IgA nephropathy (IgAN), the most prevalent primary chronic glomerulonephritis worldwide, has three major risk factors: hypertension, proteinuria >1 g/day, and severe renal lesions. Obesity also portends a poor prognosis. A Japanese boy with IgAN showed nephrotic syndrome at presentation. Pathological features resembled those of membranoproliferative glomerulonephritis (MPGN), although IgA deposition differed from MPGN and IgAN. Combination therapy improved renal lesions, but rebound deterioration of proteinuria occurred in this patient, who had marked obesity and hypertension. Serial kidney biopsy specimens were compatible with obesity-related glomerulopathy (ORG). Rebound proteinuria was apparently attributable to ORG rather than relapse and flaring up of IgAN.
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http://dx.doi.org/10.1007/s13730-015-0208-8 | DOI Listing |
Eur Radiol
January 2025
Department of Ultrasound, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Objectives: To develop and validate an ultrasomics-based machine-learning (ML) model for non-invasive assessment of interstitial fibrosis and tubular atrophy (IF/TA) in patients with IgA nephropathy (IgAN).
Materials And Methods: In this multi-center retrospective study, 471 patients with primary IgA nephropathy from four institutions were included (training, n = 275; internal testing, n = 69; external testing, n = 127; respectively). The least absolute shrinkage and selection operator logistic regression with tenfold cross-validation was used to identify the most relevant features.
Rev Med Suisse
January 2025
Service de néphrologie, Département de médecine, Hôpitaux universitaires de Genève, Genève 14.
Certain molecules, such as GLP-1 agonists and endothelin antagonists, possess nephroprotective properties. When treating IgA nephropathy, endothelin antagonists and sibeprenlimab have shown effectiveness in slowing the progression of chronic kidney isease. Additionally, the infusion of amino acids can reduce the incidence of mild acute kidney injury following cardiac surgery.
View Article and Find Full Text PDFFront Transplant
January 2025
Division of Gastroenterology, Hepatology and Nutrition, University of Minnesota, Minneapolis, MN, United States.
Introduction: The clinical characteristics of inflammatory bowel disease (dnIBD) diagnosed after solid organ transplant (SOT) are not well-described, particularly since the advent of biologic therapy for treatment of IBD.
Methods: We conducted a single-center, retrospective review of SOT recipients between 2010 and 2022 at the University of Minnesota Medical Center who were diagnosed with IBD after transplant.
Results: Of 89 patients at our center with IBD and a history of SOT, five (5.
Kidney Med
February 2025
Department of Medicine, Translational Transplant Research Center (TTRC), Renal Division, Icahn School of Medicine at Mount Sinai, New York, NY.
Curr Opin Nephrol Hypertens
January 2025
The University of Melbourne Department of Medicine (Melbourne Health and Northern Health), Royal Melbourne Hospital, Parkville, Victoria, AUSTRALIA.
Purpose Of Review: The recent widespread availability of genetic testing has resulted in the diagnosis of many more people with Alport syndrome. This increased recognition has been paralleled by advances in understanding clinical consequences, genotype-phenotype correlations and in the development of new therapies.
Recent Findings: These include the international call for a change of name to 'Alport spectrum' which better reflects the diverse clinical features seen with autosomal dominant and X-linked Alport syndrome; the demonstration of how common Alport syndrome is in people with haematuria, proteinuria, or kidney failure; the inability of current genetic testing to detect all pathogenic variants in suspected Alport syndrome; the different genotype-phenotype correlations for autosomal dominant and X-linked disease; and the novel treatments that are available including SGLT2 inhibitors for persistent albuminuria despite renin-angiotensin-aldosterone blockade, as well as early studies of gene-modifying agents.
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