FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1974072757> ?p ?o ?g. }

• W1974072757 endingPage "834" @default.
• W1974072757 startingPage "823" @default.
• W1974072757 abstract "What is the difference between IgA nephropathy and Henoch-Schönlein purpura nephritis? Henoch-Schönlein purpura nephritis (HSPN) and IgA nephropathy (IgAN) are considered to be related diseases since both can be encountered consecutively in the same patient, they have been described in twins, and bear identical pathological and biological abnormalities. Apart from the presence of extrarenal clinical signs found only in HSPN, other differences are noticed between the two diseases. The peak age ranges between 15 and 30 years for a diagnosis of IgAN, whereas HSPN is mainly seen in childhood. Nephritic and/or nephrotic syndromes are more often seen at presentation in HSPN. In contrast to IgAN, HSPN has been described in association with hypersensitivity. Endocapillary and extracapillary inflammations as well as fibrin deposits in the glomerulus are more frequent in HSPN. No major biological differences have been found between the two illnesses, except for a larger size of circulating IgA-containing complexes (IgA-CC) and a greater incidence of increased plasma IgE levels in HSPN. As tissue infiltration by leukocytes is a major feature of HSPN vasculitis, a possible role of a more potent activation of the latter cells by IgA-CC and/or circulating chemokines in HSPN should be considered. Further studies are required to elucidate this possible mechanism as well as the role of hypersensitivity in HSPN. What is the difference between IgA nephropathy and Henoch-Schönlein purpura nephritis? Henoch-Schönlein purpura nephritis (HSPN) and IgA nephropathy (IgAN) are considered to be related diseases since both can be encountered consecutively in the same patient, they have been described in twins, and bear identical pathological and biological abnormalities. Apart from the presence of extrarenal clinical signs found only in HSPN, other differences are noticed between the two diseases. The peak age ranges between 15 and 30 years for a diagnosis of IgAN, whereas HSPN is mainly seen in childhood. Nephritic and/or nephrotic syndromes are more often seen at presentation in HSPN. In contrast to IgAN, HSPN has been described in association with hypersensitivity. Endocapillary and extracapillary inflammations as well as fibrin deposits in the glomerulus are more frequent in HSPN. No major biological differences have been found between the two illnesses, except for a larger size of circulating IgA-containing complexes (IgA-CC) and a greater incidence of increased plasma IgE levels in HSPN. As tissue infiltration by leukocytes is a major feature of HSPN vasculitis, a possible role of a more potent activation of the latter cells by IgA-CC and/or circulating chemokines in HSPN should be considered. Further studies are required to elucidate this possible mechanism as well as the role of hypersensitivity in HSPN. Heberden was probably the first to report a case of Henoch-Schönlein purpura1Heberden W. Commentaries on the History and Cure of Diseases. T. Payne, London1801: 395Google Scholar. He described a five-year-old boy presenting with generalized edema, macroscopic hematuria associated with a purpuric rash, colicky pain, bloody stools, and arthralgia. The association between an erythematous or purpuric rash and joint pain was reported again by Schönlein2Schönlein J.L. Allgemeine Und Specielle Pathologie Und Therapie. 1847; vol 1: 48Google Scholar. Schönlein's former pupil, Henoch, described four children with a combination of rash, colic, bloody diarrhea, and joint pain3Henoch E. Über eine eigentümliche Form von Purpura.Berl Klin Wochenschr. 1874; 11: 641Google Scholar and, in a later report added hemorrhagic nephritis to the list of components of the syndrome4Henoch E. Vorlesungen über Kinderkrankheiten. 1989; vol 10: 839Google Scholar, thus completing the modern definition of the disease. The latter has been recently formulated by the International Consensus Conference on Nomenclature of Systemic Vasculitides as “a vasculitis with IgA-dominant immune deposits affecting small vessels and typically involving skin, gut, and glomeruli and associated with arthralgias or arthritis”5Jennette J.C. Falk R.J. Andrassy K. Nomenclature of systemic vasculitides: Proposal of an International Consensur Conference.Arthritis Rheumatol. 