Complete remission of primary membranous nephropathy following hepatitis E infection.

Primary membranous nephropathy (PMN) is a major cause of nephrotic syndrome in adults. Studies have shown that one-third of PMN cases undergo spontaneous remission, among which are some cases of infection-related complete remission. Herein, we report the case of a 57-year-old man who achieved complete remission of PMN shortly after the onset of acute hepatitis E infection.

Long-term outcomes of anterior chest wall arteriovenous graft with polyurethane.

Background: Anterior chest wall arteriovenous graft (ACWAVG) is one option for haemodialysis patients when vessels of the upper extremities become exhausted. We report here the long-term outcomes of ACWAVG with polyurethane.

Methods: From April 2005 to October 2015, nine ACWAVGs with polyurethane grafts were created.

Glomerulopathy with distinctive fibrillar deposits but lacking glomerular deposition of type III collagen.

A 62-year-old woman with nephrotic syndrome underwent a renal biopsy. Under light microscopy, the biopsy findings included lobulation and enlargement of glomeruli, occasional thickening of glomerular capillary walls, and narrowing of the capillary lumen by swollen endothelial cells. Congo red staining was negative for amyloid.

Acute heart failure due to chronic juxtarenal aortic occlusion in a patient with antiphospholipid antibody syndrome.

Abdominal aortic occlusions are rare, but occasionally life threatening. A 48-year-old man was hospitalized due to acute heart failure accompanied by acute kidney injury (AKI). Abdominal ultrasound revealed deteriorating blood flow in the bilateral renal arteries.

Adjusted Anion Gap Is Associated with Glomerular Filtration Rate Decline in Chronic Kidney Disease.

Background: Metabolic acidosis is known to accelerate the progression of chronic kidney disease (CKD). However, whether undetermined anions as indicated by the adjusted anion gap (aAG) are associated with estimated glomerular filtration rate (eGFR) decline in patients with CKD is unclear.

Methods: Data from 42 patients with CKD (baseline eGFR, 7.

Dephosphorylated Ser985 of c-Met is associated with acquired resistance to rechallenge injury in rats that had recovered from uranyl acetate-induced subclinical renal damage.

Background: We previously reported that rats that had recovered from mild proximal tubule (PT) injury induced by a sub-toxic dose of uranyl acetate (UA) showed partial resistance to a subsequent nephrotoxic dose of UA in association with reduced renal dysfunction and accelerated PT proliferation. We demonstrated that this resistance may involve hepatocyte growth factor (HGF)/c-Met signaling. Here, we examined whether primary cultured tubular cells derived from this model had acquired sensitivity to HGF.

The amelioration of renal damage in Skp2-deficient mice canceled by p27 Kip1 deficiency in Skp2-/- p27-/- mice.

SCF-Skp2 E3 ubiquitin ligase (Skp2 hereafter) targets several cell cycle regulatory proteins for degradation via the ubiquitin-dependent pathway. However, the target-specific physiological functions of Skp2 have not been fully elucidated in kidney diseases. We previously reported an increase in Skp2 in progressive nephropathy and amelioration of unilateral ureteral obstruction (UUO) renal injury associated with renal accumulation of p27 in Skp2(-/-) mice.

Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake.

Despite suppression of the circulating renin-angiotensin system (RAS), high salt intake (HSI) aggravates kidney injury in chronic kidney disease. To elucidate the effect of HSI on intrarenal RAS, we investigated the levels of intrarenal prorenin, renin, (pro)renin receptor (PRR), receptor-mediated prorenin activation, and ANG II in chronic anti-thymocyte serum (ATS) nephritic rats on HSI. Kidney fibrosis grew more severe in the nephritic rats on HSI than normal salt intake.

Up-regulation of Cks1 and Skp2 with TNFα/NF-κB signaling in chronic progressive nephropathy.

The cyclin-dependent kinase (CDK) inhibitor p27 level is associated with progression of renal damage. We previously reported that mRNA of Skp2, a component of Skp/Cullin/F-box (SCF)-ubiquitin ligase which targets to p27, was increased in unilateral ureteral obstructive kidneys in mice and that the nephritis was attenuated in Skp2-deficient mice. However, the details have not been fully clarified.

A case of hypokalemia-induced fatal arrhythmia caused by indapamide in an anorexic elderly patient.

An 84-year-old man was referred to our hospital for atrioventricular block and severe hypokalemia. He had been treated for hypertension since 2007 with indapamide, a thiazide-like diuretic. His laboratory data had not been tested for a long time.

Acquired resistance to rechallenge injury in rats that recovered from mild renal damage induced by uranyl acetate: accelerated proliferation and hepatocyte growth factor/c-Met axis.

