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Diabetic Nephropathy

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Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...

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Related Experiment Video

Updated: Jun 11, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

Published on: February 15, 2020

Oxidative stress in IgA nephropathy.

R Coppo¹, R Camilla, A Amore

¹Nephrology, Dialysis, Transplantation, Regina Margherita University Hospital, Turin, Italy. rosanna.coppo@unito.it

Nephron. Clinical Practice

|July 8, 2010

Summary

IgA nephropathy (IgAN) involves IgA1 deposits and oxidative stress. Systemic oxidative stress may worsen IgAN progression and kidney damage, influencing disease severity.

Area of Science:

Nephrology
Immunology
Oxidative Stress Research

Background:

IgA nephropathy (IgAN) is defined by IgA1 mesangial deposits, potentially from immune complex accumulation.
Oxidative stress is implicated in IgAN pathogenesis, observed in cultured cells and patient biopsies.
Altered oxidation-antioxidation balance is evident in IgAN patients, with markers like advanced oxidation protein products (AOPPs) linked to disease severity.

Purpose of the Study:

To explore the role of oxidative stress in IgA nephropathy.
To investigate the association between systemic oxidative stress markers and IgAN progression.
To hypothesize how the oxidative environment influences IgAN's clinical presentation and advancement.

Main Methods:

Analysis of oxidative stress markers in IgAN patient samples (serum, erythrocytes).

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Assessment of advanced oxidation protein products (AOPPs) and their correlation with proteinuria and disease progression.

Review of existing research on IgA1 nephrotoxicity and systemic oxidative stress.

Main Results:

IgAN patients exhibit signs of oxidative stress, including altered enzyme activities and increased lipoperoxides.
Elevated AOPPs are significantly associated with proteinuria and IgAN progression.
AOPPs, often bound to albumin, may exacerbate circulating oxidative stress.

Conclusions:

Systemic oxidative stress appears to play a crucial role in IgAN.
The degree of oxidative stress may modulate the nephrotoxicity of aberrant IgA1 and influence IgAN progression.
Targeting oxidative stress could be a potential therapeutic strategy for IgAN.