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IgA nephropathy
IgA nephropathy manifestations
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.
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.
IgA kidney disease symptoms
IgA nephropathy is characterized by the deposition of IgA in the glomerular mesangial regions and is a common type of glomerulonephritis. It is also a major cause of uremia. IgA nephropathy typically affects adolescents. Once diagnosed, patients primarily experience recurrent macroscopic hematuria, especially after skin infections or respiratory infections, during which blood in the urine becomes more apparent. Of course, there can also be asymptomatic hematuria and increased urinary protein. Some patients with IgA nephropathy may also experience edema, particularly in the eyelids and facial area upon waking up in the morning, and in severe cases, there may be an increase in blood pressure and a decline in kidney function. It is essential for patients with IgA nephropathy to have regular follow-ups to monitor changes in routine urine tests, kidney function, and blood pressure, and to seek active treatment if the condition worsens.
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.
IgA nephropathy is a disease.
IgA nephropathy is the most common type of primary glomerular disease, caused by the deposition of IgA-dominant immunoglobulins in the glomerular mesangial area. It has a short latency period, with symptoms appearing early. Clinical manifestations of IgA nephropathy are diverse, with approximately 40%-50% of patients experiencing macroscopic hematuria hours to two days after precursor symptoms such as upper respiratory tract infections, and some patients also suffer from severe back pain and abdominal pain. About 30%-40% of patients only present with asymptomatic hematuria or proteinuria. Approximately 5%-20% of patients exhibit severe edema and substantial proteinuria, showing symptoms of nephrotic syndrome. At the onset of the disease, about 10% of patients also have hypertension. As the disease progresses, those with hypertension can exceed 40%. Less than 10% of patients may experience acute renal failure.
Causes of hematuria in IgA nephropathy
IGA nephropathy is a type of chronic glomerulonephritis. This disease often causes patients to have blood in their urine, and can also lead to visible blood in the urine. The glomerulus is a cluster of capillaries with semi-permeable functions, allowing water and metabolic waste to pass through while preventing proteins and red blood cells from passing. The waste and water pass through the glomerular filtration barrier and enter into the urine, which is the main component of urine. If some pathological cause damages the capillaries of the glomerulus, such as in the case of IGA nephropathy where there is an inflammatory response within the glomerulus, it can damage the glomerular filtration barrier. As a result, red blood cells may pass through the capillary walls of the glomerulus into the urine, causing blood in the urine.
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.
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.
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.
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.