Pathologic classification of focal segmental glomerulosclerosis: a working proposal

D’Agati, Vivette D.; Fogo, Agnes B.; Bruijn, Jan A.; Jennette, J. Charles

doi:10.1053/j.ajkd.2003.10.024

Cited by 669 publications

(600 citation statements)

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“…Since 6 out of 19 glomeruli showed global sclerosis or glomerular collapse with glomerular ischemia in the renal biopsy samples, glomerular hyperfiltration after loss of functioning nephrons also developed in the present case. Glomerular ischemia and collapse is also known as one of the etiologies of secondary FSGS, such as arteriosclerosis and cholesterol embolism [6,7,25]. In our case, however, FSGS lesions developed mainly in non-collapse glomeruli.…”

Section: Discussionmentioning

confidence: 49%

“…The most important causes of secondary FSGS are conditions associated with high intraglomerular filtration pressure, including uncontrolled severe hypertension. In addition, loss of functioning nephrons may contribute to the augmentation of glomerular hypertension and hyperfiltration [6,7,24]. Since 6 out of 19 glomeruli showed global sclerosis or glomerular collapse with glomerular ischemia in the renal biopsy samples, glomerular hyperfiltration after loss of functioning nephrons also developed in the present case.…”

Section: Discussionmentioning

confidence: 67%

“…Since hypertension is considered to be an etiological factor of secondary FSGS [6,7], it is conceivable that secondary FSGS develops in malignant hypertension with nephrotic syndrome. Although several experimental animal studies concerning malignant hypertension and the formation of FSGS lesions in the kidney have been reported [8][9][10][11], the clinical studies of the kidney histology in malignant hypertension have generally not emphasized the prominence of FSGS [4,5].…”

Section: Discussionmentioning

confidence: 99%

“…Hemodynamic factors are generally believed to play an important role in the development of secondary FSGS [6,7,[21][22][23][24]. The most important causes of secondary FSGS are conditions associated with high intraglomerular filtration pressure, including uncontrolled severe hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, malignant hypertension often causes proteinuria, which can sometimes reach the levels seen in nephrotic syndrome [4,5]. Hypertension is one of the etiological factors of secondary focal segmental glomerulosclerosis (FSGS), which is mediated by adaptive structural-functional changes and associated initially with normal renal mass [4][5][6][7]. However, the pathology of the kidney in patients with hypertension and heavy proteinuria is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

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A case of secondary focal segmental glomerulosclerosis associated with malignant hypertension

et al. 2012

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Focal segmental glomerulosclerosis (FSGS) is associated with various clinicopathological conditions, including hypertension. We report here a case of secondary FSGS associated with malignant hypertension. A 33-yearold man with a 1-month history of visual impairment and headache visited the Department of Ophthalmology at our hospital and was found to have hypertensive retinopathy and severe hypertension (230/160 mmHg). He was referred to our department based on suspected renal dysfunction. His blood pressure on admission was 250/130 mmHg. Physical examination and laboratory tests revealed hypertensive cardiac dysfunction, focal brain edema, renal dysfunction (serum creatinine, Cr 7.07 mg/dl, blood urea nitrogen, BUN 49.9 mg/dl), massive proteinuria (10.7 g/day), and thrombotic microangiopathy. Funduscopy showed exudate, hemorrhage, and papilledema. The cause of secondary hypertension could not be identified. He was treated for primary malignant hypertension, but required hemodialysis 3 days after admission due to anuria. Treatment with antihypertensive agents resulted in the gradual recovery of renal function, although heavy proteinuria continued with nephrotic syndrome. Renal biopsy performed 1 month after admission showed features of malignant nephrosclerosis with secondary FSGS. Hemodialysis was discontinued following further improvement in renal function and the most recent laboratory tests showed proteinuria 1.8 g/day and persistent renal dysfunction (BUN 36.5 mg/dl, Cr 3.14 mg/ dl). Malignant hypertension may cause various injuries, including glomerular endothelial and epithelial cell injuries in glomerular hypertension and hyperfiltration, increase of the renin-angiotensin-aldosterone system, and endothelialepithelial interaction, resulting in the development of secondary FSGS and heavy proteinuria.

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Section: Discussionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 67%