“…This lack of information does not allow for the differentiation of different patterns of pathologic events leading to CKD: (1) one unique episode with apparent complete recovery but leading to an important nephronic reduction and CKD at long term by hyperfiltration; (2) recurrence of acute episodes; c/progressive indolent process as in IgAN. The latter is suggested by several reports of HSPN observed in patients known to have had IgAN for many years (82)(83)(84)(85). In general, there is a good relationship between the severity of initial clinical presentation and the risk of CKD at long term (14,21) (Table 1), but it is far from being a constant rule.…”
Section: Prognostic Value Of Renal Symptomsmentioning
confidence: 89%
“…HSPN might possibly progress by continuous deposition of IgA-CC inducing mesangial proliferation, ECM accumulation, and gomerulosclerosis such as IgAN (82)(83)(84)(85). Proteinuria persisting after the acute phase might be due to two different mechanisms: either hyperfiltration due to nephronic mass reduction during the acute phase or the effect of chemokines produced by persistently stimulated MCs on podocytes (47,48,116,117).…”
Section: Mesangial Proliferation Glomerulosclerosis and Proteinuriamentioning
SummaryHenoch-Schö nlein purpura nephritis is a rare kidney disease leading to chronic kidney disease in a non-negligible percentage of patients. Although retrospective studies suggest beneficial effects of some therapies, prospective randomized clinical trials proving treatment efficacy are still lacking. The dilemma of spontaneous recovery even in patients with severe clinical and histologic presentation and of late evolution to chronic kidney disease in patients with mild initial symptoms renders it difficult for clinicians to expose patients to treatment protocols that are not evidence-based. A better understanding of the pathophysiology of progression to chronic kidney disease in Henoch-Schö nlein purpura patients could be achieved by designing prospective international multicenter studies looking at determinants of clinical and histopathological evolution as well as possible circulating and urinary markers of progression. Such studies should be supported by a database available on the web and a new histologic classification of kidney lesions. This paper reports clinical, pathologic, and experimental data to be used for this strategy and to assist clinicians and clinical trial designers to reach therapeutic decisions.
“…This lack of information does not allow for the differentiation of different patterns of pathologic events leading to CKD: (1) one unique episode with apparent complete recovery but leading to an important nephronic reduction and CKD at long term by hyperfiltration; (2) recurrence of acute episodes; c/progressive indolent process as in IgAN. The latter is suggested by several reports of HSPN observed in patients known to have had IgAN for many years (82)(83)(84)(85). In general, there is a good relationship between the severity of initial clinical presentation and the risk of CKD at long term (14,21) (Table 1), but it is far from being a constant rule.…”
Section: Prognostic Value Of Renal Symptomsmentioning
confidence: 89%
“…HSPN might possibly progress by continuous deposition of IgA-CC inducing mesangial proliferation, ECM accumulation, and gomerulosclerosis such as IgAN (82)(83)(84)(85). Proteinuria persisting after the acute phase might be due to two different mechanisms: either hyperfiltration due to nephronic mass reduction during the acute phase or the effect of chemokines produced by persistently stimulated MCs on podocytes (47,48,116,117).…”
Section: Mesangial Proliferation Glomerulosclerosis and Proteinuriamentioning
SummaryHenoch-Schö nlein purpura nephritis is a rare kidney disease leading to chronic kidney disease in a non-negligible percentage of patients. Although retrospective studies suggest beneficial effects of some therapies, prospective randomized clinical trials proving treatment efficacy are still lacking. The dilemma of spontaneous recovery even in patients with severe clinical and histologic presentation and of late evolution to chronic kidney disease in patients with mild initial symptoms renders it difficult for clinicians to expose patients to treatment protocols that are not evidence-based. A better understanding of the pathophysiology of progression to chronic kidney disease in Henoch-Schö nlein purpura patients could be achieved by designing prospective international multicenter studies looking at determinants of clinical and histopathological evolution as well as possible circulating and urinary markers of progression. Such studies should be supported by a database available on the web and a new histologic classification of kidney lesions. This paper reports clinical, pathologic, and experimental data to be used for this strategy and to assist clinicians and clinical trial designers to reach therapeutic decisions.
“…In those cases, the clinical picture is very similar to that of IgAN. Both diseases may sometimes be encountered consecutively in the same patient [69]. On the other hand, IgAN may be accompanied by extra-renal symptoms such as abdominal pain, fever and myalgia [12].…”
Section: Igan and Henoch-schoenlein Purpura Nephritismentioning
“…At the same time, Urizar and coworkers [84] showed similar IgA deposits in renal biopsies of patients with HenochSchoÈ nlein purpura nephritis (HSPN). HSPN and IgAN are considered nowadays to be related diseases since both can be encountered consecutively in the same patient [68], have been described in identical twins [53] and bear similar pathological and biological abnormalities [19,45]. An overview of IgAN has been recently published in this journal [14].…”
Despite numerous studies, the pathogeny of Henoch-Schönlein nephritis remains incompletely elucidated and controlled therapeutic trials are still needed.
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