777:. 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 aggressive Berger's disease 6 months regimen of steroids in addition to other medications may lessen proteinuria and preserve renal function. 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.
380:
1091:
Julian, Bruce A.; Novak, Jan; Wyatt, Robert J.; Mucha, Krzysztof; Perola, Markus; Kristiansson, Kati; Viktorin, Alexander; Magnusson, Patrik K.; Thorleifsson, Gudmar; Thorsteinsdottir, Unnur; Stefansson, Kari; Boland, Anne; Metzger, Marie; Thibaudin, Lise; Wanner, Christoph; Jager, Kitty J.; Goto, Shin; Maixnerova, Dita; Karnib, Hussein H.; Nagy, Judit; Panzer, Ulf; Xie, Jingyuan; Chen, Nan; Tesar, Vladimir; Narita, Ichiei; Berthoux, Francois; Floege, Jürgen; Stengel, Benedicte; Zhang, Hong; Lifton, Richard P.; Gharavi, Ali G. (21 June 2012).
64:
1036:
474:
people to a lesser extent. This strongly suggests degalactosylation of IgA1 is a result of an underlying phenomenon (abnormal mucosal antigen handling) and not the ultimate cause of IgA nephropathy. Prevailing evidence suggests that both galactose-deficient o-glycans in the hinge region of IgA1 and synthesis and binding of antibodies against IgA1 are required for immunoglobulin complexes to form and accumulate in glomeruli.
435:, it has been found that although it shares the same histological spectrum as IgA nephropathy, a greater frequency of severe lesions such as glomerular necrosis and crescents were observed. Correspondingly, HSP nephritis has a higher frequency of glomerular staining for fibrin compared with IgAN, but with an otherwise similar immunofluorescence profile.
1733:
967:, accounting for almost half of all the patients with glomerular disease. However, it accounts for only about 25% of the proportion in Europeans and about 10% among North Americans, with African–Americans having a very low prevalence of about 2%. A confounding factor in this analysis is the existing policy of
722:
in these patients. There are persisting uncertainties, due to the limited number of patients included in the few controlled, randomized, studies performed to date. These studies hardly produce statistically-significant evidence regarding the heterogeneity of IgA nephropathy patients, the diversity of
538:
of aggressive Berger's disease rarely occurs in adults. In about 5% of cases, however, there is a higher chance of remission with non-aggressive Berger's disease (this is estimated to be around 7.4% of cases). There is a high chance of relapse, particularly with aggressive Berger's disease. However,
473:
that mainly affects children and can feature renal involvement that is almost indistinguishable from IgA nephritis. However, human studies have found that degalactosylation of IgA1 occurs in patients with IgA nephropathy in response only to gut antigen exposures (not systemic), and occurs in healthy
685:
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
521:
Nevertheless, IgA nephropathy, which was initially thought to be a benign disease, has been shown to not be a benign disease, particularly if the patient presents with an aggressive form. Though most reports describe Berger's disease as having an indolent evolution towards either healing or renal
1090:
Kiryluk, Krzysztof; Li, Yifu; Sanna-Cherchi, Simone; Rohanizadegan, Mersedeh; Suzuki, Hitoshi; Eitner, Frank; Snyder, Holly J.; Choi, Murim; Hou, Ping; Scolari, Francesco; Izzi, Claudia; Gigante, Maddalena; Gesualdo, Loreto; Savoldi, Silvana; Amoroso, Antonio; Cusi, Daniele; Zamboli, Pasquale;
530:
is slow as compared to most other glomerulonephritides – occurring over a time scale of 30 years or more (in contrast to the 5 to 15 years in other glomerulonephritides), however, in aggressive Berger's disease the time scale is within 5–10 years and often sooner. This may reflect the earlier
205:, and abdominal pain, and occurs more commonly in children. HSP is associated with a more benign prognosis than IgA nephropathy. In non-aggressive IgA nephropathy there is traditionally a slow progression to chronic kidney failure in 25–30% of cases during a period of 20 years.
334:; see below for more details on the association. Some HLA alleles have been suspected along with complement phenotypes as being genetic factors. Non-aggressive Berger's disease may also be associated with any of the above systemic diseases, however, this is rare.
399:
999:
Though various associations have been described, no consistent pattern pointing to a single susceptible gene has been identified to date. Associations described include those with C4 null allele, factor B Bf alleles, MHC antigens and IgA isotypes. ACE
342:
Histologically, IgA nephropathy may show mesangial widening and focal and segmental inflammation. Diffuse mesangial proliferation or crescentic glomerulonephritis may also be present. Immunofluorescence shows mesangial deposition of IgA often with
1910:
1895:
1785:
Barbour, Sean J.; Coppo, Rosanna; Zhang, Hong; Liu, Zhi-Hong; Suzuki, Yusuke; Matsuzaki, Keiichi; Katafuchi, Ritsuko; Er, Lee; Espino-Hernandez, Gabriela; Kim, S. Joseph; Reich, Heather N.; Feehally, John; Cattran, Daniel C. (2019-07-01).
