WHY IS IT CALLED IgA NEPHROPATHY AND HOW IS IT CAUSED

IgA nephropathy is very common disease, perhaps affecting several hundred million people around the globe. Although in many patients it is a rather benign disorder, it can progress to end-stage renal disease (ESRD). The clinical features of IgA nephropathy are quite variable but episodes of hematuria, often combined with persistent proteinuria, are common. Nephrotic syndrome at presentation is uncommon.

Because of the uncertain outlook, it is recommended that all people found to have IgA Nephropathy, even in its mild form, should be seen by their general practitioner and kidney specialist at regular intervals. Indeed healthy individuals with the disease should have blood pressure checks and urine examinations made by their doctor from time to time to pick up the first signs of any problems.

In those who have IgA Nephropathy regular tests of kidney function are necessary because progressive kidney failure can be detected by these tests. Even if someone with IgA Nephropathy appears to be stable, a regular review by a kidney specialist is important.

Primary IgA nephropathy (IgAN) was first described by Jean Berger. One of the difficulties in this disease3–6 is to predict at the time of the initial diagnosis the very long-term (decade) prognosis in the individual patient. This has been approached since the 1990s by the multivariate Cox regression model, taking into account the time duration of follow-up (FU) or the time elapsed since disease onset to occurrence of the events chosen as secondary or primary end points, usually chronic kidney disease (CKD, stage 3+) and end-stage renal failure (ESRF) as strong markers of progression. The predictive risk factors (RF) identified can be classified in two groups: major and the others.

So far there is no curative treatment for IgA Nephropathy. At present the most promising treatments include blood pressure lowering agents (Angiotensin Converting Enzyme (ACE) Inhibitors, Angiotensin Receptor Antagonists (ARA's) and Calcium Channel Blockers). Appropriate treatment including antibiotics for infections and diet will help in many cases, as will restriction of alcohol and tobacco intake and control of cholesterol. There is some evidence supporting the use of fish oil supplements. Rarely, other drugs, such as steroids, cyclophosphamide and mycophenolate are used for nephrotic of more rapidly progressive IgA nephropathy.

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What Factors would Influence the Prognosis of IgA Nephropathy

IgA Nephropathy is the common CKD which refers to that patients would suffer a long term of progression of kidney disease. of cause, different patients have different prognosis with the different physical conditions, life styles, treatment options and so on. Now this article would have a introduction about the factors which influence the prognosis of IgA nephropathy, which really need the attention of patients.

Many kidney patients would become very scared once they spot gross hematuria, and they would enter uremia eventually. In fact, the severity and frequency of hematuria has no direct relationship with the prognosis of the IgA Nephropathy. In general, the progression of IgA Nephropathy is slow, and this disease is less likely to progress into kidney failure than other types of kidney disease.

With that being said, patients with IgA Nephropathy should take this disease seriously. So patients should visit their doctors on a regular basis, stick with the treatment and do not cut back on medications on their own.

The major factors that influence prognosis of IgA Nephropathy include:

1. the gender of the patient: female patients tend to have better prognosis than male patients.

2. the starting age: on average, the children’s prognosis is better than adults. The prognosis for patients whose starting age is above 40 years old is usually not good.

3. patients whose GFR is already low and who has already kidney damage tend to have gloomy prognosis.

4. patients with less proteinuria tend to have better prognosis.

5. patients with normal blood pressure have better prognosis than patients with high blood pressure.

6. patients with the following pathological changes tend to worse prognosis: diffuse, proliferative glomerular damage with the formation of segmental or diffuse crescent, focal and segmental glomerular hardening or tubular atrophy, hardening arteriola, the thickening of the walls, the interstitial fibrosis and the deposits of IgA and C3.


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