Background: Rats that recovered from mild proximal tubule (PT) injury without renal dysfunction by subtoxic insult, developed partial resistance to subsequent nephrotoxic insult. This partial resistance was associated with reduced renal dysfunction and accelerated PT cell proliferation compared with vehicle treatment as the first insult. Here we assessed the role and potential mechanisms of accelerated PT proliferation in this acquired resistance model.

Cisplatin induces Sirt1 in association with histone deacetylation and increased Werner syndrome protein in the kidney.

Background: Sirt1, a mammalian homolog of silent information regulator 2 (Sir2), is the founding member of class III histone deacetylase (HDAC).

Methods: In this study, we examined whether Sirt1 is involved in the modification of acetylated histone H3, acetylated p53 and Werner syndrome protein (WRN), which is stabilized by Sirt1-mediated deacetylation, in cisplatin (CDDP)-induced acute renal failure (ARF) in rats.

Results: Administration of CDDP (5 mg/kg body weight) caused an increase in the Sirt1 protein level by 6 h; this increase peaked at day 5 and declined until day 14.

A case presenting with rapid renal damage caused by immunoglobulin D lambda-type multiple myeloma accompanied by granular lymphocyte proliferative disorder.

A 69-year-old man was referred to our hospital for severe anemia. The atypical lymphocyte count, including granular lymphocytes, was 2,750/μL. Lymphocyte surface marker analysis showed CD3+, CD5+, CD16+, and CD56+ cells.

A case with significant proteinuria caused by secreted protein from urothelial carcinoma.

58-year-old female was admitted to our hospital complaining isolated proteinuria of 1.7 g/day. Abdominal echography showed right-sided unilateral hydronephrosis, and computed tomography pointed out a tumor of the right renal pelvis, suggesting cancer of renal pelvis.

Hepatocyte Growth Factor stimulated cell scattering requires ERK and Cdc42-dependent tight junction disassembly.

The mechanism by which Hepatocyte Growth Factor (HGF) induces tight junction disassembly prior to cell scattering is largely unknown. Here, we show that HGF stimulates rapid loss of the TJ assembly protein Par6 from the TJ in an Erk-dependent manner. Erk activation by HGF is found to mediate the interaction of Par6 with GTP-loaded Cdc42.

Inhibition of podocyte FAK protects against proteinuria and foot process effacement.

Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that plays a critical role in cell motility. Movement and retraction of podocyte foot processes, which accompany podocyte injury, suggest focal adhesion disassembly. To understand better the mechanisms by which podocyte foot process effacement leads to proteinuria and kidney failure, we studied the function of FAK in podocytes.

Immunohistochemical study of heat shock protein 27 with respect to survival and regeneration of proximal tubular cells after uranyl acetate-induced acute tubular injury in rats.

This study examined the possible role of heat shock protein 27 (HSP27) expression in the survival and regeneration of proximal tubule (PT) cells after acute tubular injury. Rats were injected with a low (0.2 mg/kg) or high (4 mg/kg) dose of uranyl acetate (UA) to induce renal injury.

Rapid deterioration of renal function in a patient with multiple myeloma associated with amyloid and light chain depositions.

Here we report a 75-year-old man with multiple myeloma who developed acute deterioration of renal function. Systemic AL amyloid deposition was found in the stomach, duodenum and brachial artery. A small amount of proteinuria without significant abnormal urinary sediments, increased excretion of urinary low-molecular-weight proteins and Bence Jones protein were observed.

Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction.

Hepatocyte growth factor and its receptor, Met, activate biological pathways necessary for repair and regeneration following kidney injury. The Met receptor is expressed in multiple cell types within the kidney, each of which is capable of regulating fibrotic responses. To specifically address the role of the Met receptor in the adult collecting duct during renal injury, a conditional knockout mouse (Met(fl/fl);HoxB7-Cre) was generated and tested using unilateral ureteral obstruction, a model of nephron injury, fibrosis, and repair.

Decrease in tumor necrosis factor-alpha receptor-associated death domain results from ubiquitin-dependent degradation in obstructive renal injury in rats.

Increased expression levels of tumor necrosis factor-alpha (TNFalpha) is involved in tubulointerstitial cell proliferation and apoptosis in obstructive renal injury. Two TNFalpha receptors (TNFRs), TNFR1 and TNFR2, are known to exist. On TNFalpha binding, TNFR1 recruits TNFR-associated death domain (TRADD), an assembly platform to mediate TNFR1 signaling.

Met and the epidermal growth factor receptor act cooperatively to regulate final nephron number and maintain collecting duct morphology.

Ureteric bud (UB) branching during kidney development determines the final number of nephrons. Although hepatocyte growth factor and its receptor Met have been shown to stimulate branching morphogenesis in explanted embryonic kidneys, loss of Met expression is lethal during early embryogenesis without obvious kidney abnormalities. Met(fl/fl);HoxB7-Cre mice, which lack Met expression selectively in the UB, were generated and found to have a reduction in final nephron number.