We describe a 16-year-old Caucasian boy who presented with steroid-sensitive nephrotic syndrome aged 2 years. His clinical course was one of frequent relapses and severe steroid dependence. To manage this, he was sequentially treated with levamisole, then oral cyclophosphamide before being started on ciclosporin. A renal biopsy performed prior to commencement of ciclosporin confirmed minimal change disease on light microscopy. The immunohistochemistry and electron microscopy findings were in keeping with this. His complement levels were normal and his lupus serology negative. He remained on ciclosporin therapy for 8 years and had two further renal biopsies to detect ciclosporin-induced renal damage. Both biopsies showed evidence of increasing amounts of C1q deposition on immunohistochemistry and the presence of immune deposits on electron microscopy. As he had continued negative lupus serology, this was compatible with a diagnosis of C1q nephropathy. In addition both biopsies had changes compatible with chronic mild ciclosporin nephrotoxicity. This case is the first report describing in detail a paediatric patient with evolving C1q nephropathy who was treated successfully with rituximab. We discuss the role of C1q in this clinicopathological entity and question its significance.
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http://dx.doi.org/10.1093/ndtplus/sfp055 | DOI Listing |
Clin Nephrol Case Stud
December 2024
Nephrology Center and the Okinaka Memorial Institute for Medical Research.
A 47-year-old woman with a 12-year history of anemia and high C-reactive protein (CRP) levels was admitted to our hospital with worsening fatigue and night sweats. She had high levels of immunoglobulin G (IgG; 4182 mg/dL), IgA (630.6 mg/dL), and CRP (7.
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January 2025
Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, No.1 East Jianshe Road, Erqi District, Zhengzhou, 450052, China.
Increasing evidence points toward an essential role for complement activation in the pathogenesis of diabetic kidney disease (DKD). However, the precise molecular mechanisms remain unclear, and the pathway predominantly contributing to complement activation in DKD is of particular interest. In this study, the glomerular proteome, especially the profiles of the complement proteins, was analyzed in kidney biopsies from 40 DKD patients and 10 normal controls using laser microdissection-assisted liquid chromatography-tandem mass spectrometry (LMD-LC-MS/MS).
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December 2024
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 812-8582, Japan.
Neuron-derived neurotrophic factor (NDNF) was discovered as a target antigen in membranous nephropathy (MN) caused by syphilis. However, there have been few reports of NDNF-positive MN in Japan. A 19-year-old female patient was admitted to our hospital with nephrotic syndrome and acute kidney injury.
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February 2025
Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, Oklahoma, United States.
The rising prevalence of metabolic diseases is a significant global health concern. Beyond lifestyle management, targeting key molecules involved in metabolic regulation is essential. C1q/TNF-related protein 6 (CTRP6) is notably associated with glucose and lipid metabolism, with numerous studies highlighting its regulatory functions in metabolic diseases.
View Article and Find Full Text PDFClin Exp Nephrol
December 2024
Department of Pathology, Toranomon Hospital, Tokyo, Japan.
Renal lesions due to systemic lupus erythematosus (SLE) are defined as lupus nephritis (LN), a renal disease characterized by the deposition of immunoglobulin (Ig)G-based immune complexes in the kidney and the appearance of double-stranded DNA and Smith antibodies. In particular, deposition of IgG3, which has strong complement binding properties, under the endothelium or in the mesangium activates the classical complement pathway of C1q, C4, and C3, leading to renal damage. This step is followed by migration of inflammatory cells, including neutrophils and monocytes, which induce inflammation in the glomerular capillaries and cause mesangiolysis and endothelial cell damage, resulting in endocapillary proliferative nephritis.
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