IgA nephropathy manifestations

Written by Zhou Qi
Nephrology
Updated on September 24, 2024
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IgA nephropathy is a pathological type of chronic glomerulonephritis. The clinical manifestations of this disease are diverse, with the typical clinical presentation of IgA nephropathy being hematuria, especially visible hematuria following a cold.

However, patients may also exhibit other features, such as significant amounts of urinary protein. In some cases, this can reach the level of 3.5g in a 24-hour urine protein quantification. Patients may experience edema, such as swelling in the lower limbs, eyelids, etc. There could also be clinical presentations of high blood pressure, rapid progression of renal failure, and other symptoms.

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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.

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Written by Ji Kang
Nephrology
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How to determine the stages of IgA nephropathy?

IGA nephropathy has different grading methods, such as Lee grading and Hass grading. Both classify the pathological changes of IGA nephropathy into five stages, with similar descriptions. According to the Lee grading: Grade 1: Most glomeruli are normal, with occasional mild mesangial widening or without cellular proliferation, and no tubulointerstitial changes. Grade 2: Glomeruli show focal mesangial proliferation, with no tubulointerstitial changes. Grade 3: Glomeruli exhibit diffuse mesangial proliferation, with occasional segmental focal lesions, rare crescents, and adhesions, focal interstitial edema, and rare cellular infiltration. Grade 4: Glomeruli show diffuse severe mesangial proliferation and sclerosis, partial or segmental glomerulosclerosis, crescent formation observed but less than 45%, tubular atrophy, interstitial infiltration. Grade 5: The nature of the lesions is similar to grade 4 but more severe. Crescent formation in glomeruli is greater than 45%.

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Written by Hu Lin
Nephrology
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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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Written by Li Liu Sheng
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Foods to Avoid with IgA Nephropathy

IgA nephropathy patients are a very common type of glomerular disease. For IgA nephropathy patients, it is crucial to adhere to a light diet, meaning they should avoid foods such as pickles, salted vegetables, kimchi, cured products, smoked products, and barbecues, focusing primarily on fresh vegetables and fruits. Of course, if IgA nephropathy patients also suffer from renal insufficiency, they must avoid various soy products including tofu, bean sprouts, soybean sprouts, mung bean sprouts, and nut-based foods. These foods contain a lot of plant proteins, which can increase the burden on the kidneys, leading to potential renal insufficiency. Additionally, they should not consume foods high in potassium, such as oranges, bananas, pineapples, etc. Therefore, it is essential for IgA nephropathy patients to be cautious with their diet.

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Written by Hu Lin
Nephrology
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IgA kidney disease's etiology

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.