1994; 37: 187-192Crossref PubMed Scopus (3362) Google Scholar. In 1968, Berger and Hinglais reported for the first time a form of glomerulonephritis characterized by mesangial accumulation of IgA associated with less intense deposits of IgG and/or C36Berger J. Hinglais N. Les dépôts intercapillaires d'IgA-IgG.J Urol Nephrol. 1968; 74: 694-695PubMed Google Scholar. Light microscopy revealed mainly focal and segmental mesangial proliferation and matrix expansion, whereas electron-dense deposits were demonstrated by electron microscopy between the glomerular basement membrane and mesangial cells (MCs). The finding of glomerular IgA deposits led later on to the denomination of IgA nephropathy (IgAN). At the same time, Urizar et al showed similar pathological findings in renal biopsies of patients with Henoch-Schönlein purpura nephritis (HSPN)7Urizar R.E. Michael A. Sisson S. Anaphylactoid purpura. II. Immunofluorescent and electron microscopy studies of the glomerular lesions.Lab Invest. 1968; 19: 437-440PubMed Google Scholar. Henoch-Schönlein purpura nephritis and IgAN currently are considered to be related diseases since both can be encountered consecutively in the same patient8Ravelli A. Carnevale-Maffe G. Ruperto N. IgA nephropathy and Henoch-Schönlein syndrome occurring in the same patient.Nephron. 1996; 72: 111-112Crossref PubMed Scopus (15) Google Scholar, have been described in identical twins9Meadow S.R. Scott D.G. Berger disease: Henoch-Schönlein without the rash.J Pediatr. 1985; 106: 27-32Abstract Full Text PDF PubMed Scopus (108) Google Scholar, and bear identical pathological and biological abnormalities10Knight J.F. The rheumatic poison: A survey of some published investigations of the immunopathogenesis of Henoch-Schönlein purpura.Pediatr Nephrol. 1990; 4: 533-541Crossref PubMed Scopus (43) Google Scholar, 11Davin J.C. Weening J.J. Berger disease: Thirty years later.Eur J Pediatr. 1999; 158: 437-443Crossref PubMed Scopus (8) Google Scholar. The present review points out the similarities and differences between the two diseases in order to propose pathogenetic mechanisms that may explain the occurrence of systemic vasculitis in HSPN only Tables 1 and 2.Table 1Similarities of IgAN and HSPNClinical features More frequent in male Gross hematuria simultaneous to a respiratory infection Frequent evolution to chronic renal insufficiency Relapse after transplantationHistology Predominant mesangial IgA1 deposits Electron dense deposits in the mesangium Mesangial proliferation Cutaneous IgA depositsIgA immunological abnormalities Abnormal IgA1 glycosylation pattern Increased IgA plasma levels Increased IgA1 plasma levels Increased polymeric IgA plasma levels Circulating IgA-containing complexes Increased IgA synthesis by B lymphocytesOther immunological abnormalities Reduced function of the reticuloendothelial system Low grade complement activation High IgE plasma levels High incidence of C4B null phenotype Increased TNF-α and IL-1 urinary excretionAbnormalities of mucosal barriers Increased intestinal permeability to 51Cr EDTA Increased long carbon monoxide diffusionCoagulation abnormalities Intact cross-linked fibrin (XFb) Increased von Willebrand factor plasma levelsAbbreviations are: TNF-α, tumor necrosis factor-α; IL-1, interleukin-1. Open table in a new tab Table 2Differences between IgAN and HSPNIgANHSPNClinical features Extra-renal symptoms-+ Age at onset>15 y<15 y Nephritic/nephrotic syndrome+/-+++ Risk of chronic renal failure (CRF)+++ Hypersensitivity-+ Secondary forms+++/-Histology Endocapillary proliferation+/-++ Epithelial crescents+/-++ Perivascular glomerular IgA+/-++ Subepithelial/subendothelial dense deposits+/-++ Increased lambda/kappa ratio+- Fibrin deposits+/-++Circulatory IgA abnormalities IgA-containing complexes size7S-19S>19SOther blood immunologic abnormalities High IgE plasma levels+++ High eosinophil cationic protein (ECP) plasma levels-+ Open table in a new tab Abbreviations are: TNF-α, tumor necrosis factor-α; IL-1, interleukin-1. IgA nephropathy represents 1.6% of all new cases of end-stage renal failure (ESRF) recorded in the European Dialysis and Transplantation Association registry for the year 198812Fassbinder W. Brunner F.P. Brynger H. Combined report on regular dialysis and transplantation in Europe, XX, 1989.Nephrol Dial Transplant. 