481:
rather than the kidney itself. Remarkably, the IgA1 that accumulates in the kidney does not appear to originate from the mucosa-associated lymphoid tissue (MALT), which is the site of most upper respiratory tract infections, but from the
407:
371:) are usually not seen. Electron microscopy confirms electron-dense deposits in the mesangium that may extend to the subendothelial area of adjacent capillary walls in a small subset of cases, usually those with focal proliferation.
237:
will persist, it is however more common with aggressive Berger's disease for gross hematuria to persist rather than microscopic hematuria. Renal function usually remains normal with non-aggressive Berger's disease, though rarely
249:(less than 2 gram/day). These patients may be asymptomatic and only picked up due to urinalysis. Hence, the disease is more commonly diagnosed in situations where screening of urine is compulsory (e.g., schoolchildren in
861:
The events that tend to progressive kidney failure are not unique to IgA nephropathy and non-specific measures to reduce the same would be equally useful. These include a low-protein diet and optimal control of
1872:
442:
for IgA have not been identified in the kidney, but it is possible that this antigen has been cleared before the disease manifests itself. It has also been proposed that IgA itself may be the antigen.
1349:
Suzuki, Hitoshi; Kiryluk, Krzysztof; Novak, Jan; Moldoveanu, Zina; Herr, Andrew; Renfrow, Matthew; Wyatt, Robert; Scolari, Francesco; Mestecky, Jiri; Gharavi, Ali; Julian, Bruce (October 1, 2011).
959:
Men are affected three times as often as women. There is also marked geographic variation in the prevalence of IgA nephropathy throughout the world. It is the most common glomerular disease in the
330:. Diagnosis of Berger's disease and a search for any associated disease occasionally reveals such an underlying serious systemic disease. Occasionally, there are simultaneous symptoms of
405:
404:
401:
400:
694:
and failure of other major organs. 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
406:
917:
has shown discordant results with most studies showing a better prognosis, perhaps related to the early diagnosis, except for one group which reported a poorer prognosis.
854:. However, these results have not been reproduced by other study groups and in two subsequent meta-analyses. However, fish oil therapy does not have the drawbacks of
403:
178:
IgA nephropathy is the most common glomerulonephritis worldwide; the global incidence is 2.5/100,000 per year amongst adults. Aggressive Berger's disease is on the
2090:
578:
causes of hematuria. In children and younger adults, the history and association with respiratory infection can raise the suspicion of IgA nephropathy. A kidney
2229:
811:, made them an unfavorable choice for use in young adults. However, one recent study, in a carefully selected high risk population of patients with declining
2021:
1517:
Kobayashi Y, Hiki Y, Kokubo T, Horii A, Tateno S (1996). "Steroid therapy during the early stage of progressive IgA nephropathy. A 10-year follow-up study".
2085:
445:
A recently advanced theory focuses on abnormalities of the IgA1 molecule. IgA1 is one of the two immunoglobulin subclasses (the other is IgD) that is
2095:
885:(Tarpeyo) was approved for medical use in the US to reduce proteinuria in adults with primary IgA nephropathy at risk of rapid disease progression.
179:
871:
2207:
2180:
2168:
2146:
2137:
1710:
269:
226:
1634:
Strippoli GF, Manno C, Schena FP (2003). "An "evidence-based" survey of therapeutic options for IgA nephropathy: assessment and criticism".
1490:
Clarkson AR, Seymour AE, Woodroffe AJ, McKenzie PE, Chan YL, Wootton AM (1980). "Controlled trial of phenytoin therapy in IgA nephropathy".
402:
1925:
1020:
2062:
875:
218:
290:
and other symptoms of kidney failure, in people who probably had longstanding undetected microscopic hematuria and/or proteinuria)
2219:
2014:
466:
432:
331:
194:
190:
2190:
542:
Overall, the current 10-year survival rate for aggressive Berger's disease is 25% and 73% for non-aggressive Berger's disease.
477:
From the fact that IgAN can recur after renal transplant, it can be postulated that the disease is caused by a problem in the
654:
627:
379:
803:
in patients with
Aggressive Berger's disease, however, the side effect profile of these drugs, including long term risk of
2067:
1093:"Geographic Differences in Genetic Susceptibility to IgA Nephropathy: GWAS Replication Study and Geospatial Risk Analysis"
2280:
1716:
360:
307:
465:
of the IgA molecules in tissues, especially the glomerular mesangium. A similar mechanism has been claimed to underlie
197:), which is considered by many to be a systemic form of IgA nephropathy. IgA vasculitis presents with a characteristic
2007:
1069:, with co-author, the electron microscopist Nicole Hinglais, was the first to describe IgA deposition in this form of
734:
has been claimed to reduce the frequency of those episodes. However, it does not reduce the incidence of progressive
539:
given the evolution of this disease, the longer term (10–20 years) outcome of such patients is not yet established.
