The characteristics of proteinuria in IgA nephropathy

Written by Zhou Qi
Nephrology
Updated on September 06, 2024
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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 Zhou Qi
Nephrology
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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.

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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 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 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.