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{{SK}} IgA nephritis; IgAN; Berger's disease; synpharyngitic glomerulonephritis
{{SK}} IgA nephritis; IgAN; Berger's disease; synpharyngitic glomerulonephritis
==Therapy==
The ideal treatment for IgAN would remove IgA from the glomerulus and prevent further IgA deposition.  This goal still remains a remote prospect. There are a few additional caveats that have to be considered while treating IgA nephropathy. IgA nephropathy has a very variable course, ranging from a benign recurrent [[hematuria]] up to a rapid progression to [[chronic renal failure]]. Hence the decision on which patients to treat should be based on the prognostic factors and the risk of progression. Also, IgA nephropathy recurs in [[transplant]]s despite the use of [[ciclosporin]], [[azathioprine]] or [[mycophenolate mofetil]] and [[steroid]]s in these patients. There are persisting uncertainties, due to the limited number of patients included in the few controlled randomized studies performed to date, which hardly produce statistically significant evidence regarding the heterogeneity of IgA nephropathy patients, the diversity of study treatment protocols, and the length of follow-up.
Patients with isolated hematuria, [[proteinuria]] < 1 g/day and normal [[renal function]] have a benign course and are generally just followed up annually. In cases where [[tonsillitis]] is the precipitating factor for episodic hematuria, [[tonsillectomy]] has been claimed to reduce the frequency of those episodes. However, it does not reduce the incidence of progressive [[chronic renal failure|renal failure]]{{ref|Xie}}. Also, the natural history of the disease is such that episodes of frank [[hematuria]] reduce over time, independent of any specific treatment. Similarly, [[prophylactic]] [[antibiotic]]s have not been proven to be beneficial.  Dietary [[gluten]] restriction, used to reduce mucosal [[antigen]] challenge, also has not been shown to preserve [[renal function]]. [[Phenytoin]] has been also been tried without any benefit{{ref|Clarkson}}.
A subset of IgA nephropathy patients, who have [[minimal change disease]] on light [[microscopy]] and clinically have [[nephrotic syndrome]], show an exquisite response to [[steroid]]s, behaving more or less like [[minimal change disease]]. In other patients, the evidence for steroids is not compelling.  Short courses of high dose steroids have been proven to lack benefit.  However, in patients with preserved [[renal function]] and proteinuria (1-3.5 g/day), a recent prospective study has shown that 6 months regimen of steroids may lessen proteinuria and preserve renal function{{ref|Kobayashi}}. However, the risks of long-term steroid use have to be weighed in such cases.  It should be noted that the study had 10 years of patient follow-up data, and did show a benefit for steroid therapy; there was a lower chance of reaching end-stage renal disease (renal function so poor that dialysis was required) in the steroid group.  Importantly, angiotensin-converting enzyme inhibitors were used in both groups equally.
[[Cyclophosphamide]] had been used in combination with antiplatelets / [[anticoagulant]]s in unselected IgA nephropathy patients with conflicting results. Also, the side effect profile of this drug, including long term risk of [[malignancy]] and [[infertility|sterility]], made it an unfavorable choice for use in young adults. However, one recent study, in a carefully selected high risk population of patients with declining GFR, showed that a combination of steroids and [[cyclophosphamide]] for the initial 3 months followed by [[azathioprine]] for a minimum of 2 years resulted in a significant preservation of renal function {{ref|Ballardie}}. Other agents such as [[mycophenolate mofetil]], [[ciclosporin]] and mizoribine have also been tried with varying results.
A study from Mayo Clinic did show that long term treatment with omega-3 fatty acids results in reduction of progression to [[renal failure]], without, however, reducing [[proteinuria]] in a subset of patients with high risk of worsening [[kidney function]]{{ref|Donadio}}. However, these results have not been reproduced by other study groups and in two subsequent meta-analyses {{ref|Strippoli}}{{ref|Dillon}}. However, fish oil therapy does not have the drawbacks of [[immunosuppressive therapy]].  Also, apart from its unpleasant taste and abdominal discomfort, it is relatively safe to consume.
The events that tend to progressive renal failure are not unique to IgA nephropathy and non-specific measures to reduce the same would be equally useful. These include low-protein diet and optimal control of [[blood pressure]].  The choice of the [[antihypertensive]] agent is open as long as the blood pressure is controlled to desired level.  However, [[Angiotensin converting enzyme inhibitor]]s and [[Angiotensin II receptor antagonist]]s are favoured due to their anti-proteinuric effect.


==References==
==References==

Revision as of 22:18, 27 September 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: IgA nephritis; IgAN; Berger's disease; synpharyngitic glomerulonephritis

References

  1. ^ Xie Y, Chen X, Nishi S, Narita I, Gejyo F. Relationship between tonsils and IgA nephropathy as well as indications of tonsillectomy. Kidney Int. 2004;65(4):1135-44. PMID 15086452
  2. ^ Clarkson AR, Seymour AE, Woodroffe AJ, et al. Controlled trial of phenytoin therapy in IgA nephropathy. Clin Nephrol. 1980;13(5):215-8. PMID 6994960
  3. ^ Kobayashi Y, Hiki Y, Kokubo T, et al: Steroid therapy during the early stage of progressive IgA nephropathy: A 10-year follow-up study. Nephron. 1996;72:237-242 PMID 8684533.
  4. ^ Ballardie FW, Roberts IS: Controlled prospective trial of prednisolone and cytotoxics in progressive IgA nephropathy. J Am Soc Nephrol. 2002;13:142-148 PMID 11752031.
  5. ^ Donadio JV Jr, Bergstralh EJ, Offord KP, Spencer DC, Holley KE: A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology Collaborative Group.N Engl J Med. 1994;331(18):1194-9 PMID 7935657
  6. ^ Strippoli G, Mano C, Schena F. An ‘evidence-based’ survey of therapeutic options for IgA nephropathy: assessment and criticism. Am J Kidney Dis. 2003;41:1129–1139 PMID 12776264
  7. ^ Dillon JJ. Fish oil therapy for IgA nephropathy: efficacy and interstudy variability. J Am Soc Nephrol. 1997;8:1739–1744 PMID 9355077
  8. ^ Bartosik LP, Lajoie G, Sugar L, Cattran DC. Predicting progression in IgA nephropathy. Am J Kidney Dis. 2001;38(4):728-35. PMID 11576875


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