1991; 6: 5-35Google Scholar. In a large series of children with ESRF recorded in France13Broyer M. Fréquence et cause de l'-insuffisance rénale chez l'enfant,.Néphrologie Pédiatrique. edited by Royer P, Habib Matthieu H, et al. Flammarion Médecine-Sciences, Paris1983: 425-433Google Scholar, 1.3% had IgAN. The overall prevalence of IgAN is not known. However, the overall frequency of IgAN in renal biopsies has been reported in several series as reviewed by Emancipator14Emancipator S.N. Primary and secondary forms of IgA nephritis and Schönlein–Henoch syndrome,.Pathology of the Kidney. edited by Heptinstall RH. London, Little, Brown, Toronto1993: 389-476Google Scholar. The frequency varies from 4 to 44% of all renal biopsies. This wide range depends on criterion for performing a biopsy, but also on racial features14Emancipator S.N. Primary and secondary forms of IgA nephritis and Schönlein–Henoch syndrome,.Pathology of the Kidney. edited by Heptinstall RH. London, Little, Brown, Toronto1993: 389-476Google Scholar. IgAN seems to be a relative rarity in blacks, in both the United States and Africa. American Indians, on the other hand, have a higher incidence of IgAN than the world population at large. The peak age at the time of the first clinical manifestations of primary IgAN ranges between 15 and 30 years15Schena F.P. IgA nephropathies,.Oxford Textbook of Clinical Nephrology. edited by Cameron S, Davison AM, Grünfeld JP, et al. Oxford University Press, Oxford1992: 339-369Google Scholar. Affected children do not present symptoms before the age of three years; thereafter, they are evenly spread through childhood16Levy M. Gonzales-Burchard G. Broyer M. Berger's disease in children: Natural history and outcome.Medicine (Baltimore). 1985; 64: 157-180PubMed Google Scholar. Worldwide, the male-to-female sex ratio is 2:114Emancipator S.N. Primary and secondary forms of IgA nephritis and Schönlein–Henoch syndrome,.Pathology of the Kidney. edited by Heptinstall RH. London, Little, Brown, Toronto1993: 389-476Google Scholar. The proportion of HSPN as cause of ESRF in adults is minimal17Haycock G.B. The nephritis of Henoch-Schönlein purpura,.Oxford Textbook of Clinical Nephrology. edited by Cameron S, Davison AM, Grünfeld J-P, et al. New York, Tokyo, Oxford University Press, Oxford1992: 595-612Google Scholar, whereas it can reach up to 5.1% in children13Broyer M. Fréquence et cause de l'-insuffisance rénale chez l'enfant,.Néphrologie Pédiatrique. edited by Royer P, Habib Matthieu H, et al. Flammarion Médecine-Sciences, Paris1983: 425-433Google Scholar. The prevalence of HSP is difficult to assess from previously reported studies. Epidemiological studies on HSP performed to date have not taken into account the presence of IgA deposits in tissue as a diagnostic criterium. This is important since the latter is the gold standard of distinguishing HSP from other vasculitides such as hypersensitivity vasculitis5Jennette J.C. Falk R.J. Andrassy K. Nomenclature of systemic vasculitides: Proposal of an International Consensur Conference.Arthritis Rheumatol. 1994; 37: 187-192Crossref PubMed Scopus (3362) Google Scholar. However, it is generally agreed that the incidence of HSP decreases with age17Haycock G.B. The nephritis of Henoch-Schönlein purpura,.Oxford Textbook of Clinical Nephrology. edited by Cameron S, Davison AM, Grünfeld J-P, et al. New York, Tokyo, Oxford University Press, Oxford1992: 595-612Google Scholar. The lack of using appropriate diagnostic criteria possibly explains why the proportion of patients presenting with renal involvement varies considerably among the different reports (20 to 100%) according to a review from White and Yoshikawa18White R.H.R. Yoshikawa N. Henoch-Schönlein nephritis,.Pediatric Nephrology. edited by Barratt TM, Holiday M. Williams & Wilkins, Baltimore1993: 729-738Google Scholar. Another explanation might reside in the use of different criteria for diagnosing HSPN, since many of the earlier studies did not utilize serial routine urinalysis, and transient