Treatment of IgA nephropathy

被引:120
作者
Barratt, J. [1 ]
Feehally, J. [1 ]
机构
[1] Univ Leicester, Leicester Gen Hosp, Dept Infect Immun & Inflmmat, John Walls Renal Unit, Leicester LE5 4PW, Leics, England
关键词
IgA deposition; IgA; IgA nephropathy; treatment;
D O I
10.1038/sj.ki.5000419
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
IgA nephropathy (IgAN) is an important cause of progressive kidney disease with 25-30% of patients developing end-stage renal disease within 20 years of diagnosis. There is still no treatment to modify mesangial IgA deposition and available treatments are those extrapolated from the management of other patterns of chronic glomerulonephritis. There remains no consensus on the use of immunosuppressive agents for treatment of progressive IgAN and this is compounded by the relative lack in IgAN of randomized controlled trials relevant to current clinical practice. Patients with recurrent macroscopic hematuria or isolated microscopic hematuria and proteinuria < 1 g/24 h require no specific treatment. Those with nephrotic syndrome and minimal change on renal biopsy should be managed as for minimal change nephropathy. There is no evidence to support the use of corticosteroids for nephrotic IgAN outside this group of patients. Patients presenting with acute renal failure require evaluation to distinguish acute tubular necrosis, which requires supportive therapy only, from crescentic IgAN, for which treatment with cyclophosphamide and corticosteroids in a regimen similar to that for renal small vessel vasculitis is indicated in the absence of significant chronic histologic injury. Patients at greatest risk of progressive renal impairment are those with hypertension, proteinuria > 1 g/24 h, and reduced glomerular filtration rate at diagnosis. All such patients should be treated to a blood pressure of 125/75 mm Hg with dual blockade of the renin-angiotensin system with angiotensin-converting enzyme inhibition and angiotensin receptor blockade. At present, there is insufficient evidence for the additional use of immunosuppressive agents, antiplatelet agents, or anticoagulants.
引用
收藏
页码:1934 / 1938
页数:5
相关论文
共 27 条
[1]  
Ballardie FW, 2002, J AM SOC NEPHROL, V13, P142, DOI 10.1681/ASN.V131142
[2]  
Chen Xiangmei, 2002, Zhonghua Yi Xue Za Zhi, V82, P796
[3]   MESANGIAL IMMUNOGLOBULIN A DEPOSITS IN MINIMAL CHANGE NEPHROTIC SYNDROME - A REPORT OF AN OLDER PATIENT AND REVIEW OF THE LITERATURE [J].
CLIVE, DM ;
GALVANEK, EG ;
SILVA, FG .
AMERICAN JOURNAL OF NEPHROLOGY, 1990, 10 (01) :31-36
[4]   Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome [J].
D'Amico, G .
SEMINARS IN NEPHROLOGY, 2004, 24 (03) :179-196
[5]  
Donadio JV, 1999, J AM SOC NEPHROL, V10, P1772
[6]  
FEEHALLY J, 2002, THERAPY NEPHROLOGY H
[7]   Recurrent IgA nephropathy after renal transplantation [J].
Floege, J .
SEMINARS IN NEPHROLOGY, 2004, 24 (03) :287-291
[8]   Mycophenolate mofetil (MMF) vs placebo in patients with moderately advanced IgA nephropathy:: a double-blind randomized controlled trial [J].
Frisch, G ;
Lin, J ;
Rosenstock, J ;
Markowitz, G ;
D'Agati, V ;
Radhakrishnan, J ;
Preddie, D ;
Crew, J ;
Valeri, A ;
Appel, G .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2005, 20 (10) :2139-2145
[9]  
FURUSE A, 1985, INT J PED NEPHROL, V6, P205
[10]   ANCA-associated crescentic glomerulonephritis with mesangial IgA deposits [J].
Haas, M ;
Jafri, J ;
Bartosh, SM ;
Karp, SL ;
Adler, SG ;
Meehan, SM .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2000, 36 (04) :709-718