A Case of IgA Nephropathy and Renal Hemosiderosis Associated with Primary Hemochromatosis

Nakayama, Masaru; Kaizu, Yoshiki; Uesugi, Noriko; Nakashita, Satsuki; Suehiro, Takaichi

doi:10.1080/08860220802249033

Cited by 4 publications

(2 citation statements)

References 8 publications

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“…An increased urinary iron excretion and renal iron deposition has been found in hemochromatosis (HH) mice [ 120 ]. Clinical case reports also indicate that HH can lead to hemosiderin deposition in kidneys and injured kidneys [ 121 , 122 ]. Hemochromatosis is an inherited disorder most commonly caused by mutations in the HFE gene that result in misfolding of the HFE protein, loss of function in sensing iron concentration and defective hepcidin synthesis in hepatocytes, which in turn leads to reduced ubiquitinated degradation of FPN, elevated FPN levels and increased release of cellular iron, resulting in elevated circulating iron levels [ 123 ].…”

Section: Renal Iron Homeostasis and Cellular Dysfunction In Kidney Di...mentioning

confidence: 99%

Advance in Iron Metabolism, Oxidative Stress and Cellular Dysfunction in Experimental and Human Kidney Diseases

Xie,

Yao,

2024

Antioxidants

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Kidney diseases pose a significant global health issue, frequently resulting in the gradual decline of renal function and eventually leading to end-stage renal failure. Abnormal iron metabolism and oxidative stress-mediated cellular dysfunction facilitates the advancement of kidney diseases. Iron homeostasis is strictly regulated in the body, and disturbance in this regulatory system results in abnormal iron accumulation or deficiency, both of which are associated with the pathogenesis of kidney diseases. Iron overload promotes the production of reactive oxygen species (ROS) through the Fenton reaction, resulting in oxidative damage to cellular molecules and impaired cellular function. Increased oxidative stress can also influence iron metabolism through upregulation of iron regulatory proteins and altering the expression and activity of key iron transport and storage proteins. This creates a harmful cycle in which abnormal iron metabolism and oxidative stress perpetuate each other, ultimately contributing to the advancement of kidney diseases. The crosstalk of iron metabolism and oxidative stress involves multiple signaling pathways, such as hypoxia-inducible factor (HIF) and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways. This review delves into the functions and mechanisms of iron metabolism and oxidative stress, along with the intricate relationship between these two factors in the context of kidney diseases. Understanding the underlying mechanisms should help to identify potential therapeutic targets and develop novel and effective therapeutic strategies to combat the burden of kidney diseases.

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Section: Renal Iron Homeostasis and Cellular Dysfunction In Kidney Di...mentioning

confidence: 99%

Advance in Iron Metabolism, Oxidative Stress and Cellular Dysfunction in Experimental and Human Kidney Diseases

Xie,

Yao,

2024

Antioxidants

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“…Nakayama et al described a patient with primary hemochromatosis who developed IgAN. The 55-year-old man had a severe disease course with a rapid decline in his renal function [ 55 ]. Steroid treatment improved the renal state, lowering the serum creatinine.…”

Section: Iga Nephropathy Secondary To Liver Diseasesmentioning

confidence: 99%

Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic Review of Case Reports

Tota

Baron

Musial

et al. 2023

JCM

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Primary (pIgAN), secondary IgA nephropathy (sIgAN), and IgA-associated nephropathy can be distinguished. While pIgAN has been thoroughly studied, information about the etiology of sIgAN remains scarce. As concerns sIgAN, several studies suggest that different etiologic factors play a role and ultimately lead to a pathophysiologic process similar to that of pIgAN. In this article, we review a vast number of cases in order to determine the novel putative underlying diseases of sIgAN. Moreover, updates on the common pathophysiology of primary disorders and sIgAN are presented. We identified liver, gastrointestinal, oncological, dermatological, autoimmune, and respiratory diseases, as well as infectious, iatrogenic, and environmental factors, as triggers of sIgAN. As novel biological therapies for listed underlying diseases emerge, we suggest implementing drug-induced sIgAN as a new significant category. Clinicians should acknowledge the possibility of sIgAN progression in patients treated with TNF-α inhibitors, IL-12/IL-23-inhibitors, immune checkpoint inhibitors, CTLA-4, oral anticoagulants, thioureylene derivatives, and anti-vascular endothelial growth factor drugs.

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The multifaceted role of iron in renal health and disease

2019

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A Case of IgA Nephropathy and Renal Hemosiderosis Associated with Primary Hemochromatosis

Cited by 4 publications

References 8 publications

Advance in Iron Metabolism, Oxidative Stress and Cellular Dysfunction in Experimental and Human Kidney Diseases

Advance in Iron Metabolism, Oxidative Stress and Cellular Dysfunction in Experimental and Human Kidney Diseases

Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic Review of Case Reports

The multifaceted role of iron in renal health and disease

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