microscopic hematuria was probably missed18White R.H.R. Yoshikawa N. Henoch-Schönlein nephritis,.Pediatric Nephrology. edited by Barratt TM, Holiday M. Williams & Wilkins, Baltimore1993: 729-738Google Scholar. Finally, an underestimation could result from the existence of renal lesions without any clinical signs and the delay that can occur between the initial signs and renal symptoms. Indeed, the incidence of renal involvement increases with time after HSP diagnosis in children19Kaku Y. Nohara K. Honda S. Renal involvement in Henoch-Schönlein purpura: A multivariate analysis of prognostic factors.Kidney Int. 1998; 53: 1755-1759Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar. Kaku, Nohara, and Honda have shown that the latter percentage increased progressively to reach 35.4% after one year and continued to increase thereafter19Kaku Y. Nohara K. Honda S. Renal involvement in Henoch-Schönlein purpura: A multivariate analysis of prognostic factors.Kidney Int. 1998; 53: 1755-1759Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar. In contrast to studies in children, the incidence of renal involvement in HSP in adults has been more precisely assessed in one study using a cohort of patients in whom the diagnosis was made by showing the characteristic leukocytoklastic skin vasculitis accompanied by IgA deposits20Tancrede-Bohin E. Ochonisky S. Vignon-Pennamen M.D. Schönlein-Henoch purpura in adult patients: Predictive factors for IgA glomerulonephritis in a retrospective of 57 cases.Arch Dermatol. 1997; 133: 438-442Crossref PubMed Google Scholar. This study demonstrated that 49% of patients presented with abnormal urinary signs. In HSPN also, the sex ratio (male:female ratio 1.5) shows an increased frequency in males21Habib R. Cameron J.S. Schönlein-Henoch purpura,.The Kidney: Rheumatic Disease. edited by Bacon PA, Hadler NM. Butterworth Scientific, London1982: 178Google Scholar. The most prominent clinical feature of IgAN is synpharyngitic macroscopic hematuria. Less often, macroscopic hematuria in IgAN is accompanied by other infections (pulmonary, intestinal, or urinary)22Clarkson A.R. Clinical and laboratory features of IgA nephropathy,.IgA Nephropathy. edited by Clarkson, AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 9-15Crossref Google Scholar. In Western countries, macroscopic hematuria is the most frequent initial presentation in children (76 to 100%)23Hogg R.G. Silva F.G. IgA nephropathy in children,.IgA Nephropathy. edited by Clarkson AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 16-38Crossref Google Scholar, followed by the fortuitous finding of microscopic hematuria accompanied or not by proteinuria (0 to 19%). In contrast to children, microscopic hematuria and/or proteinuria are the most frequent initial presentations in adults (28 to 61% vs. 12 to 43% for macroscopic hematuria)24Davin J.C. Contribution à l'étude de la pathogénie des néphropathies à IgA: Thèse d'Aggrégation. Université de Liège, Liège1993Google Scholar. Renal insufficiency and hypertension are less often encountered as initial signs, but are more frequent at first presentation in adults (15 to 36% and 31 to 43%, respectively)24Davin J.C. Contribution à l'étude de la pathogénie des néphropathies à IgA: Thèse d'Aggrégation. Université de Liège, Liège1993Google Scholar than in children (4 to 12% and 0 to 18%, respectively)23Hogg R.G. Silva F.G. IgA nephropathy in children,.IgA Nephropathy. edited by Clarkson AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 16-38Crossref Google Scholar. In a few cases, a nephrotic or a nephritic syndrome can be the first sign in adults (4 to 13%)24Davin J.C. Contribution à l'étude de la pathogénie des néphropathies à IgA: Thèse d'Aggrégation. Université de Liège, Liège1993Google Scholar but also in children (4 to 8%)23Hogg R.G. Silva F.G. IgA nephropathy in children,.IgA Nephropathy. edited by Clarkson AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 16-38Crossref Google Scholar. Finally, in some adult patients, the diagnosis is made when ESRF is already present25Goldstein A.R. White R.H.R. Akuse R. Long-term follow-up of childhood Henoch-Schönlein nephritis.Lancet. 