How is IgA nephropathy caused?

Written by Li Liu Sheng
Nephrology
Updated on January 16, 2025
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IgA nephropathy is a common glomerular disease and a major cause of uremia. However, the exact cause of IgA nephropathy is not very clear. Current research suggests that it is caused by factors such as infections which stimulate the production of autoantibodies, forming immune complexes that deposit in the glomeruli. This leads to inflammation of the glomeruli, eventually stimulating mesangial cell proliferation and accumulation of extracellular matrix, causing glomerulosclerosis and interstitial fibrosis. IgA nephropathy is a very covert disease, often presenting as asymptomatic hematuria or increased urine protein. Many patients discover this condition incidentally during physical examinations. Some individuals have a history of upper respiratory or gastrointestinal infections before the onset of the disease, followed by the discovery of gross hematuria. IgA nephropathy is more common in children and adolescents.

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Written by Zhou Qi
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The characteristics of proteinuria in IgA nephropathy

IgA nephropathy is a pathological type of chronic glomerulonephritis, which can cause patients to exhibit symptoms such as proteinuria and hematuria. Regarding the characteristics of proteinuria, it is generally primarily glomerular proteinuria. In the classification of patients' proteinuria, glomerular proteinuria accounts for a large proportion. If IgA nephropathy presents as chronic nephritis or nephrotic syndrome, the patient's level of proteinuria will be quite severe, with significant amounts of proteinuria, where the 24-hour urinary protein quantification may exceed 1g or even reach more than 3.5g. However, not all patients with IgA nephropathy have such high levels of proteinuria; some may only have mild proteinuria.

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Written by Niu Yan Lin
Nephrology
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Can patients with IgA nephropathy eat peaches?

Patients with IgA nephropathy vary greatly in the severity of their condition, and whether they can eat peaches depends on their individual disease state. If a patient does not have increased creatinine levels and no edema, they can eat peaches like a normal person without any restrictions on quantity. If the patient has increased creatinine levels, they need to control the amount of peaches they consume. This is because, in patients with elevated creatinine, the glomerular filtration rate is decreased, and a decrease in glomerular filtration rate can lead to an inability to expel excess potassium ions from the body. Peaches are a fruit with a high potassium content, and if such patients consume too many peaches, it can lead to hyperkalemia. Mild cases may experience weakness and numbness in the limbs, while severe cases can lead to potentially fatal cardiac arrhythmias.

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Written by Li Liu Sheng
Nephrology
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Does stage 2 IgA nephropathy require treatment?

IgA nephropathy can be divided into five stages, where stages one to two are relatively mild, early stages, and generally have a good prognosis. For patients with stage two IgA nephropathy, it is rare for the condition to progress to uremia, but whether treatment is needed largely depends on the clinical manifestations of the IgA nephropathy. If a patient with IgA nephropathy has a 24-hour urinary protein quantification greater than 0.5g, it is advisable to use an angiotensin-converting enzyme inhibitor or an angiotensin II receptor antagonist to protect kidney function and reduce urinary protein. If a stage two IgA nephropathy patient only shows microscopic hematuria, drug treatment is not necessary. However, routine urinalysis and kidney function monitoring should be conducted in daily life, and if an infection occurs, timely anti-infection treatment should be administered. If a stage two IgA nephropathy patient has significant proteinuria, steroid treatment is often required. (Medication should be taken under the guidance of a doctor.)

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Written by Zhou Qi
Nephrology
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IgA kidney disease causes

IgA nephropathy is a type of chronic nephritis. Patients with this disease have inflammatory reactions within their glomeruli. This inflammation is caused by the deposition of IgA immune complexes in the glomeruli. The reason why patients are prone to IgA immune complex deposition is still not very clearly explained in current medical literature and remains unclear. It is possible that such patients produce defective IgA immunoglobulins, often related to mucosal inflammatory infections, such as tonsillitis, enteritis, proctitis, etc. Inflammation of these mucosal areas might cause defective secretory IgA to circulate through the bloodstream to the kidneys, triggering an inflammatory response. The production of defective IgA immunoglobulins in patients may be related to genetic and environmental factors, but the specific mechanism is still not very clear.

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Written by Li Liu Sheng
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IgA nephropathy stages 1, 2, 3 criteria

According to the standards of the World Health Organization, IgA nephropathy is classified into five stages pathologically. The first stage is where most glomeruli appear normal under light microscopy, with only minor mesangial proliferation or associated cellular proliferation, generally showing slight changes without damage to the tubules and interstitium; The second stage indicates mild lesions where over fifty percent of the glomeruli are normal, with only a small portion of the glomeruli showing mesangial cell proliferation, glomerular sclerosis adhesion, and other changes, without the formation of crescents; The third stage is focal segmental glomerulonephritis, characterized by diffuse proliferation of mesangial cells and widening of the mesangial areas, with the lesions exhibiting focal segmental changes and comparatively mild interstitial lesions.