Subcellular localization of glucocorticoid receptor protein in the human kidney glomerulus

Subcellular localization of glucocorticoid receptor protein in the human kidney glomerulus.BackgroundThe detailed mechanisms of glucocorticoid action in idiopathic nephrotic syndrome and progressive glomerulonephritides have not been clearly elucidated. The pharmacological actions of glucocorticoids are mediated by their binding to an intracellular protein, the glucocorticoid receptor (GR). The determination of GR localization in normal glomerular cells is essential to elucidate the mechanisms of glucocorticoid action in various glomerular diseases.MethodsWe carried out an immunoblot examination using antihuman GR-specific antibody and homogenates of isolated normal human glomeruli and mesangial cells in culture. Immunohistochemical examinations were also performed on normal human kidney specimens at light and electron microscopic levels. The nuclear translocation of GRs elicited by ligand binding was further investigated by confocal laser-scanning microscopic inspection of freshly isolated glomeruli and mesangial cells cultured with dexamethasone.ResultsAn immunoblot examination demonstrated the presence of a 94 kDa protein, a molecular weight consistent with that of GRs, in the homogenates of glomeruli and cultured mesangial cells. By light microscopic examination, GRs were strongly detected in the nucleus and moderately in the cytoplasm of all glomerular cells, parietal and visceral epithelial cells, endothelial cells, and mesangial cells. By electron microscopic examination, the nuclear GRs of all glomerular cells were found to be diffusely distributed in the euchromatin. Additionally, the immunofluorescence intensities of nuclear GRs in isolated glomeruli and mesangial cells in culture became more intense by the addition of dexamethasone.ConclusionsOur findings suggest that all subsets of human glomerular cells definitely express the GR protein, which potentially undergoes translocation by glucocorticoids

膀胱頸部に発生した前立腺嚢胞による下部尿路閉塞の2例

We report two cases of symptomatic prostatic cysts, which were arising around the bladder neck, in a 39-year-old man without clinical evidence of benign prostatic hyperplasia and a 72-year-old man with refractory bladder outlet obstruction. The lesions were found by abdominal ultrasound examination for post-voiding residual at the first visit. Transurethral unroofing of the cysts was performed with successful resolution of voiding symptoms.われわれは, 膀胱頸部に発生した症候性前立腺嚢胞の2例を経験した。1つは臨床的に前立腺肥大症を認めない39歳にみられ, もう1つは難治性排尿障害を認めていた72歳にみられた。これらの病変は初診時の残尿測定における超音波検査で同定された。経尿道的嚢胞開窓術により排尿症状は改善された。(著者抄録

Nutahara K. Renal disease progression in autosomal dominant polycystic kidney disease. Clin Exp Nephrol

Abstract Backgroun

Transtibial Pullout Repair of Lateral Meniscus Posterior Root Tear with Tissue Loss: A Case with Anterior Cruciate Ligament Injury and Medial Meniscus Tear

Lateral meniscus (LM) posterior root tear (LMPRT) is mainly caused by trauma, especially trauma associated with anterior cruciate ligament (ACL) injuries. Although a transtibial pullout repair or a side-to-side repair is commonly performed for LMPRT, to the best of our knowledge, there is no clinical report of LMPRT with tissue loss using the pullout technique. Thus, the purpose of this report was to describe a clinical, radiographic, and arthroscopic outcome after pullout repair for a case of LMPRT with a large defect with a chronic ACL tear and complex medial meniscus (MM) tears. A 31-year-old man complained of knee pain and restricted range of motion after twisting his knee when he stepped on an iron pipe. The patient had a football-related injury to his right knee 14 years before presentation, and since then, the patient's knee has given out more than 10 times but was left unassessed. Magnetic resonance imaging showed LMPRT with tissue loss, ACL tears, and complex MM tears. Transtibial pullout repair of the LMPRT with ACL reconstruction and MM repairs were performed. Following the pullout repair of the LMPRT, an approximately 6 mm gap remained between the LM posterior root and root insertion. However, magnetic resonance imaging and second-look arthroscopy at 1 year postoperatively revealed meniscal healing, gap filling with some regeneration tissue, of the LM posterior root. Furthermore, the lateral meniscus extrusion in the coronal plane improved from 3.1 mm (preoperative) to 1.6 mm (1 year postoperatively). Transtibial pullout repair with the remaining gap could be a viable treatment option for LMPRT with tissue loss, combined with ACL reconstruction

Genotypes of autosomal dominant polycystic kidney disease in Japanese

Abstract Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary disorders. The prevalence of the ADPKD genotype in the Caucasian and Latin populations has been reported. Here, we used linkage analysis to demonstrate the prevalence of the genotype and the correlation between phenotypes and genotypes among 21 Japanese ADPKD families consisting of 96 individuals and including 57 affected members. Six polymorphic markers, each linked to either the polycystic kidney disease 1 (PKD1) or polycystic kidney disease 2 (PKD2) gene, were used for polymerase chain reaction analysis. Seventeen families (81%) showed linkage to PKD1, two families (10%) showed linkage to PKD2, and two families did not show linkage to either PKD1 or PKD2. One of the PKD1-linked families was indicated to have different mutations of PKD1 gene in the same family. PKD2-linked families did not have milder symptoms than PKD1-linked families