Immunoglobulin-A nephropathy is the most common chronic glomerulonephritis worldwide. Metabolic risk factors, such as hyperuricaemia and hypertriglyceridaemia, are associated with the progression of this condition.

Prognosis
Although considered as a benign glomerulopathy, IgA nephropathy is now a well-known cause of end-stage renal disease (ESRD). Fifty percent of people suffering from gA nephropathy develop renal insufficiency and 20 to 30% may reach ESRD after 20 to 25 years of evolution.

Main Symptoms
Main symptoms are painless macrohematuria or microhematuria.

Natural Treatment of IgA Nephropathy
Treatment of IgA nephropathy with natural supplements has hardly been studied. I have listed a few supplements and herbs that have been looked at, but before starting a natural treatment program with these supplements, make sure you discuss with your doctor.

Fish oils are found in cold water fish and as supplements. It is certainly worthwhile to consider adding omega-3 fish oils to one's supplement regimen.
Antioxidants such as Vitamins C, E, and alpha lipoic acid antioxidant
Cordyceps mushroom
White peony root herb
Perilla frutescens herb

One option is to try each supplement for a period of 2 months, have a 2 week interval in between each one, and to see which one of these natural IgA nephropathy treatment options works best.

Fish oils, omega-3 fatty acids
The effect of EPA in patients with IgA nephropathy is not pronounced, but these results suggest that EPA is a safe and worthwhile supplement to the drugs used to treat this disease. Ther Apher Dial. 2010. Effects of eicosapentaenoic acid supplementation on immunoglobulin A nephropathy.

Treatment of severe IgA nephropathy with omega-3 fatty acids: the effect of a "very low dose" regimen.
Ren Fail. 2004.
The effect of a "very low dose" of purified omega-3 fatty acids (PFA) in the progression of severe IgA nephropathy was tested, in a randomized, prospective, controlled trial. Fourteen patients were assigned to receive a "very low dose" of PFA (0.85 g EPA and 0.57 g PHA) and 14 patients were treated symptomatically and used as controls. Both groups were similar in terms of serum creatinine (Scr) and glomerular filtration rate (GFR) at baseline. Patients were treated for 4 years. A "very low dose" of PFA is also effective in slowing renal progression in high-risk patients with IgA Nephropathy and particularly those with advanced renal disease.

Effect of 12-month therapy with omega-3 polyunsaturated acids on glomerular filtration response to dopamine in IgA nephropathy.
Am J Nephrol. 2004.
Omega-3 polyunsaturated acids therapy is efficient in primary IgA nephropathy. It is unknown whether doses of omega-3 smaller than those given previously are still effective. The aim of the study was to examine the effect of omega-3 therapy on renal vascular function in relation to proteinuria and urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). 20 IgA Nephropathy patients aged 36.5 +/- 10 with creatinine clearance (Cr(cl)) 105 +/- 27 ml/min and proteinuria 3 +/- 2 g/24 h were given orally 810 mg EPA and 540 mg DHA daily for 12 months. Omega-3 supplementation is associated with the improvement of both renal vascular function and tubule function in IgA Nephropathy patients.

Oxidized omega-3 fatty acids inhibit pro-inflammatory responses in glomerular endothelial cells.
Nephron Exp Nephrol. 2004.
Department of Pathology, University of Iowa of Iowa Hospitals and Clinics, Iowa City, Iowa
Omega-3 fatty acids have beneficial effects in chronic inflammatory diseases that are characterized by accumulation of leukocytes and leukocyte-mediated tissue injury. Accumulation of leukocytes occurs, in part, due to pro-inflammatory responses in endothelial cells, such as increase in expression of leukocyte adhesion receptors and chemokines, such as MCP-1 and IL-8. These studies show that the beneficial effects of fish oil in chronic inflammatory diseases, including IgA nephropathy, may result from the inhibitory effects of oxidized omega-3 fatty acids on pro-inflammatory events in endothelial cells via inhibition of NF-kappaB activation.