1992; 339: 280-282Abstract PubMed Scopus (320) Google Scholar. A history of a recent or simultaneous infection is also common in HSP. Indeed, the latter is reported in one third to two thirds according to the studies17Haycock G.B. The nephritis of Henoch-Schönlein purpura,.Oxford Textbook of Clinical Nephrology. edited by Cameron S, Davison AM, Grünfeld J-P, et al. New York, Tokyo, Oxford University Press, Oxford1992: 595-612Google Scholar. Although any of the four major components of the syndrome (rash, joint pain, abdominal symptoms, and renal disease) may be present before the other, it is rare for the renal disease to do so17Haycock G.B. The nephritis of Henoch-Schönlein purpura,.Oxford Textbook of Clinical Nephrology. edited by Cameron S, Davison AM, Grünfeld J-P, et al. New York, Tokyo, Oxford University Press, Oxford1992: 595-612Google Scholar. According to a single series from a tertiary center25Goldstein A.R. White R.H.R. Akuse R. Long-term follow-up of childhood Henoch-Schönlein nephritis.Lancet. 1992; 339: 280-282Abstract PubMed Scopus (320) Google Scholar, initial signs of HSPN are hematuria and proteinuria in 50% of patients, acute nephritic syndrome in 8%, nephrotic syndrome in 13%, and an association of nephritic and nephrotic syndrome in 29% of patients25Goldstein A.R. White R.H.R. Akuse R. Long-term follow-up of childhood Henoch-Schönlein nephritis.Lancet. 1992; 339: 280-282Abstract PubMed Scopus (320) Google Scholar. As expected, the incidence of mild symptoms is higher in unselected series26Koskimies O. Rapola J. Savilahti E. Renal involvement in Schönlein-Henoch purpura.Acta Paediatr Scand. 1974; 63: 357-363Crossref PubMed Scopus (35) Google Scholar, 27Nielsen H.E. Epidemiology of Schönlein-Henoch purpura.Acta Paediatr Scand. 1988; 77: 125-131Crossref PubMed Scopus (130) Google Scholar. Unfortunately, none of the latter studies used cutaneous IgA deposits as a diagnostic criterion, and therefore, their results must be considered with caution. At 10 years after diagnosis, 15% of adult patients with IgAN reach ESRF, rising to 25 to 34% at 20 years after diagnosis24Davin J.C. Contribution à l'étude de la pathogénie des néphropathies à IgA: Thèse d'Aggrégation. Université de Liège, Liège1993Google Scholar, 28D'Amico G. Natural history and treatment of idiopathic IgA nephropathy,.Nephrology. edited by Robinson RR. Springer, New York1984: 686-699Crossref Google Scholar. Studies about the prognosis of IgAN in children are contradictory. Yoshikawa, Ito, and Nakamura have shown that 10% of children with IgAN display chronic renal failure after 20 years of follow-up29Yoshikawa N. Ito H. Nakamura H. IgAN in children from Japan.Child Nephrol Urol. 1989; 9: 191-199Google Scholar. In contrast, Wyatt et al have shown a similar prognosis in children and in adults30Wyatt R.J. Kritchevsky S.B. Woodford S.Y. IgA nephropathy: Long-term prognosis for pediatric patients.J Pediatr. 1995; 127: 913-919Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar. In children as well as in adults, the intensity of proteinuria and hypertension and the severity of histologic findings are related with evolution to chronic renal failure14Emancipator S.N. Primary and secondary forms of IgA nephritis and Schönlein–Henoch syndrome,.Pathology of the Kidney. edited by Heptinstall RH. London, Little, Brown, Toronto1993: 389-476Google Scholar, 22Clarkson A.R. Clinical and laboratory features of IgA nephropathy,.IgA Nephropathy. edited by Clarkson, AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 9-15Crossref Google Scholar, 23Hogg R.G. Silva F.G. IgA nephropathy in children,.IgA Nephropathy. edited by Clarkson AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 16-38Crossref Google Scholar. Recurrence in the transplanted kidney is observed in about two thirds of patients and leads to graft failure in 25% of them31Hartung R. Livingstone B. Excell L. Recurrence of IgA deposits/disease in grafts: An Australian Registry Survey 1980-1990.Contrib Nephrol. 1995; 111: 13-17Crossref PubMed Google Scholar. According to a national multicentric Italian study, the risk of ESRF in adults with HSPN 10 years after diagnosis is about 15% and therefore does not differ from that of IgAN32Coppo R. Mazzuco G. Cagnoli L. Long-term prognosis of Henoch-Schönlein nephritis in adults and children.Nephrol Dial Transplant. 