2116:
812:
229:, which occurs some time (weeks) after initial infection. With both aggressive and non-aggressive Berger's disease
2172:
1055:
855:
2275:
2224:
2150:
1936:
988:
987:) and any suspicious abnormality is pursued with a kidney biopsy, which might partly explain the high observed
972:
929:
579:
503:
1868:
1259:
Maverakis E, Kim K, Shimoda M, Gershwin M, Patel F, Wilken R, Raychaudhuri S, Ruhaak LR, Lebrilla CB (2015).
1011:. However, more than 90% of cases of IgA nephropathy are sporadic, with a few large pedigrees described from
1007:(D allele) is associated with progression of kidney failure, similar to its association with other causes of
522:
damage, a more aggressive course is occasionally seen associated with extensive crescents, and presenting as
670:
555:
189:
in the glomerulus. There are other diseases associated with glomerular IgA deposits, the most common being
2057:
1059:
1008:
1004:
933:
774:
758:
735:
691:
527:
368:
344:
323:
279:
273:
1553:
294:
A variety of systemic diseases are associated with aggressive IgA nephropathy (Berger's disease) such as
1670:
824:
823:
for a minimum of 2 years resulted in a significant preservation of renal function. Other agents such as
707:
666:
662:
595:
515:
234:
1062:, a student of Schönlein's, further associated abdominal pain and renal involvement with the syndrome.
163:. Aggressive Berger's disease (a rarer form of the disease) can attack other major organs, such as the
2158:
2111:
968:
858:. Also, apart from its unpleasant taste and abdominal discomfort, it is relatively safe to consume.
535:
523:
499:
428:
383:
311:
265:
239:
31:
1914:
1310:"O-glycosylation of serum IgA1 antibodies against mucosal and systemic antigens in IgA nephropathy"
839:
591:
424:
387:
156:
2254:
2249:
2132:
2077:
2049:
2040:
1070:
1058:
described a syndrome of purpura associated with joint pain and urinary precipitates in children.
766:
650:
639:
635:
587:
518:
and isolated mesangial IgA will be included and improve the prognosis of that particular series.
420:
319:
260:
148:
1750:
Bartosik LP, Lajoie G, Sugar L, Cattran DC (2001). "Predicting progression in IgA nephropathy".
514:
will be excluded. If, in contrast, all such patients are biopsied, then the group with isolated
498:, there is considerable possibility for variation in any population studied depending upon the
1976:
1947:
1809:
1767:
1692:
1651:
1616:
1575:
1534:
1499:
1472:
1380:
1331:
1290:
1241:
1192:
1151:
1124:
796:
658:
81:
74:
1711:"FDA approves first drug to decrease urine protein in IgA nephropathy, a rare kidney disease"
486:. This, too, suggests an immune pathology rather than direct interference by outside agents.
1817:
1799:
1759:
1682:
1643:
1606:
1565:
1554:"Controlled prospective trial of prednisolone and cytotoxics in progressive IgA nephropathy"
1526:
1462:
1370:
1362:
1321:
1280:
1272:
1231:
1223:
1182:
1114:
1104:
1046:, the elder, first described the disease in 1801 in a 5-year-old child with abdominal pain,
1043:
867:
816:
780:
711:
695:
352:
245:
A smaller proportion (20–30%), usually the older population, have microscopic hematuria and
112:
71:
2185:
1451:"Relationship between tonsils and IgA nephropathy as well as indications of tonsillectomy"
902:
851:
631:
611:
599:
427:. The mesangium by light microscopy may be hypercellular and show increased deposition of
213:
The classic presentation for the non-aggressive form (in 40–50% of the cases) is episodic
63:
1187:
1170:
1595:"A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology Collaborative Group"
1171:"What is the difference between IgA nephropathy and Henoch-Schönlein purpura nephritis?"
2030:
1822:
1375:
1350:
1285:
1260:
1236:
1211:
1119:
1092:
964:
941:
906:
863:
843:
747:
571:
303:
140:
35:
1919:
1647:
1035:
870:
agent is open as long as the blood pressure is controlled to desired level. However,
582:
is necessary to confirm the diagnosis. The biopsy specimen shows proliferation of the
494:
Since IgA nephropathy commonly presents without symptoms through abnormal findings on
2269:
1787:
1737:
1467:
1450:
1398:
1142:
D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy".
800:
731:
615:
567:
478:
446:
315:
295:
268:(either as a complication of the frank hematuria, when it usually recovers or due to
182:
list of rare diseases. Primary IgA nephropathy is characterized by deposition of the
144:
17:
1804:
506:
assumes a critical role; if it is a policy to simply observe patients with isolated
2211:
1999:
1066:
1051:
948:
932:
such as interstitial scarring which are associated with a poor prognosis. ACE gene
922:
898:
820:
792:
715:
703:
287:
152:
90:
1987:
1941:
1109:
1971:
1836:
Heberden W. Commentarii Di
Morborium Historia et Curatione. London: Payne, 1801.
