scholarly journals Serum glomerular albumin permeability activity: association with rapid progression to end-stage renal disease in focal segmental glomerulosclerosis

SpringerPlus ◽  
2016 ◽  
Vol 5 (1) ◽  
Author(s):  
Sudhindra Pudur ◽  
Tarak Srivastava ◽  
Mukut Sharma ◽  
Ram Sharma ◽  
Sergey Tarima ◽  
...  
2020 ◽  
Vol 10 (4) ◽  
pp. e43-e43
Author(s):  
Luísa Helena Pereira ◽  
Ana Cabrita ◽  
Mário Góis ◽  
Helena Viana ◽  
Sandra Sampaio ◽  
...  

Focal segmental glomerulosclerosis (FSGS) is a recognized cause of renal disease worldwide. The collapsing variant is distinct from the others, characterized clinically by a more severe nephrotic syndrome generally resistant to immunosuppressive therapy. It is known that a great number of patients progress to end-stage renal disease. Recognizing this lesion in biopsy is frequently challenging owing to the focal nature of the process which highlights the need for keeping a high index of suspicion for the diagnosis. We report and discuss a case of a non-HIV collapsing FSGS, followed by a complete (unexpected) renal recovery after an oral corticosteroid course.


1999 ◽  
Vol 10 (9) ◽  
pp. 1900-1907
Author(s):  
MELVIN M. SCHWARTZ ◽  
JONI EVANS ◽  
RAY BAIN ◽  
STEPHEN M. KORBET

Abstract. The cellular lesion (CELL), seen in some patients with primary focal segmental glomerulosclerosis (FSGS), comprises proliferation, hypertrophy, and pathologic changes in the cells overlying the glomerular scar. The prognosis of the cellular lesion was retrospectively studied in 100 patients with FSGS (43 had FSGS-CELL and 57 had FSGS without the cellular lesion (classic segmental scar [CS]). Patients with the FSGS-CELL lesion were more often black and severely proteinuric and developed more end-stage renal disease (ESRD). Nephrotic patients with FSGS-CELL (n = 39) were more proteinuric at presentation than patients with FSGS-CS (n = 36). ESRD developed more frequently in patients with the FSGS-CELL (17 of 39, 44% versus 5 of 36, 14%, P = 0.005), and patients with extensive FSGS-CELL (≥ 20% glomeruli) were mainly black (94%), severely nephrotic (67%, >10 g/d), and had a poor response to treatment (23% remission). In nephrotic patients, initial serum creatinine, interstitial expansion ≥20%, and CELL independently predicted ESRD. However, the rates of remission in treated nephrotic patients with FSGS-CELL and FSGS-CS were the same (9 of 17, 53% versus 17 of 39, 52%), and patients in both groups who achieved a remission had a 5-yr survival of 100%. Steroid treatment was the only variable that predicted remission. Patients with the FSGS-CELL have an increased prevalence of ESRD, but the improved prognosis associated with remission is so significant that a therapeutic trial is warranted in all nephrotic FSGS patients, regardless of the presence of the cellular lesion.


2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Cyril Cyrus ◽  
Shahanas Chathoth ◽  
Chittibabu Vatte ◽  
Nafie Alrubaish ◽  
Othman Almuhanna ◽  
...  

Background. End-stage renal disease (ESRD) is the result of hypertensive nephrosclerosis and chronic glomerular diseases and is associated with high morbidity and mortality. There are strong heritable components in the manifestation of the disease with a genetic predisposition to renal disorders, including focal segmental glomerulosclerosis and arterionephrosclerosis. Recent studies in genetics have examined modifiable risk factors that contribute to renal disease, and this has provided a deep insight into progressive kidney disease. Single-nucleotide polymorphisms at the proximity of SHROOM3, CST3, SLC7A9, and MYH9 genes have been associated with an increased risk of developing CKD and ESRD. Methods. A total of 160 CKD patients and 189 control subjects of Saudi origin participated in the study. Eight polymorphisms (SHROOM3-rs9992101, rs17319721; SLC7A9-rs4805834; MYH9-rs4821480, rs4821481, rs2032487, rs3752462; CST3-rs13038305) were genotyped using TaqMan assay, and the haplotype analysis was done using the HaploView 4.2 software. Results. Haplotype analysis revealed a novel haplotype “E6”-GTTT to be associated significantly with an increased risk for ESRD (p=0.0001) and CKD (p=0.03). Conclusion. CKD is often silent until symptomatic uremia during the advanced stages of the disease. The newly identified haplotype will help recognize patients at risk for a rapid progression of CKD to ESRD. Accurate detection and mapping of the genetic variants facilitates improved risk stratification and development of improved and targeted therapeutic management for CKD.


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