1997; 12: 2277-2283Crossref PubMed Scopus (172) Google Scholar. In childhood, the prognosis of HSPN seems to be worse than that of IgAN. HSPN leads to chronic renal failure in 20% of children 20 years after the diagnosis18White R.H.R. Yoshikawa N. Henoch-Schönlein nephritis,.Pediatric Nephrology. edited by Barratt TM, Holiday M. Williams & Wilkins, Baltimore1993: 729-738Google Scholar compared with 10% of children with IgAN after the same follow-up period29Yoshikawa N. Ito H. Nakamura H. IgAN in children from Japan.Child Nephrol Urol. 1989; 9: 191-199Google Scholar. The risk of chronic renal failure is related to the initial clinical presentation Figure 118White R.H.R. Yoshikawa N. Henoch-Schönlein nephritis,.Pediatric Nephrology. edited by Barratt TM, Holiday M. Williams & Wilkins, Baltimore1993: 729-738Google Scholar, 25Goldstein A.R. White R.H.R. Akuse R. Long-term follow-up of childhood Henoch-Schönlein nephritis.Lancet. 1992; 339: 280-282Abstract PubMed Scopus (320) Google Scholar. Chronic renal failure will be encountered in less than 5% when clinical signs at presentation are hematuria and/or minimal proteinuria, 15% when proteinuria is heavy but not nephrotic or in case of acute nephritic syndrome, 40% in case of nephrotic syndrome, and more than 50% when nephritic and nephrotic syndromes are associated. Of interest, even minimal urinary abnormalities can lead to chronic renal failure after decades25Goldstein A.R. White R.H.R. Akuse R. Long-term follow-up of childhood Henoch-Schönlein nephritis.Lancet. 1992; 339: 280-282Abstract PubMed Scopus (320) Google Scholar. The general opinion is that HSP has a worse prognosis in adults than in children [reviewed in33Lahita R.G. Influence of age on Henoch Schönlein purpura.Lancet. 1997; 350: 1116-1117Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar. However, in their study of patients with a clinical presentation that warranted renal biopsy, Coppo et al showed that HSPN had a similar prognosis in children and adults32Coppo R. Mazzuco G. Cagnoli L. Long-term prognosis of Henoch-Schönlein nephritis in adults and children.Nephrol Dial Transplant. 1997; 12: 2277-2283Crossref PubMed Scopus (172) Google Scholar. Several risk factors for renal involvement have been reported in children19Kaku Y. Nohara K. Honda S. Renal involvement in Henoch-Schönlein purpura: A multivariate analysis of prognostic factors.Kidney Int. 1998; 53: 1755-1759Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar: older age, abdominal symptoms, low factor XIII activity, and persisting purpura. In adults—unlike children—the patients with renal involvement do not seem to differ from those without, according to any clinical parameter such as sex, prevalence of bullous or necrotic lesions of the skin, or gastrointestinal and joint involvement20Tancrede-Bohin E. Ochonisky S. Vignon-Pennamen M.D. Schönlein-Henoch purpura in adult patients: Predictive factors for IgA glomerulonephritis in a retrospective of 57 cases.Arch Dermatol. 1997; 133: 438-442Crossref PubMed Google Scholar. Interestingly, remissions of Henoch-Schönlein purpura have been reported during pregnancy or sex-hormone therapy34Merrill J. Lahita R.G. Henoch-Schönlein purpura remitting in pregnancy and during sex steroid therapy.Br J Rheumatol. 1994; 33: 586-588Crossref PubMed Scopus (24) Google Scholar. The latter observation as well as the mean sex ratio (male:female 1.5) is in favor of a pathogenic role of male hormones. As in IgAN, recurrence can affect the transplanted kidney and lead to graft loss in 11 to 35% of patients five years after transplantation [reviewed in35Meulders Q. Pirson Y. Cosyns J.P. Course of Henoch-Schönlein nephritis after renal transplantation: Report on ten patients and review of the literature.Transplantation. 