1611:
1594:
1212:"New developments in the genetics, pathogenesis, and therapy of IgA nephropathy"
918:
894:
847:
828:
808:
727:
699:
619:
483:
246:
1276:
438:
There is no clear known explanation for the accumulation of the IgA. Exogenous
1952:
1904:
1423:
980:
910:
882:
832:
804:
762:
646:
607:
559:
495:
470:
86:
1813:
1982:
1763:
1261:"Glycans in the immune system and The Altered Glycan Theory of Autoimmunity"
1047:
984:
914:
751:
687:
603:
583:
551:
511:
507:
454:
391:
348:
214:
202:
1771:
1671:"Fish oil therapy for IgA nephropathy: efficacy and interstudy variability"
1655:
1579:
1476:
1384:
1366:
1335:
1326:
1309:
1294:
1245:
1196:
1128:
242:
may occur (see below). This presentation is more common in younger adults.
1696:
1620:
1538:
1503:
1155:
411:
The pathophysiology, signs and symptoms, and treatment of IgA nephropathy.
1687:
1012:
960:
937:
674:
563:
416:
233:
can also occur. The gross hematuria may resolve after a few days, though
186:
1887:
1788:"Evaluating a New International Risk-Prediction Tool in IgA Nephropathy"
1570:
1227:
788:
784:
770:
743:
719:
575:
462:
458:
439:
198:
1846:
Berger J, Hinglais N (1968). "Les depots intercapillaires d'IgA-IgG".
1530:
602:) are not usually biopsied since this is associated with an excellent
1899:
739:
622:, usually less than 2 grams per day, also may be present. Other
461:-rich hinge region. Aberrant glycosylation of IgA appears to lead to
450:
299:
283:
160:
1593:
Donadio JV, Bergstralh EJ, Offord KP, Spencer DC, Holley KE (1994).
1034:
1016:
976:
623:
397:
378:
250:
172:
164:
1736:
This article incorporates text from this source, which is in the
1930:
1873:
National
Institute of Diabetes and Digestive and Kidney Diseases
1024:
1001:
838:
A study from Mayo Clinic did show that long-term treatment with
230:
168:
2003:
364:
356:
327:
183:
124:
118:
217:, which usually starts within a day or two of a non-specific
947:
Disease progression in IgAN can be predicted at the time of
502:
policy. Similarly, the local policy for performing kidney
127:
30:"Berger's disease" redirects here. Not to be confused with
925:
are the most powerful prognostic factors in this group.
723:
study treatment protocols, and the length of follow-up.
1073:
and therefore it is sometimes called Berger's disease.
1065:
In 1968, Jean Berger (1930–2011), a pioneering French
936:
has been recently shown to have an impact with the DD
730:
is the precipitating factor for episodic hematuria, a
677:
levels can show increased IgA in 50% of all patients.
598:(i.e. without associated proteinuria and with normal
562:
are usually done first to pinpoint the source of the
1877:
1308:
Smith AC, Molyneux K, Feehally J, Barratt J (2006).
913:
concentrations are markers of a poor outcome. Frank
850:
in a subset of patients with high risk of worsening
115:
2242:
2206:
2167:
2145:
2129:
2104:
2076:
2048:
2037:
1962:
1881:
878:are favoured due to their anti-proteinuric effect.
121:
80:
51:
46:
1449:Xie Y, Chen X, Nishi S, Narita I, Gejyo F (2004).
256:Very rarely (5% each), the presenting history is:
431:proteins. In terms of the renal manifestation of
419:(IgA) in a granular pattern in the mesangium (by
757:A subset of IgA nephropathy patients, who have
746:challenge, also has not been shown to preserve
842:results in slight reduction of progression to
415:The disease derives its name from deposits of
351:and smaller amounts of other immunoglobulins (
2230:Eosinophilic granulomatosis with polyangiitis
2015:
1355:Journal of the American Society of Nephrology
975:as an investigative tool. School children in
940:associated more commonly with progression to
8:
815:, showed that a combination of steroids and
928:There are certain other features on kidney
909:, older age, familial disease and elevated
835:have also been tried with varying results.
2142:
2045:
2022:
2008:
2000:
1878:
43:
1821:
1803:
1686:
1610:
1569:
1466:
1374:
1325:
1284:
1235:
1186:
1118:
1108:
754:has also been tried without any benefit.
1351:"The Pathophysiology of IgA Nephropathy"
872:Angiotensin converting enzyme inhibitors
2096:Membranoproliferative/mesangiocapillary
1082:
991:of IgA nephropathy in those countries.
531:diagnosis made due to frank hematuria.
