IgA Nephropathy

Wyatt, Robert; Julian, Bruce A.

doi:10.1056/nejmra1206793

Cited by 1,040 publications

(1,036 citation statements)

References 79 publications

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“…This elderly patient had none of the classic features of IgAV such as palpable purpura and gastrointestinal manifestations, including abdominal pain, bleeding, infarction, and intussusceptions (9). IgA nephropathy is the most common cause of glomerulonephritis, and symptoms can range from asymptomatic hematuria to RPGN (10). Although our patient is a woman in her 60s with a history of heavy smoking, the absence of pulmonary symptoms and negative antibodies to NC1 of type IV collagen in the GBM excludes Goodpasture's syndrome as the cause of her renal disease (11,12).…”

Section: Differential Diagnosismentioning

confidence: 97%

“…She had periorbital edema as well as bilateral lower extremity pitting edema to the knees. Laboratory evaluation in the emergency room showed normocytic anemia, blood urea nitrogen of 44 mg/dl (normal range [7][8][9][10][11][12][13][14][15][16][17][18], and a creatinine level of 3.8 mg/dl (normal range 0.6 -1.2). Her estimated creatinine clearance was 11.9 ml/minute/1.73 m 2 (normal range 80 -125) with a fractional excretion of sodium of 2.5%.…”

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confidence: 99%

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An Unusual Case of Hematuria

Najem

Sfeir

Estrada

et al. 2014

Arthritis Care & Research

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Section: Differential Diagnosismentioning

confidence: 97%

mentioning

confidence: 99%

An Unusual Case of Hematuria

Najem

Sfeir

Estrada

et al. 2014

Arthritis Care & Research

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“…The clinical manifestation of IgA nephropathy is highly variable, ranging from non-progressive benign disease to variably progressive course leading ultimately to end-stage renal disease [5,6]. IgA nephropathy can manifest as asymptomatic microscopic haematuria, gross haematuria, nephritic syndrome, nephrotic syndrome or acute renal injury from heavy glomerular haematuria with tubular occlusion and/or damage by red cells or from crescentic glomerulonephritis [7].…”

Section: Introductionmentioning

confidence: 99%

Crescentic IgA nephropathy following bone fracture

Karkar¹,

Ghacha²,

Abdelrahman³

2017

Nephrol Renal Dis

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Immunoglobulin A (IgA) nephropathy is the commonest form of primary glomerulonephritis with variable clinical presentation. It has been associated with several infectious and non-infectious diseases but with only few reported cases following traumatic bone fracture. The present case report describes a 55 years old male patient who developed acute kidney injury within 3 months following bone fracture. Urine examination showed microscopic haematuria and proteinuria together with rapid deterioration in renal function. Light microscopic examination of kidney biopsy sections showed glomerular mesangial proliferation with fibro-cellular crescent formation in few glomeruli, two glomeruli were sclerosed, in addition to interstitial inflammation and tubular atrophy. Immunofluorescence microscopy showed mesangial IgA and C3 deposits. The renal function improved substantially following a course of steroids and mycophenolate mofetil without dialysis support. The development of acute IgA nephropathy is possibly followed the incident of traumatic bone fracture.

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“…1 The disease is characterized by the deposition of IgA immunocomplexes (IC) onto the renal glomeruli, activating mesangial proliferation and stimulating production of inflammatory cytokines, leading to progressive kidney failure. Although the pathogenesis of this condition is poorly understood, it is likely that kidneys, like in other IC related diseases, represent 'innocent bystanders'.…”

Section: Introductionmentioning

confidence: 99%

A SPRY2 mutation leading to MAPK/ERK pathway inhibition is associated with an autosomal dominant form of IgA nephropathy

Milillo¹,

Carpia²,

Costanzi

et al. 2015

Eur J Hum Genet

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IgA nephropathy (IgAN) represents the most common primary glomerulonephritis worldwide with a prevalence of 25-50% among patients with primary glomerulopathies. In~5-10% of the patients the disease segregates with an autosomal dominant (AD) pattern. Association studies identified loci on chromosomes 1q32, 6p21, 8p23, 17p13, 22q12, whereas classical linkage studies on AD families identified loci on chromosomes 2q36, 4q26-31, 6q22, 17q12-22. We have studied a large Sicilian family where IgAN segregates with an AD transmission. To identify the causal gene, the exomes of two affected and one unaffected individual have been sequenced. From the bioinformatics analysis a p.(Arg119Trp) variant in the SPRY2 gene was identified as the probable disease-causing mutation. Moreover, functional characterization of this variant showed that it is responsible for the inhibition of the MAPK/ERK1/2 pathway. The same effect was observed in two sporadic IgAN patients carriers of wild-type SPRY2, suggesting that downregulation of the MAPK/ERK1/2 pathway represents a common mechanism leading to IgAN.

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IgA Nephropathy

Cited by 1,040 publications

References 79 publications

An Unusual Case of Hematuria

An Unusual Case of Hematuria

Crescentic IgA nephropathy following bone fracture

A SPRY2 mutation leading to MAPK/ERK pathway inhibition is associated with an autosomal dominant form of IgA nephropathy

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