Idiopathic IgA Mesangial Nephropathy

D’Amico, Giuseppe

doi:10.1159/000183538

Cited by 68 publications

(26 citation statements)

References 64 publications

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“…We think that the IgA nephropathy contributed to this unhabitual evolution of renal function. Our patient had a high urinary protein excretion at the time of the diagnosis, and the renal biopsy specimen showed lesions of focal glomerular scle rosis; these two factors correlate well with the impaired renal function and the subsequent clinical outcome of our patient [13,14].…”

Section: Discussionsupporting

confidence: 58%

IgA Nephropathy and Polycystic Kidney Disease

Panisello

Martínez-Vea²,

García³

et al. 1988

Am J Nephrol

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We report a patient with polycystic kidney disease, advanced renal failure, and nephrotic-range proteinuria. Kidney biopsy revealed IgA nephropathy with lesions of focal and segmental glomerular sclerosis. This association had not been previously described and is probably coincidental. This case supports the assumption that the nephrotic-range proteinuria observed in some polycystic patients could be the consequence of another superimposed glomerular disease. This glomerulopathy can worsen the course of azotemia in these patients.

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Section: Discussionsupporting

confidence: 58%

IgA Nephropathy and Polycystic Kidney Disease

Panisello

Martínez-Vea²,

García³

et al. 1988

Am J Nephrol

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“…Initial reports suggested that primary IgA nephropathy has a benign course; however, progression to end-stage renal failure was subsequently observed from 8 to 33% [4,5]. Crescentic formation in IgA nephropathy, histologically characterized by extensive extracapillary proliferation, is assumed to have a poor prognosis [6].…”

mentioning

confidence: 99%

Idiopathic IgA Nephropathy with Diffuse Crescent Formation

Tang

Wang

et al. 2002

Am J Nephrol

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Objective: To investigate the clinicopathological features and outcome of idiopathic IgA nephropathy with diffuse crescent formation in Chinese patients. Methods: Twenty-five patients with diffuse crescentic IgA nephropathy (DCIgAN), 15 males and 10 females with median age of 28.5, and median disease duration of 5.1 months, were studied. Their clinical, laboratory and pathological features and outcome were investigated. Twenty-one were administered pulse immunosuppressive therapy, and 15 were followed up for more than 6 months. Results: 1.14% had total IgA nephropathy, and 16.4% total diffuse crescentic glomerulonephritis. Clinically, most of patients (88%) showed rapidly progressive glomerulonephritis associated with a high level of serum creatinine (418 ± 264 µmol/l). Gross hematuria was noted in 72%, hypertension in 64%, and nephrotic syndrome in 48%. Pathologically, except for diffuse crescent formation (a median 65% and range 50–95%), we observed segmental necrosis of glomerular capillaries in 60%, glomerular infiltrating cells in 48%, endothelial cells proliferation in 32%, and rupture of Bowmans’ capsule in 24%. Severe tubular interstitial damage was also found, tubular atrophy in 64%, interstitial fibrosis in 60%, diffuse interstitial infiltrating cells in 74%, and interstitial vasculitis in 40%. Immunopathologically, four phenotypes were observed; however, IgA associated with IgM deposition was higher than that in patients with general IgA nephropathy (IgAN). In addition, the infiltrating CD4+, CD8+, CD68+ and PCNA+ cells in renal tissue were significantly high compared with that in controls. In a follow-up study, 66.7% of patients had life-sustaining renal function, 4 of them had normal range of serum creatinine (<124 µmol/l), and only 5 were dialysis-dependent. Conclusions: The patients with crescentic IgA nephropathy mostly show rapidly progressive nephritis associated with more severe pathological changes including glomerular, tubular interstitial and vascular lesions than in patients with general IgAN. The infiltrates in glomeruli may contribute to the crescentic formation, and the intensive immune suppressing treatment is useful to improve renal damage in patients with DCIgAN.

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“…It is possible, however, that the other investigators deliberately chose to study IgA nephropathy, which is the glomerular disease most commonly associated with gross haematuria [22]. From our findings one can infer that acute renal failure from gross haematuria can be found in all haematuric glomerulonephritides, especially when they are accompanied by glomerular necrotizing lesions.…”

Section: Discussionmentioning

confidence: 74%

Reversible acute renal failure from gross haematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction

Fogazzi

Imbasciati

Moroni

et al. 1995

Nephrology Dialysis Transplantation

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Abstract. Seven patients with acute renal failure due to gross haematuria caused by glomerulonephritis are described. Gross haematuria lasting 4-40 days led to acute impairment of renal function of variable severity (peak plasma creatinine 1.3-12 mg/dl) and duration. While partial recovery of renal function occurred in all patients within few days, complete remission was observed only some months later. Three patients had IgA nephropathy (2 the primary form and 1 nephritis secondary to Schonlein-Henoch purpura), two patients had acute postinfectious glomerulonephritis, and two others had focal necrotizing (pauci-immune) glomerulonephritis. The glomerular changes seen in the renal biopsy were not enough to explain per se the renal function impairment. Tubular changes, however, were severe and consisted of tubular necrosis, erythrocyte casts, erythrocyte phagocytosis by tubular cells, accompanied by interstitial damage (oedema, red-cell extravasation, and inflammatory infiltrates). Study of the renal biopsies by immunofluorescence revealed no retrodiffusion of Tamm-Horsfall protein into the glomerular Bowman's space, a sign of obstructed tubular flow in any case. It is concluded that acute renal failure due to gross haematuria in glomerulonephritic patients may not occur only in IgA nephropathy, as reported so far, and is not associated with intratubular obstruction.

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Idiopathic IgA Mesangial Nephropathy

Cited by 68 publications

References 64 publications

IgA Nephropathy and Polycystic Kidney Disease

IgA Nephropathy and Polycystic Kidney Disease

Idiopathic IgA Nephropathy with Diffuse Crescent Formation

Reversible acute renal failure from gross haematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction

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