510:, a group with a generally favourable
270:rapidly progressive glomerulonephritis
819:for the initial 3 months followed by
649:done to aid in the diagnosis include
626:causes of isolated hematuria include
282:(no previous symptoms, presents with
227:post-streptococcal glomerulonephritis
7:
1403:The Lecturio Medical Concept Library
1188:10.1046/j.1523-1755.2001.059003823.x
1054:, and purpura of the legs. In 1837,
795:have commonly been used, often with
742:restriction, used to reduce mucosal
1021:Online Mendelian Inheritance in Man
876:Angiotensin II receptor antagonists
550:For an adult patient with isolated
390:of a patient with Henoch-Schönlein
594:. However, patients with isolated
25:
1552:Ballardie FW, Roberts IS (2002).
219:upper respiratory tract infection
137:synpharyngitic glomerulonephritis
2220:Granulomatosis with polyangiitis
2031:Disease of the kidney glomerules
1731:
1468:10.1111/j.1523-1755.2004.00486.x
769:, show an exquisite response to
111:
62:
56:IgA nephritis, Berger's disease
1805:10.1001/jamainternmed.2019.0600
147:; specifically it is a form of
628:thin basement membrane disease
526:. In general, the entry into
1:
1648:10.1016/S0272-6386(03)00344-5
1210:Magistroni, Riccardo (2015).
846:, without, however, reducing
773:, behaving more or less like
690:up to a rapid progression to
566:. These tests would rule out
1717:Food and Drug Administration
1110:10.1371/journal.pgen.1002765
951:by a risk-prediction tool.
361:classical complement pathway
308:systemic lupus erythematosus
2091:Endocapillary proliferative
1612:10.1056/NEJM199411033311804
897:(especially > 2 g/day),
359:). Early components of the
2297:
1428:National Kidney Foundation
1277:10.1016/j.jaut.2014.12.002
29:
2173:Type III hypersensitivity
856:immunosuppressive therapy
423:), a region of the renal
143:(or nephropathy) and the
70:
61:
2225:Microscopic polyangiitis
2151:Type II hypersensitivity
983:(as do army recruits in
467:Henoch–Schönlein purpura
433:Henoch–Schönlein purpura
332:Henoch–Schönlein purpura
195:Henoch–Schönlein purpura
2086:Mesangial proliferative
1764:10.1053/ajkd.2001.27689
671:Protein electrophoresis
586:, with IgA deposits on
135:) (and variations), or
1792:JAMA Internal Medicine
1367:10.1681/ASN.2011050464
1327:10.1681/ASN.2006060658
1060:Eduard Heinrich Henoch
1056:Johann Lukas Schönlein
1040:
1009:chronic kidney failure
775:minimal change disease
759:minimal change disease
692:chronic kidney failure
614:, usually as red cell
528:chronic kidney failure
457:residues in a special
412:
395:
324:ankylosing spondylitis
280:Chronic kidney failure
274:chronic kidney failure
2191:diffuse proliferative
1038:
866:. The choice of the
825:mycophenolate mofetil
708:mycophenolate mofetil
634:, the latter being a
596:microscopic hematuria
516:microscopic hematuria
410:
382:
272:which often leads to
235:microscopic hematuria
141:disease of the kidney
27:Disease of the kidney
18:Berger's disease
2159:Goodpasture syndrome
1688:10.1681/ASN.V8111739
1216:Kidney International
1175:Kidney International
765:and clinically have
524:acute kidney failure
429:extracellular matrix
312:rheumatoid arthritis
266:Acute kidney failure
240:acute kidney failure
2281:Autoimmune diseases
1675:J. Am. Soc. Nephrol
1571:10.1681/ASN.V131142
1558:J. Am. Soc. Nephrol
1228:10.1038/ki.2015.252
1169:C, Davin J (2001).
840:omega-3 fatty acids
698:despite the use of
592:electron microscopy
574:, two other common
386:showing IgA in the
193:(formerly known as
2255:glomerulonephrosis
2250:glomerulonephritis
2181:Post-streptococcal
1963:External resources
1721:. 17 December 2021
1669:Dillon JJ (1997).
1430:. 24 December 2015
1071:glomerulonephritis
1041:
971:and use of kidney
881:In December 2021,
767:nephrotic syndrome
642:and eye problems.
640:hearing impairment
636:hereditary disease
588:immunofluorescence
558:of the kidney and
421:immunofluorescence
413:
396:
320:reactive arthritis
261:Nephritic syndrome
209:Signs and symptoms
149:glomerulonephritis
2263:
2262:
2238:
2237:
2125:
2124:
2050:Non-proliferative
1997:
1996:
1752:Am. J. Kidney Dis
1636:Am. J. Kidney Dis
1531:10.1159/000188848
1424:"IgA Nephropathy"
1399:"IgA Nephropathy"
1361:(10): 1795–1803.
