IgA Nephropathy Is Not Terrible

Studies with the highest power and evidence levels include:
In 1999 Pozzi et al published a randomly assigned to supportive therapy only for additional corticosteroids. In a recently published, up to 10 years follow up of that population, serum creatinine had doubled in one of 43 patients in the steroid group versus 13 of 43 in the control group.
In 1999 Yoshikawa et al published a randomized controlled trial in Japanese children with normal GFR treated with supportive therapy or immunosuppression. During two years follow up proteinuria decreased from 1.0 to 0.9 in controls and from 1.4 to 0.2g/day in the immunosuppressed group. GFR remained normal in all but on child. Side effects in immunosuppressed children include growth retardation.
In 2000 Shoji published a randomized trial in which 8 patients were randomized to receive antiplatelet therapy only, while 11patienst receive additional oral prednisolone for one year. Proteinuria and histology were improved at one year in the steroid group. The study mainly dealt with low-risk patients.
In 2002 Ballardie et al published a randomized controlled single center study on IgA Nephropathy patients with progressive loss of renal function. Patients were randomized to prednisolone and cytotoxic agents or supportive therapy only. Renal survival in treated patients showed significantly better preservation of function at 5 years. 72% compared to 6% in controls. Morbidity attributable to treatment include one case of azathioprine-induced marrow suppression and one of secondary diabetes mellitus.
In 2003, Katafuchi et al published a randomized controlled trial in which 43 patients receive oral prednisolone as compared to 47 patients in the control group. Whereas renal survival was not improved by the steroid therapy, proteinuria decreased in the steroid group only. An unexplained, significantly higher baseline proteinuria in the steroid group considerable limits interpretation of this study.
In 2004, Maes et al described a prospective study in 34 patients with IgA Nephropathy and impaired renal function, who were randomized to 2g mycophenolate mefetil or placebo. After 3 years of follow up, insulin clearances and proteinuria did not different between the groups.

IgA Nephropathy

Iga nephropathy is the most common form of primary glomerulonephritis in the developed world and it is also an important cause of end stage renal failure. Prevalence seems much higher in Asia, Australia, Finland and south Europe. In UK, Canada and US, the prevalence rate is much lower.
Normally, immunofluorescent tagging of antibodies to detect antigens in tissues and percutaneous renal biopsy, along the discovery of an new immunoglobulin present in serum and in tissue secretions all collided to prepare the way for the seminal observations.
It is now fully recognized that IgA Nephropathy is not always a benign disease. It has a cumulative renal survival of 89% after five years, 81% after ten years and 65% after 20 years. The unfavorable long term prognostic indices are proteinuria of more than 1g/day, hypertension, glomerulosclerosis exceeding 20%, presence pf crescents, and medial hyperplasia of blood vessels on renal biopsy. Especially, patients who have uncontrolled hypertension seems to have a more rapid clinical course progressing to end stage within a few years. A small subset of patients with heavy proteinuria behaves clinically like minimal change disease. Their proteinuria responds to steroid and this subset was recognized as an overlapping syndrome if IgA Nephropathy and lipoid nephrosis. Otherwise, sever nephrotic range proteinuria is not common in IgA Nephropathy, but nephrotic-range proteinuria in the absence of minimal change disease is associated with poor prognosis.

How Does IgA Nephropathy Occur?

According to the clinical observation, there are more or less common points among IgA Nephropathy patients, such as mesangial cells proliferation, increasing mesangial matrix, glomerulosclerosis, crescent, interstitial fibrosis, renal tubule atrophy, etc. The only difference is just the severity. So, how to understand it more clearly? The main cause of most nephritis is immune complex deposition. The blood vessel in kidney is circuitous and massive, the blood amount is also more. Based on this, the immune complex circulating with blood circulation is easy to deposit here. If the amount of immune complex is temporary and in less amount , mesangial cells can remove them, so hematuria or proteinuria can disappear also. For example, many patients will have more serious hematuria and proteinuria after getting tonsillitis, but hematuria and proteinuria will become less serious after a few days. Therefore, we suggest antibiotics after patients getting infection. This is not used to treat IgA Nephropathy, but to prevent more immune complex formation so as to reduce the damage in mesangial cells.
If immune complex is in huge amount and lasts for a long time, mesangial cells can not deal with them completely. In order to face such condition, it will produce more mesangial cells to do this work and at the same time each mesangial cells is also in larger size. At this time, if biopsy is taken, more mesangial cells and broadening mesangial area can be found, and it is called mesangial cell proliferation.
However, everything should be controlled in some degree. If such condition lasts for long time, kidney will be damaged more. During mesangial cell proliferation, some other materials will be secreted at the same time. It is not easy to see clearly about their structure of these materials, but they looks like glass or coagulated cement.These materials are called mesangial matrix. And, under biopsy, it is mesangial matrix proliferation.
What's worse, with time passing, under the reaction of cell factors, mesangial will not have enough ability to remove these mesangial matrix. Besides, more mesangial matrix will also cause pressure to surrounding cells or even take the place of other health cells. Then gradually, sclerosis occurs. No matter it is glomerulosclerosis, or segmental sclerosis, it is irreversible. Therefore, during the whole treatment, preventing more glomeruli being sclerosed is the most basic and important aspect.
Crescent is formed due to the inflammation. If the inflammation due to immune complex is too active, filtration membrane will be damaged, and then some blood leak out. These blood can stimulate the epithelial cells in glomerular capsule, thus causing glomerular capsule epithelial cells proliferation. Finally, cellular crescent forms, and then cellulose crescent. Once crescent become to cellulose crescent, it is more serious, and it is difficult to reverse.
Interstitial fibrosis is just found in recent years. It can not cause hematuria or proteinuria, but it has close relationship with kidney function decline. The severity of interstitial fibrosis is an important point to estimate the prognosis of IgA Nephropathy.

The New Treatment Way for IgA Nephropathy

We all  know IgA Nephropathy is a kind of immune system disease. Here, I attached a picture, which may make it more clear.

We know that IgA Nephropathy is caused by inflammation reaction in kidney due to immune complex IgA deposit in mesangial area. Thus mesangial cells will be damaged first. With more and more IgA deposit, pathological damage will certainly happen in mesangial area. Mesangial area has the function of adjusting blood pressure, so IgA Nephropathy patients will have high blood pressure with the progression of the disease gradually. With the disease progressing, the pathological damage will also involves  to the endothelial cells and basement membrane. Basement membrane has the filtrating function. When filtrating function declines more, protein leaks out with urine. Actually, the more protein in urine, the more serious damage in basement membrane. Besides, according to the research, the prognosis is more serious if patients protein in urine can not be treated well.

From the above, we should also begin to know how the treatment is taken.

Firstly, the inflammation should be stopped first so as to prevent more damage in mesangial area. In most hospitals or countries, hormones or immune suppressant are suggested. However, these medicine can not only inhibit the abnormal immune reaction in kidney, but also inhibit the whole body immunity, which makes people have lower immunity. Therefore, the side effects is also a great problem.

Then, after stop inflammation reaction, the deposit immune complex should also be removed and in this way, there is no new inflammation anymore. Of course, the existed damage in mesangial area should also be repaired. Then, the disease can be controlled well. At the same time, using treatment to adjust patient whole body immunity. To be honest, a systematic treatment should contain the above points. However, most doctors only keep their treatment or medications at the first step, which is the main reason of the disease relapse.

Besides, due to low immunity, IgA Nephropathy patients are also easy to get low immunity, which makes them are easy to get various infection. Thefore, preventing infection is very important.