Docosahexaenoic acid attenuates mycotoxin-induced immunoglobulin a nephropathy, interleukin-6 transcription, and mitogen-activated protein kinase phosphorylation in mice.
J Nutr. 2004. Jia Q, Zhou HR, Bennink M, Pestka JJ. Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI
The purpose of this investigation was to evaluate the dose-dependent effects of docosahexaenoic acid (DHA) on deoxynivalenol (DON)-induced IgA nephropathy in mice and their relation to proinflammatory gene expression and mitogen-activated protein kinase (MAPK) activation. Taken together, the results indicate that DHA dose-dependently inhibited DON-induced IgA dysregulation and nephropathy, and that impairment of MAPK activation and expression of COX-2 and IL-6 are potential critical upstream mechanisms.

Docosahexaenoic acid and eicosapentaenoic acid, but not alpha-linolenic acid, suppress deoxynivalenol-induced experimental IgA nephropathy in mice.
J Nutr. 2004.
Department of Food Science and Human Nutrition, and Center for Integrative Toxicology, Michigan State University, East Lansing, MI
Diets enriched in the (n-3) PUFAs, docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and their precursor alpha-linolenic acid (ALA), were evaluated for efficacy in ameliorating the development of IgA nephropathy induced in mice by the mycotoxin deoxynivalenol (DON). Taken together, both DHA and EPA, but not ALA, ameliorated the early stages of IgA Nephropathy, and these effects might be related to a reduced capacity for IL-6 production.

The role of fish oil/omega-3 fatty acids in the treatment of IgA nephropathy.
Semin Nephrol. 2004. Division of Nephrology, the Department of Medicine, and the Department of Laboratory Medicine and Pathology, Mayo Clinic & Mayo Foundation, Rochester, MN
Fish and marine oils are the most abundant and convenient sources of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the two major n-3 fatty acids that serve as substrates for cyclooxygenase and lipoxygenase pathways leading to less potent inflammatory mediators than those produced through the n-6 PUFA substrate, arachidonic acid. N-3 PUFA can also suppress inflammatory and/or immunologic responses through eicosanoid-independent mechanisms. Although the pathophysiology of IgA nephropathy is incompletely understood, it is likely that n-3 PUFA prevents renal disease progression by interfering with a number of effector pathways triggered by mesangial immune-complex deposition. In addition, potential targets of n-3 PUFA relevant to renal disease progression could be similar to those involved in preventing the development and progression of cardiovascular disease by lowering blood pressure, reducing serum lipid levels, decreasing vascular resistance, or preventing thrombosis. In IgA nephropathy, efficacy of n-3 PUFA contained in fish oil supplements has been tested with varying results. The largest randomized clinical trial performed by our collaborative group provided strong evidence that treatment for 2 years with a daily dose of 1.8 g of EPA and 1.2 g of DHA slowed the progression of renal disease in high-risk IgA Nephropathy patients. These benefits persisted after 6 years of follow up.

The long-term outcome of patients with IgA nephropathy treated with fish oil in a controlled trial. Mayo Nephrology Collaborative Group.
J Am Soc Nephrol. 1999.
Department of Internal Medicine, Mayo Clinic & Foundation, Rochester, Minnesota
It was reported previously that dietary fish oil supplementation retarded the progression of renal disease in patients with IgA nephropathy in a multicenter, placebo-controlled, randomized, 2-yr clinical trial. The aim of this study was to determine the long-term influence of fish oil treatment on renal progression in observations on the study cohort of 106 patients extending beyond the 2-yr trial. After a mean follow-up of 6.4 yr, 46 patients-17 in the fish oil group versus 29 in the placebo group-reached the primary end point, and 27 patients-eight in the fish oil group versus 19 in the placebo group-developed ESRD. At the end of the 2-yr trial, 75 patients (45 fish oil, 30 placebo) remained at risk for the primary end point. This is also when the double-blind part of the trial ended, allowing physicians to stop supplements, switch original placebo-assigned patients to fish oil, and continue fish oil in original fish oil-assigned patients. A significantly greater number of nonsupplemented placebo patients developed the primary end point and ESRD compared with long-term supplemented fish oil patients. By intention, BP control, primarily treated with angiotensin-converting enzyme inhibition, was equal in the fish oil and placebo groups. Proteinuria was modestly reduced in both groups. It is concluded that early and prolonged treatment with fish oil slows renal progression for high-risk patients with IgA nephropathy.