686:benign recurrent
408:
225:), as opposed to
105:), also known as
96:
95:
41:Medical condition
32:Buerger's disease
16:(Redirected from
2288:
2143:
2046:
2024:
2017:
2010:
2001:
1879:
1856:
1855:
1843:
1837:
1834:
1828:
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1825:
1807:
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1776:
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1747:
1741:
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1734:
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1728:
1726:
1707:
1701:
1700:
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1590:
1584:
1583:
1573:
1549:
1543:
1542:
1514:
1508:
1507:
1487:
1481:
1480:
1470:
1446:
1440:
1439:
1437:
1435:
1420:
1414:
1413:
1411:
1409:
1395:
1389:
1388:
1378:
1346:
1340:
1339:
1329:
1314:J Am Soc Nephrol
1305:
1299:
1298:
1288:
1256:
1250:
1249:
1239:
1207:
1201:
1200:
1190:
1166:
1160:
1159:
1139:
1133:
1132:
1122:
1112:
1087:
1044:William Heberden
979:undergo routine
868:antihypertensive
817:cyclophosphamide
781:Cyclophosphamide
712:cyclophosphamide
638:associated with
554:, tests such as
417:immunoglobulin A
409:
134:
133:
130:
129:
126:
123:
120:
117:
107:Berger's disease
72:Immunoglobulin A
66:
44:
21:
2296:
2295:
2291:
2290:
2289:
2287:
2286:
2285:
2276:Kidney diseases
2266:
2265:
2264:
2259:
2234:
2202:
2163:
2136:
2131:
2121:
2100:
2072:
2063:Focal segmental
2039:
2033:
2028:
1998:
1993:
1992:
1958:
1957:
1890:
1869:IGA Nephropathy
1865:
1860:
1859:
1845:
1844:
1840:
1835:
1831:
1784:
1783:
1779:
1749:
1748:
1744:
1732:
1724:
1722:
1709:
1708:
1704:
1681:(11): 1739–44.
1668:
1667:
1663:
1633:
1632:
1628:
1605:(18): 1194–99.
1599:N. Engl. J. Med
1592:
1591:
1587:
1551:
1550:
1546:
1516:
1515:
1511:
1489:
1488:
1484:
1448:
1447:
1443:
1433:
1431:
1422:
1421:
1417:
1407:
1405:
1397:
1396:
1392:
1348:
1347:
1343:
1320:(12): 3520–28.
1307:
1306:
1302:
1258:
1257:
1253:
1209:
1208:
1204:
1168:
1167:
1163:
1150:(245): 709–27.
1141:
1140:
1136:
1103:(6): e1002765.
1089:
1088:
1084:
1079:
1033:
997:
957:
891:
852:kidney function
748:kidney function
726:In cases where
683:
632:Alport syndrome
612:red blood cells
600:kidney function
548:
492:
490:Natural history
449:on a number of
398:
377:
375:Pathophysiology
340:
211:
114:
110:
99:IgA nephropathy
89:
47:IgA nephropathy
42:
39:
28:
23:
22:
15:
12:
11:
5:
2294:
2292:
2284:
2283:
2278:
2268:
2267:
2261:
2260:
2258:
2257:
2252:
2246:
2244:
2240:
2239:
2236:
2235:
2233:
2232:
2227:
2222:
2216:
2214:
2204:
2203:
2201:
2200:
2195:
2194:
2193:
2183:
2177:
2175:
2165:
2164:
2162:
2161:
2155:
2153:
2140:
2127:
2126:
2123:
2122:
2120:
2119:
2114:
2108:
2106:
2102:
2101:
2099:
2098:
2093:
2088:
2082:
2080:
2074:
2073:
2071:
2070:
2065:
2060:
2058:Minimal change
2054:
2052:
2043:
2035:
2034:
2029:
2027:
2026:
2019:
2012:
2004:
1995:
1994:
1991:
1990:
1979:
1967:
1966:
1964:
1960:
1959:
1956:
1955:
1944:
1933:
1922:
1907:
1891:
1886:
1885:
1883:
1882:Classification
1876:
1875:
1864:
1863:External links
1861:
1858:
1857:
1848:J Urol Nephrol
1838:
1829:
1777:
1742:
1702:
1661:
1642:(6): 1129–39.
1626:
1585:
1544:
1509:
1482:
1461:(4): 1135–44.
