IgA kidney disease's etiology

Written by Hu Lin
Nephrology
Updated on September 07, 2024
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IgA nephropathy can be divided into primary and secondary IgA nephropathy. Secondary IgA nephropathy includes, for example, lupus nephritis, allergic purpura nephritis, liver disease-related kidney damage, rheumatoid arthritis kidney damage, and so on. The etiology of primary IgA nephropathy is mainly due to the deposition of a type of immunoglobulin, IgA, in the mesangial area of the glomeruli, leading to a series of immune responses, which in turn cause inflammatory damage, resulting in a chronic glomerulonephritis. This form of IgA nephropathy is mainly related to mucosal immune defense, meaning it is linked to certain infectious factors. Additionally, some patients have high reactivity of their mucosa to certain food antigens, which leads to a series of immune-mediated inflammatory responses.

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How is IgA nephropathy diagnosed?

The diagnosis of IgA nephropathy relies on pathological examination. The name "IgA nephropathy" itself is a term used in immunopathological diagnosis, describing a type of chronic glomerulonephritis. There are many reasons that can cause inflammatory reactions in the kidneys, and the underlying mechanisms of the disease vary. Specifically, IgA nephropathy refers to the abnormal deposition of IgA immune complexes in the mesangial areas of the glomeruli. Therefore, a pathological examination is necessary for diagnosis. Typically, under a light microscope, proliferation of mesangial cells and widening of the mesangial areas can be observed. Additionally, immunofluorescence testing is conducted to detect a large presence of IgA immune complexes in the glomerular mesangial areas, confirming the diagnosis of IgA nephropathy.

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Written by Li Liu Sheng
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Is IgA nephropathy grade 3 serious?

IgA nephropathy is divided into five stages pathologically, with stage three being the focal proliferative type. The higher the stage, the more severe the condition of IgA nephropathy. Stage three is in the early to middle phase, where generally the condition of the patients is comparatively good, and rarely worsens to uremia, belonging to the low-risk group. Clinically, patients with stage three IgA nephropathy often exhibit repeated occurrences of gross hematuria or persistent microscopic hematuria. Some patients may also experience varying degrees of increased urinary protein. Patients with this stage of IgA nephropathy rarely suffer from hypertension or renal insufficiency, but it is essential in daily life to avoid nephrotoxic drugs, prevent infections, seek medical attention promptly upon infection, and regularly follow up on routine urine and renal function changes. If the condition tends to worsen, active treatment should be pursued.

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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.

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IgA kidney disease symptoms

The clinical manifestations of IgA nephropathy are diverse. The most common clinical manifestations include episodic gross hematuria, asymptomatic hematuria, and proteinuria. Episodic gross hematuria often occurs several hours after an upper respiratory tract infection, or a day or two later. Patients may notice that their urine is dark tea-colored, brown, or fresh red, light red, and this type of gross hematuria tends to recur. The second type is asymptomatic microscopic hematuria, with or without proteinuria, also known as asymptomatic urinalysis. This is often discovered during physical examinations when patients show no symptoms and tests reveal hidden blood and protein positivity in the urine. The third major category is proteinuria, which in some patients may present as nephrotic syndrome-like proteinuria. The fourth is hypertension; the fifth, acute kidney injury; and the sixth, chronic kidney failure. Most patients with IgA nephropathy gradually progress to chronic kidney failure within 10 to 20 years of diagnosis.

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How to treat occult blood in IgA nephropathy

IGA disease is a pathological type of chronic glomerulonephritis. This type of glomerular lesion often leads to positive occult blood in urine, and in some cases, may even cause gross hematuria visible to the naked eye. However, the relationship between hematuria and the severity or prognosis of the patient's condition is not very clear, so clinically, hematuria is not considered as a treatment target. Generally, during the active phase of the disease, patients can be treated with corticosteroids and other medications, especially those with more than 1g of protein in a 24-hour urine collection. Otherwise, most patients choose ACE inhibitors or ARBs as antihypertensive drugs to reduce the pressure inside the glomerulus. Additionally, avoiding colds can also help reduce occult blood in urine. (Specific medications should be administered under the guidance of a physician)