1994; 58: 1179-1186Crossref PubMed Google Scholar. Secondary forms of IgAN have been extensively reviewed by Emancipator14Emancipator S.N. Primary and secondary forms of IgA nephritis and Schönlein–Henoch syndrome,.Pathology of the Kidney. edited by Heptinstall RH. London, Little, Brown, Toronto1993: 389-476Google Scholar and Mustonen and Pasternak36Mustonen J. Pasternak A. Associated diseases in IgA nephropathy,.IgA Nephropathy. edited by Clarkson AR. Dordrecht, Lancaster, Martinus Nijhoff, Boston1987: 47-65Crossref Google Scholar. A high proportion of patients presenting with diseases involving the liver (for example, alcoholic cirrhosis and biliary ectasy) or secretory mucosae (celiac and Crohn's disease, chronic infection or cancer) have mesangial deposits of IgA indistinguishable from those with primary IgAN. Secondary forms of IgAN can also be observed in lymphoproliferative disorders (for example, IgA gammopathies and non-Hodgkin lymphomas). Finally, autoimmune and hypersensitivity diseases such as dermatitis herpetiformis, ankylosing spondylitis, scleritis, and sundry collagen-vascular diseases are also seen in association with mesangial IgAN. In the secondary forms, however, the association of complement with IgA deposits is much less frequent than in IgAN, and thus, pathological and clinical signs of inflammatory disease are usually absent. Most patients with secondary IgAN have been recognized at autopsy and had never been observed to have had urinary or renal functional abnormalities. Episodic macroscopic hematuria and/or renal insufficiency or proteinuria are rarely reported but do occur. In contrast to IgAN, HSPN has been described in association with hypersensitivity. Indeed, several drugs such as ciprofloxacin, acetylsalicylic acid, vancomycin, carbidopa/levodopa, cocaine, angiotensin-converting enzyme inhibitors, carbamazepine, and streptokinase have been implicated in HSP induction37Moots R.J. Keeling P.J. Morgan S.H. Adult Schönlein-Henoch purpura after enalapril.Lancet. 1992; 340: 304-305Abstract PubMed Scopus (20) Google Scholar, 38Disdier P. Harle J.R. Verrot D. Adult Schönlein-Henoch purpura after lisinopril.Lancet. 1992; 340: 985Abstract PubMed Scopus (8) Google Scholar, 39Drago F. Arditi M.R. Rebora R. Henoch-Schönlein induced by fluoroquinolones.Br J Dermatol. 1994; 131: 448Crossref PubMed Scopus (16) Google Scholar, 40Prajapati C. Casson I.F. Henoch-Schönlein purpura associated with ranitidine.Int J Clin Pract. 1997; 51: 251PubMed Google Scholar, 41Chevalier X. Rostoker G. Larget-Piet B. Schönlein-Henoch purpura with necrotizing vasculitis after cocaine snorting.Clin Nephrol. 1995; 43: 348-349PubMed Google Scholar, 42Kaneko K. Igarashi J. Suzuki Y. Carbamazepine-induced thrombocytopenia and leucopenia complicated by Henoch-Schönlein purpura symptoms.Eur J Pediatr. 1993; 152: 769-770Crossref PubMed Scopus (23) Google Scholar, 43Niedermaier G. Briner V. Henoch–Schönlein syndrome induced by carbidopa/levodopa.Lancet. 1997; 349: 1071-1072Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar, 44Michail S. Vaiopoulos G. Nakopoulou L. Henoch-Schönlein purpura and acute interstitial nephritis after intravenous vancomycin administration in a patient with a staphylococcal infection.Scand J Rheumatol. 1998; 27: 233-235Crossref PubMed Scopus (27) Google Scholar, 45Sola Alberich R. Jammoul A. Masana L. Henoch-Schönlein purpura associated with acetyl salicylic acid.Ann Intern Med. 1997; 126: 665Crossref Scopus (14) Google Scholar. Henoch-Schönlein purpura is much less frequently associated with other diseases than IgAN. Cancer46Cairns S.A. Mallick N.P. Lawler W. Squamous cell carcinoma of bronchus presenting with Henoch-Schönlein purpura.Br Med J. 1978; 2: 474-475Crossref PubMed Scopus (54) Google Scholar, blunt trauma47Talbot D. Craig R. Falconer S. Henoch-Schönlein purpura secondary to trauma.Arch Dis Child. 1988; 63: 1114-1115Crossref PubMed Scopus (7) Google Scholar, monoclonal IgA gammopathy48Dosa S. Cairns S.A. Mallick M.P. Relapsing Henoch-Schönlein syndrome with renal involvement in a patient with an IgA monoclonal gammopathy.Nephron. 1980; 26: 145-148Crossref PubMed Google Scholar, Wiskott-Aldrich syndrome carrier status49Lasseur K. Allen A.C. Deminière C. Henoch-Schönlein purpura with IgA nephropathy and abnormalities of IgA in a Wiskott-Aldrich syndrome carrier.Am J Kidney Dis. 1997; 2: 285-287Abstract Full Text PDF Scopus (20) Google Scholar, and chronic alcoholic liver disease50Feriozzi S. Onetti Muda A. Faragg" @default.
• W1974072757 created "2016-06-24" @default.
• W1974072757 creator A5014916890 @default.
• W1974072757 creator A5029094113 @default.
• W1974072757 creator A5039978343 @default.
• W1974072757 date "2001-03-01" @default.
• W1974072757 modified "2023-10-18" @default.