1441:
1415:
1390:
1341:
1300:
1251:
1202:
1161:
1134:
1081:
1080:
1078:
1075:
1039:Dr Jean Berger
1032:
1029:
996:
993:
965:Southeast Asia
956:
953:
942:kidney failure
907:hyperlipidemia
890:
887:
864:blood pressure
844:kidney failure
801:anticoagulants
736:kidney failure
682:
679:
675:immunoglobulin
572:bladder cancer
547:
544:
491:
488:
463:polymerisation
447:O-glycosylated
384:Immunostaining
376:
373:
339:
336:
304:celiac disease
292:
291:
277:
263:
223:synpharyngitic
210:
207:
191:IgA vasculitis
94:
93:
84:
78:
77:
68:
67:
59:
58:
53:
49:
48:
40:
36:IgA vasculitis
26:
24:
14:
13:
10:
9:
6:
4:
3:
2:
2293:
2282:
2279:
2277:
2274:
2273:
2271:
2256:
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2251:
2248:
2247:
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2226:
2223:
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2213:
2209:
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2196:
2192:
2189:
2188:
2187:
2184:
2182:
2179:
2178:
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2174:
2170:
2166:
2160:
2157:
2156:
2154:
2152:
2148:
2144:
2141:
2139:
2134:
2128:
2118:
2115:
2113:
2110:
2109:
2107:
2103:
2097:
2094:
2092:
2089:
2087:
2084:
2083:
2081:
2079:
2078:Proliferative
2075:
2069:
2066:
2064:
2061:
2059:
2056:
2055:
2053:
2051:
2047:
2044:
2042:
2036:
2032:
2025:
2020:
2018:
2013:
2011:
2006:
2005:
2002:
1989:
1985:
1984:
1980:
1978:
1974:
1973:
1969:
1968:
1965:
1961:
1954:
1950:
1949:
1945:
1943:
1939:
1938:
1934:
1932:
1928:
1927:
1923:
1921:
1917:
1916:
1912:
1908:
1906:
1902:
1901:
1897:
1893:
1892:
1889:
1884:
1880:
1874:
1870:
1867:
1866:
1862:
1853:
1849:
1842:
1839:
1833:
1830:
1824:
1819:
1815:
1811:
1806:
1801:
1797:
1793:
1789:
1781:
1778:
1773:
1769:
1765:
1761:
1758:(4): 728–35.
1757:
1753:
1746:
1743:
1739:
1738:public domain
1720:
1718:
1712:
1706:
1703:
1698:
1694:
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1684:
1680:
1676:
1672:
1665:
1662:
1657:
1653:
1649:
1645:
1641:
1637:
1630:
1627:
1622:
1618:
1613:
1608:
1604:
1600:
1596:
1589:
1586:
1581:
1577:
1572:
1567:
1564:(1): 142–48.
1563:
1559:
1555:
1548:
1545:
1540:
1536:
1532:
1528:
1525:(2): 237–42.
1524:
1520:
1513:
1510:
1505:
1501:
1498:(5): 215–18.
1497:
1493:
1492:Clin. Nephrol
1486:
1483:
1478:
1474:
1469:
1464:
1460:
1456:
1452:
1445:
1442:
1429:
1425:
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1301:
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1287:
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1274:
1270:
1266:
1262:
1255:
1252:
1247:
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1238:
1233:
1229:
1225:
1222:(5): 974–89.
1221:
1217:
1213:
1206:
1203:
1198:
1194:
1189:
1184:
1181:(3): 823–34.
1180:
1176:
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1157:
1153:
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1145:
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1130:
1126:
1121:
1116:
1111:
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1102:
1098:
1097:PLOS Genetics
1094:
1086:
1083:
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1072:
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1063:
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1014:
1010:
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994:
992:
990:
986:
982:
978:
974:
970:
966:
962:
954:
952:
950:
949:kidney biopsy
945:
943:
939:
935:
931:
926:
924:
920:
916:
912:
908:
904:
900:
896:
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877:
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818:
814:
810:
806:
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797:anti-platelet
794:
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782:
778:
776:
772:
768:
764:
760:
755:
753:
749:
745:
741:
737:
733:
732:tonsillectomy
729:
724:
721:
717:
713:
709:
705:
701:
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693:
689:
680:
678:
676:
672:
668:
664:
660:
656:
652:
648:
643:
641:
637:
633:
629:
625:
621:
617:
616:urinary casts
613:
609:
605:
601:
597:
593:
589:
585:
581:
577:
573:
569:
568:kidney stones
565:
561:
557:
553:
545:
543:
540:
537:
532:
529:
525:
519:
517:
513:
509:
505:
501:
497:
489:
487:
485:
480:
479:immune system
475:
472:
468:
464:
460:
456:
452:
448:
443:
441:
436:
434:
430:
426:
422:
418:
393:
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385:
381:
374:
372:
370:
366:
362:
358:
354:
350:
346:
337:
335:
333:
329:
325:
321:
317:
316:heart failure
313:
309:
305:
301:
297:
296:liver failure
289:
285:
281:
278:
275:
271:
267:
264:
262:
259:
258:
257:
254:
252:
248:
243:
241:
236:
232:
228:
224:
220:
216:
208:
206:
204:
200:
196:
192:
188:
185:
181:
176:
174:
170:
166:
162:
158:
154:
150:
146:
145:immune system
142:
138:
132:
108:
104:
100:
92:
88:
85:
83:
79:
76:
73:
69:
65:
60:
57:
54:
50:
45:
37:
33:
19:
2212:Pauci-immune
2208:Type III RPG
2197:
2105:By condition
1981:
1970:
1946:
1935:
1924:
1909:
1894:
1851:
1847:
1841:
1832:
1795:
1791:
1780:
1755:
1751:
1745:
1723:. Retrieved
1714:
1705:
1678:
1674:
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1635:
1629:
1602:
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1522:
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1491:
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1432:. Retrieved
1427:
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1406:. Retrieved
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1100:
1096:
1085:
1067:nephrologist
1064:
1052:hematochezia
1042:
1005:polymorphism
998:
958:
955:Epidemiology
946:
934:polymorphism
927:
923:hypertension
899:hypertension
892:
880:
860:
837:
821:azathioprine
793:Isotretinoin
779:
756:
738:. Dietary
725:
716:Isotretinoin
704:azathioprine
684:
644:
549:
541:
533:
520:
508:bloody urine
493:
476:
444:
437:
414:
341:
293:
288:hypertension
255:
244:
222:
212:
177:
153:inflammation
136:
106:
102:
98:
97:
91:Rheumatology
55:
2169:Type II RPG
2117:Amyloidosis
1972:MedlinePlus
1725:18 December
1271:(6): 1–13.
