Vesicoureteral Reflux, Reflux Nephropathy, and End-Stage Renal Disease

Brakeman, Paul

doi:10.1155/2008/508949

Cited by 40 publications

(30 citation statements)

References 35 publications

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“…[1][2][3] Likewise, we observed that proteinuria appeared in the presence of RS and increased with grade of VUR. In addition, significant microalbuminuria (MA) found in our RS (þ) children supported previous reports postulating MA was an early indicator of glomerulosclerosis and hyperfiltration in RN.…”

Section: Discussionmentioning

confidence: 70%

“…However, clinical progression from VUR to renal scarring (RS) and nephropathy has not been completely elucidated although both the immune system and inflammatory process have been implicated. 2,3 Interleukin-18 (IL-18) is primarily a macrophage-derived pro-inflammatory cytokine; additionally expressed in bone marrow and renal parenchymal cells. It may promote immune and non-immune tissue damage through several mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-18, CRP and procalcitonin levels in vesicoureteral reflux and reflux nephropathy

2013

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Background: Some patients with vesicoureteral reflux (VUR) develop reflux nephropathy (RN) and a number of them progress to chronic kidney disease (CKD). However, it is unclear to predict which patient will develop RN and/or CKD. The aim of this study is to evaluate the role of Interleukin-18 (IL-18), C-reactive protein (CRP) and procalcitonin (PCT) as an indicator of RN in VUR. Methods: Ninety-three children aged 3.5-16 years with primary VUR were enrolled. Patients were divided into two groups according to the presence of renal scarring (RS). CRP, PCT, blood urea nitrogen (BUN), serum creatinine (Scr), urinary protein (Up), creatinine (Ucr) and microalbumin (Umalb), serum and urine IL-18 levels were determined during urinary tract infection (UTI) free episode. Results: BUN, Scr, Up/Ucr and Umalb/Ucr concentrations were higher whereas calculated creatinine clearance (Ccr) values were lower in RS (þ) group compared to RS (À) group. CRP, PCT, serum and urine IL-18 levels and mean urine IL-18/Cr concentrations were similar in both groups. Serum and urine IL-18 levels did not differ according to the grade of VUR. No significant correlation was found between CRP, PCT and IL-18. Conclusions: Proteinuria and microalbuminuria are valuable hallmarks of RN. CRP and PCT seem not to be reliable indicators of RN in VUR patients. Moreover, serum and urine IL-18 might not predict RN.

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Interleukin-18, CRP and procalcitonin levels in vesicoureteral reflux and reflux nephropathy

2013

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“…In a recent review Brakeman identifies the principal risk factors of progression of VUR to CKD: reduced glomerular filtration rate (GFR), bilateral VUR and/or renal scarring, grade V VUR, proteinuria, and hypertension. [57]. Ardissino et al found an estimated risk of end stage renal disease (ESRD) of 56% in italian children by age 20 years [58] …”

Section: Urinary Tract Infections and Vesico-ureteral Refluxmentioning

confidence: 99%

Risk Factors for Renal Failure: From Infancy to Adulthood

Maringhini¹,

Azzolina²,

Cusumano³

et al. 2012

Renal Failure - The Facts

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“…This condition may be associated with urinary tract infection and renal parenchymal abnormality, with the latter due to either congenital dysplasia or acquired scarring [2,3]. Studies carried out in several countries have found that the VURassociated renal abnormality is a cause of childhood and adolescent chronic renal failure (CRF) [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Mutations in the ROBO2 and SLIT2 genes are rare causes of familial vesico-ureteral reflux

Bartik

Zhao

et al. 2009

Pediatr Nephrol

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Familial clustering of vesico-ureteral reflux (VUR) suggests that genetic factors play an important role in the pathogenesis of this condition. The SLIT2 protein and its receptor, ROBO2, have key functions in the formation of the ureteric bud. Two recent studies have found that ROBO2 gene missense mutations are associated with VUR. In the study reported here, we investigated the genetic contribution of the SLIT2 and ROBO2 genes in non-syndromic familial VUR by mutation screening of 54 unrelated patients with primary VUR. Direct sequencing of all 26 exons and the exon-intron boundaries revealed six ROBO2 gene variants, two of which were new. Direct sequencing of all 37 exons and the exon-intron boundaries identified 20 SLIT2 gene variants, two of which were new. One variant, c.4253C > T, which was found in two families, leads to an amino acid substitution in a relatively well-conserved amino acid, p.Ala1418Val, which was predicted to cause an altered secondary structure but to have little impact on the three-dimensional structure. This missense variant did not segregate with VUR in these two families and was not found in 96 control subjects. We conclude that gene variants in ROBO2 and SLIT2 are rare causes of VUR in humans. Our results provide further evidence for the genetic heterogeneity of this disorder.

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Vesicoureteral Reflux, Reflux Nephropathy, and End-Stage Renal Disease

Cited by 40 publications

References 35 publications

Interleukin-18, CRP and procalcitonin levels in vesicoureteral reflux and reflux nephropathy

Interleukin-18, CRP and procalcitonin levels in vesicoureteral reflux and reflux nephropathy

Risk Factors for Renal Failure: From Infancy to Adulthood

Mutations in the ROBO2 and SLIT2 genes are rare causes of familial vesico-ureteral reflux

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