respect to the disease course and complications, such as acute kidney injury (AKI). We therefore performed a retrospective review to characterize the clinical presentations, steroid responsiveness and complications of adult-onset MCNS patients in our hospital.

Patients And Methods: We retrospectively reviewed 40 cases of idiopathic adult-onset MCNS who had been investigated and treated at a single center.

[Case of HIV-associated nephropathy accompanied by nephrotic syndrome and acute worsening of kidney function].

A previously healthy black man presented with acute kidney injury wtih nephrotic syndrome. His serum creatinine and albumin concentrations were 8.0 mg/dL and 0.

Autophagy guards against cisplatin-induced acute kidney injury.

Autophagy is a highly conserved bulk protein degradation pathway involved in cellular homeostasis. Although emerging evidence indicates involvement of autophagy in various conditions, efforts to clarify the role of autophagy in renal tubules are beginning to be elucidated. In the present study, we examined the hypothesis that autophagy guards against acute kidney injury (AKI) by modulating several deteriorative pathways that lead to tubular cell death using a cisplatin-induced model of AKI.

Gene polymorphisms contributing to hypertension in immunoglobulin A nephropathy.

Background: Hypertension, which is affected by genetic and environmental factors, is one of the major risk factors for chronic kidney disease. Identification of the genetic factor contributing to hypertension in patients with chronic kidney disease may potentially refine a therapeutic strategy.

Methods: In the present multicenter cross-sectional study, 240 patients were eligible (aged 15-50 years with urinary protein ≥0.

A case of MPO-ANCA-positive polyarteritis nodosa complicated by exudative otitis media, mononeuritis multiplex, and acute renal failure.

In December 2008, a 69-year-old Japanese woman was admitted to the Department of Otorhinolaryngology because of hearing impairment due to bilateral exudative otitis media, and was discharged without complete recovery despite conventional treatment. Two weeks later, she was readmitted for worsened deafness, numbness, gait disturbance, and general fatigue. She was referred to our department for general investigation.

Autophagy protects the proximal tubule from degeneration and acute ischemic injury.

Autophagy is a bulk protein degradation system that likely plays an important role in normal proximal tubule function and recovery from acute ischemic kidney injury. Using conditional Atg5 gene deletion to eliminate autophagy in the proximal tubule, we determined whether autophagy prevents accumulation of damaged proteins and organelles with aging and ischemic renal injury. Autophagy-deficient cells accumulated deformed mitochondria and cytoplasmic inclusions, leading to cellular hypertrophy and eventual degeneration not observed in wildtype controls.

[Case of AL amyloidosis associated with a remarkable histological progress in a short period].

AL amyloidosis is the most common form of systemic amyloidosis. Although kidney biopsy often is the method by which the disease is identified, small amounts of amyloid in kidney biopsy specimens may be missed on routine examination unless specifically investigated. We present here a previously healthy 60-year-oldmissed on routine examination unless specifically investigated.

Azelnidipine-induced chyloperitoneum in a patient with microscopic polyangiitis.

A 76-year-old man developed fever and appetite loss, and then was referred to our hospital because of rapidly progressive renal insufficiency; his serum creatinine increased from 1.2 to 5.9 mg/dl within 1 month.

Successful treatment of HCV-related cryoglobulinemic glomerulonephritis with double-filtration plasmapheresis and interferon combination therapy.

A 67-year-old, hepatitis C virus (HCV)-positive woman was admitted to our hospital because of proteinuria and leg edema. Laboratory examination showed decreased serum albumin and complement activity and positive cryoglobulin. The HCV RNA genotype was 1b with high viral load.

[Clinical characteristics of five elderly patients with severe hypokalemia induced by glycyrrhizin derivatives].

Although hypokalemia is a common clinical problem, symptoms generally do not become manifest unless the serum potassium (K) falls rapidly. We encountered five cases with symptomatic severe hypokalemia (K<2.0 mEq/L) hospitalized for the past 15 months at our hospital.

[Adult case of severe Henoch-Schönlein purpura associated with steroid-resistant nephrotic syndrome successfully treated with intravenous cyclophosphamide].

Henoch-Schönlein purpura (HSP) is a systemic disorder characterized by small vessel vasculitis with the deposition of IgA immune complexes. Renal involvement is the major cause of morbidity and mortality in patients with HSP. We report here a 37-year-old female patient with HSP nephritis (HSPN) associated with steroid-resistant nephrotic syndrome and renal dysfunction despite conventional therapy.