1265:J Autoimmun
919:Proteinuria
895:proteinuria
848:proteinuria
829:ciclosporin
783:(traded as
728:tonsillitis
700:ciclosporin
696:transplants
647:blood tests
620:Proteinuria
484:bone marrow
247:proteinuria
201:skin rash,
52:Other names
2270:Categories
2147:Type I RPG
2068:Membranous
1948:DiseasesDB
1798:(7): 942.
1455:Kidney Int
1077:References
981:urinalysis
911:creatinine
893:Male sex,
883:budesonide
833:mizoribine
805:malignancy
763:microscopy
659:complement
610:will show
608:urinalysis
576:urological
560:cystoscopy
556:ultrasound
496:urinalysis
471:vasculitis
425:glomerulus
388:glomerulus
338:Morphology
87:Nephrology
2133:nephritic
2130:Primarily
2041:nephrotic
2038:Primarily
1983:eMedicine
1854:: 694–95.
1814:2168-6106
1048:hematuria
989:incidence
985:Singapore
969:screening
915:hematuria
889:Prognosis
809:sterility
761:on light
752:Phenytoin
688:hematuria
681:Treatment
604:prognosis
584:mesangium
552:hematuria
546:Diagnosis
536:remission
534:Complete
512:prognosis
500:screening
455:threonine
392:nephritis
349:properdin
231:loin pain
215:hematuria
203:arthritis
157:glomeruli
82:Specialty
2112:Diabetic
1772:11576875
1656:12776264
1580:11752031
1477:15086452
1385:21949093
1336:17093066
1295:25578468
1246:26376134
1197:11231337
1129:22737082
1023:(OMIM):
1013:Kentucky
995:Genetics
961:Far East
938:genotype
771:steroids
720:steroids
661:levels,
564:bleeding
440:antigens
199:purpuric
187:antibody
2243:General
1988:med/886
1942:D005922
1823:6583088
1697:9355077
1621:7935657
1539:8684533
1519:Nephron
1504:6994960
1434:27 July
1408:27 July
1376:3892742
1286:4340844
1237:4653078
1156:3329736
1144:Q J Med
1120:3380840
1031:History
903:smoking
789:cytoxan
785:endoxan
744:antigen
459:proline
221:(hence
159:of the
155:of the
139:, is a
1977:000466
1931:161950
1820:
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973:biopsy
930:biopsy
791:) and
787:&
740:gluten
665:, and
645:Other
580:biopsy
504:biopsy
451:serine
300:cancer
284:anemia
161:kidney
151:or an
2186:Lupus
1920:583.9
1905:N02.8
1719:(FDA)
1715:U.S.
1017:Italy
977:Japan
624:renal
251:Japan
173:heart
165:liver
75:dimer
1953:1353
1937:MeSH
1926:OMIM
1915:9-CM
1810:ISSN
1768:PMID
1727:2021
1693:PMID
1652:PMID
1617:PMID
1576:PMID
1535:PMID
1500:PMID
1473:PMID
1436:2021
1410:2021
1381:PMID
1332:PMID
1291:PMID
1242:PMID
1193:PMID
1152:PMID
1125:PMID
1015:and
1002:gene
963:and
921:and
874:and
831:and
807:and
718:and
673:and
630:and
606:. A
590:and
570:and
469:, a
453:and
347:and
326:and
180:NORD
171:and
169:skin
103:IgAN
2198:IgA
2138:RPG
1911:ICD
1896:ICD
1871:on
1818:PMC
1800:doi
1796:179
1760:doi
1683:doi
1644:doi
1607:doi
1603:331
1566:doi
1527:doi
1463:doi
1371:PMC
1363:doi
1322:doi
1281:PMC
1273:doi
1232:PMC
1224:doi
1183:doi
1115:PMC
1105:doi
1027:).
813:GFR
706:or
667:LDH
663:ANA
655:ESR
653:or
651:CRP
367:or
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