• W1974072757 title "What is the difference between IgA nephropathy and Henoch-Schönlein purpura nephritis?" @default.
• W1974072757 cites W1512976152 @default.
• W1974072757 cites W1517365537 @default.
• W1974072757 cites W1565766912 @default.
• W1974072757 cites W157736347 @default.
• W1974072757 cites W1595865874 @default.
• W1974072757 cites W1838497045 @default.
• W1974072757 cites W1892347675 @default.
• W1974072757 cites W1935866677 @default.
• W1974072757 cites W1967374404 @default.
• W1974072757 cites W1970559120 @default.
• W1974072757 cites W1973212712 @default.
• W1974072757 cites W1974106289 @default.
• W1974072757 cites W1974369780 @default.
• W1974072757 cites W1978150018 @default.
• W1974072757 cites W1982127939 @default.
• W1974072757 cites W1982372195 @default.
• W1974072757 cites W1982979766 @default.
• W1974072757 cites W1985397540 @default.
• W1974072757 cites W1986079204 @default.
• W1974072757 cites W1988938707 @default.
• W1974072757 cites W1990611521 @default.
• W1974072757 cites W1992322707 @default.
• W1974072757 cites W1993025001 @default.
• W1974072757 cites W1993237352 @default.
• W1974072757 cites W2001255622 @default.
• W1974072757 cites W2001481302 @default.
• W1974072757 cites W2003054773 @default.
• W1974072757 cites W2006601787 @default.
• W1974072757 cites W2007463241 @default.
• W1974072757 cites W2010963412 @default.
• W1974072757 cites W2013030718 @default.
• W1974072757 cites W2013195964 @default.
• W1974072757 cites W2014007651 @default.
• W1974072757 cites W2017973167 @default.
• W1974072757 cites W2022015207 @default.
• W1974072757 cites W2022152115 @default.
• W1974072757 cites W2022433281 @default.
• W1974072757 cites W2022791095 @default.
• W1974072757 cites W2023471197 @default.
• W1974072757 cites W2024030696 @default.
• W1974072757 cites W2025156220 @default.
• W1974072757 cites W2026580967 @default.
• W1974072757 cites W2027085139 @default.
• W1974072757 cites W2027562676 @default.
• W1974072757 cites W2029157024 @default.
• W1974072757 cites W2032272196 @default.
• W1974072757 cites W2033154962 @default.
• W1974072757 cites W2035494890 @default.
• W1974072757 cites W2036447451 @default.
• W1974072757 cites W2038528125 @default.
• W1974072757 cites W2041037954 @default.
• W1974072757 cites W2041231237 @default.
• W1974072757 cites W2044218649 @default.
• W1974072757 cites W2045494764 @default.
• W1974072757 cites W2046691405 @default.
• W1974072757 cites W2048965288 @default.
• W1974072757 cites W2051625250 @default.
• W1974072757 cites W2054935974 @default.
• W1974072757 cites W2056107593 @default.
• W1974072757 cites W2058167418 @default.
• W1974072757 cites W2061406879 @default.
• W1974072757 cites W2061979167 @default.
• W1974072757 cites W2064536780 @default.
• W1974072757 cites W2066158183 @default.
• W1974072757 cites W2066834432 @default.
• W1974072757 cites W2067012218 @default.
• W1974072757 cites W2068758060 @default.
• W1974072757 cites W2069136584 @default.
• W1974072757 cites W2069353550 @default.
• W1974072757 cites W2069717619 @default.
• W1974072757 cites W2069778758 @default.
• W1974072757 cites W2071708371 @default.
• W1974072757 cites W2073014968 @default.
• W1974072757 cites W2078006327 @default.
• W1974072757 cites W2078301944 @default.
• W1974072757 cites W2079344868 @default.
• W1974072757 cites W2080883395 @default.
• W1974072757 cites W2082105506 @default.
• W1974072757 cites W2083190467 @default.
• W1974072757 cites W2086475918 @default.
• W1974072757 cites W2088889072 @default.
• W1974072757 cites W2090766494 @default.
• W1974072757 cites W2092089608 @default.
• W1974072757 cites W2099831017 @default.
• W1974072757 cites W2100063226 @default.
• W1974072757 cites W2115950497 @default.
• W1974072757 cites W2122078316 @default.
• W1974072757 cites W2125247444 @default.
• W1974072757 cites W2132736935 @default.
• W1974072757 cites W2133280563 @default.

• next