IGA Nephropathy Treatment research
Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy.
J Zhejiang Univ Sci B. 2005. Division of Nephrology, School of Medicine, Zhejiang University, Hangzhou China.
To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy patients' bodies. Seventy-two IgA nephropathy patients  and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric methods. Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgA nephropathy group were significantly increased, while those of VC, VE and beta-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgA nephropathy group were significantly decreased. Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those of VC, VE, beta-CAR, SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually; and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, beta-CAR, SOD, CAT and GPX were decreased gradually. The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgA nephropathy patients were 73%-92%, and the correct rates for the HAV were 70%-91% when independent discriminant analysis was used; and the correct rate for the IgA nephropathy patients was increased to 98%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. A series of free radical chain reactions caused serious pathological aggravation in the IgA nephropathy patients'  bodies, thus resulting in oxidative damage in their bodies. In treating IgA nephropathy, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Pathogenesis of IgA nephropathy.
Semin Nephrol. 2004.
In IgA nephropathy, there is dysregulation of the IgA response to a wide range of antigens. The dysregulation promotes synthesis of polymeric IgA1 (pIgA1) with physicochemical characteristics that favor mesangial deposition, including altered O-glycosylation of the hinge region. This may be the synthesis of IgA in the systemic compartment, which has the phenotype of mucosal IgA. There is not a change in IgA1 structure to an entirely abnormal form; rather, there is a shift that results in a proportional increase in forms of IgA1 also found in healthy individuals. Altered O-glycosylation could favor pIgA1 deposition by promoting formation of macromolecular IgA and immune complexes. Mesangial injury follows through interactions of pIgA1 with the cells and extracellular matrix proteins of the mesangium and the activation of complement. The final clinical expression of IgA Nephropathy also depends on generic factors, including hypertension and proteinuria, and a fibrotic renal response. No single IgA Nephropathy gene has been identified, and it is likely that multiple interacting genes will eventually prove to underlie susceptibility to IgA Nephropathy and the risk of progressive renal disease.

Clinical study on dan shao tang in treating IgA nephropathy of deficiency of yin with damp-heat symptom
Zhong Yao Cai. 2003.
To explore the effect of Dan Shao Tang in treating IgA nephropathy of deficiency of Yin with damp-heat symptom. METHODS: 90 patients with IgA nephropathy of deficiency of Yin with damp-heat symptom were randomly divided into two groups. 50 patients in treatment group were treated with Dan Shao Tang and western medicine and 40 patients in control group were treated only with western medicine. The effects and changes of the indexes including renal function, hematuria, proteinuria, blood IgA before and after treatment were observed. After six months treatment, the general effective rate in treatment group was 70%, which was markedly higher than that in control group. Treatment group is obviously better than control group on decreasing hematuria, proteinuria, blood IgA and improving renal function. Dan Shao Tang is effective on IgA nephropathy of deficiency of Yin with damp-heat symptom.

The effect of the extract from Radix Paeoniae alba on IgA Glomerulonephritis in mice
Zhong Yao Cai. 2003.
To observe the effect of the extract from Radix Paeoniae Alba ( white peony root )on IgA glomerulonephritis in mice. METHODS: IgA glomerulonephritis was induced by injection of dextran and sephadex-150. After administrating the extract, the contents of urinary protein, BUN and Cr in serum were determined. RESULTS: The extract could inhibit the decline of mouse weight, and decrease urinary protein content and BUN content in serum. While, the extract had no effect on Cr in serum. The extract from Radix Paeoniae Alba had therapeutical effect on IgA glomerulonephritis.

