Why doesn't IgA nephropathy cause swelling?

Written by Zhou Qi
Nephrology
Updated on September 02, 2024
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IgA nephropathy refers to the abnormal deposition of IgA immunoglobulin in the glomeruli of patients, which causes an inflammatory response and damages the glomerular capillaries. The extent of this damage varies, so not all patients will experience swelling. If the condition is severe, causing significant proteinuria, patients may develop hypoproteinemia and consequent decrease in plasma colloidal osmotic pressure, leading to swelling. If renal failure has occurred, the kidneys' ability to excrete water decreases, which can also cause swelling. Some patients may experience swelling due to damage to the renal tubules, which increases the reabsorption capacity for water. Otherwise, patients may not show obvious swelling, such as those with only mild proteinuria and hematuria, whose clinical symptoms are not pronounced.

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Written by Zhou Qi
Nephrology
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Can IgA nephropathy patients eat watermelon?

IgA nephropathy is a chronic glomerulonephritis with varying degrees of severity and diverse clinical manifestations. Whether patients can eat watermelon depends on their kidney function and the presence of edema symptoms. If patients have kidney failure and noticeable edema, it is advised that they avoid eating watermelon, as it contains a significant amount of potassium ions. Consuming watermelon may lead to hyperkalemia due to the intake of large amounts of potassium ions. The main component of watermelon is water, and if patients have noticeable symptoms of edema, eating watermelon may exacerbate these symptoms and even cause issues like hypertension. If patients do not have noticeable edema and their kidney function is normal, eating small amounts of watermelon should not be a major concern.

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Written by Li Liu Sheng
Nephrology
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How is IgA nephropathy caused?

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
Nephrology
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Can IgA nephropathy be cured?

IgA nephropathy cannot be completely cured. IgA nephropathy is a type of chronic glomerulonephritis and is a chronic disease. Currently, it is incurable in medical practice. However, many patients have only mild symptoms, such as mild hematuria, proteinuria, and minor kidney damage, and timely long-term management of the disease usually does not lead to severe consequences. Some patients, on the other hand, have relatively severe conditions and require treatment with steroid medications. Most of these patients can achieve relatively good treatment outcomes and ultimately avoid severe kidney failure. However, a very small number of patients may eventually experience significant proteinuria and even severe renal failure.

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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
Nephrology
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How to control IgA nephropathy?

IgA nephropathy is a very common type of glomerular disease in clinical practice and is also a major cause of uremia. Therefore, sufficient attention should be given to IgA nephropathy by patients, and active treatment is required. The treatment of IgA nephropathy usually depends on the clinical manifestations and pathological types of the patient, meaning that the treatment approaches for patients with different clinical manifestations of IgA nephropathy are not exactly the same. For patients who frequently experience gross hematuria, if it is related to tonsil infection, it is recommended that the patient undergo tonsillectomy. For patients with IgA nephropathy who only have microscopic hematuria, there is generally no need for special medication treatment. However, in daily life, regular monitoring of routine urine tests, kidney function, and blood pressure is necessary, and the use of drugs that are toxic to the kidneys should be avoided. For patients with IgA nephropathy who also have significant proteinuria, even nephrotic syndrome, treatment often requires the use of steroids, and even immunosuppressants. For patients with mild to moderate proteinuria, it is recommended to use angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Only in this way can the condition of IgA nephropathy be controlled.