Suppressive effects of Perilla frutescens on IgA nephropathy in HIGA mice.
Nephrol Dial Transplant. 2003.
Perilla frutescens (perilla) is a herbal medicine used in Japanese traditional Kampo medicine. The present study was conducted to evaluate the anti-nephritic effects of perilla in HIGA mice that spontaneously develop high levels of serum immunoglobulin A (IgA) along with mesangial IgA deposition. A perilla decoction and its major active constituent, rosmarinic acid (RsA), were orally administrated to 10-week-old HIGA mice for 16 weeks. Perilla suppressed proteinuria, proliferation of glomerular cells, serum levels of IgA, glomerular IgA and IgG depositions in HIGA mice. Cultured Peyer's patch cells and spleen cells from perilla-treated mice produced significantly less IgA than controls. Rosmarinic acid, by itself, suppressed serum IgA levels and glomerular IgA deposition in HIGA mice. Cultured spleen cells from RsA-treated mice produced less IgA than controls. The perilla decoction may suppress IgA nephropathy, in part, through modulation of the intestinal mucosal immune system. These effects were caused by rosaminic acid acting synergistically with other constituents.

Clinical study on Shenning Mixture in treating IgA nephropathy
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000.
To study the clinical therapeutic effect of Shenning Mixture (SNM) in treating IgA nephropathy. Patients were treated separately with SNM or prednisone by randomized grouping. The criteria, including clinical symptoms, signs, hematuria, albuminuria and immune globulin were observed. The total effective rate and the complete remission rate in the SNM group were 97% and 45% respectively, while in the control group, they were 37% and 8% respectively. Comparison of the two groups showed that the therapeutic effect in the former was better than that in the latter significantly. The hematuria and albuminuria extenuated and serum IgA lowered more significantly in the SNM group than those in the control group. SNM has obvious therapeutic effect on the hematuria and albuminuria in treating IgA nephropathy.

Inhibition of activated human mesangial cell proliferation by the natural product of Cordyceps sinensis (H1-A): an implication for treatment of IgA mesangial nephropathy.
J Lab Clin Med. 1999.
Cordyceps sinensis is a parasitic fungus that has been used as a Chinese medicine for a long time in the treatment of nephritis. Today, the hypothesis about the pathogenesis of immunoglobulin A nephropathy is that nephritogenic IgA immune complexes (IgAIC) go to the kidney to stimulate resting mesangial cells to release cytokines and growth factors. These cytokines and growth factors cause mesangial cell proliferation and release matrix, chemical mediators that lead to the glomerular injury. However, nephritogenic IgAIC in humans is still unknown. To solve this problem previously, we established an in vitro model that showed that cultured human mesangial cells (HMC) stimulated with interleukin-1 (IL-1) plus IL-6 can cause mesangial cell proliferation, increasing production of chemical mediators and superoxide anion. An in vivo model also proved that this culture medium may lead to renal injury with hematuria and proteinuria. These results give us a new regimen for the treatment of patients with IgA Nephropathy in the future. iga nephropathy bergers disease cause of iga nephropathy.

Managing Henoch-Schonlein purpura in children with fish oil and ACE inhibitor therapy.
Nephrology (Carlton). 2004.
Department of Pediatrics, Steele Memorial Children's Research, University of Arizona, Tucson, Arizona
The kidney biopsy in Henoch-Schonlein purpura shows IgA deposits and fish-oil therapy has proven to be promising in halting the progression of IgA nephropathy. Five children with biopsy-proven HSP with repeated episodes of haematuria and proteinuria were treated with fish oil (1 g orally twice daily). In three of the five patients an angiotensin-converting enzyme inhibitor (ACEI) was added for hypertension. This is the first report of abatement of Henoch-Schonlein purpura with fish oil and ACEI in children. There is a need for randomized prospective trials to confirm this observation.

Emails
Have you seen any research with idebenone and this kidney disorder?
   I have not.