Renal Histology in Ureteropelvic Junction Obstruction: Are Histological Changes a Consequence of Hyperfiltration?

Pascual, Luis A.; Oliva, Julio; Vega-P., Jose; Principi, Iliana; Vallés, Patricia G.

doi:10.1016/s0022-5347(01)62674-0

Cited by 30 publications

(16 citation statements)

References 13 publications

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“…In our study, 26% of patients did not reach the minimal reference value of urinary osmolality. Hyperfiltration in the hydronephrotic kidney is correlated with an increased excretion of proteins and may have a synergistic effect on the progression of histopathologic changes in the kidney [31]. In our study, there was mild proteinuria (up to 1.13 g/24 h per m 2 ) detected in 11.5% patients.…”

Section: Tubular Functionsupporting

confidence: 43%

Long-term follow-up of renal function in patients after surgery for obstructive uropathy

et al. 2008

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In this prospective study, selected biochemical markers of glomerular and tubular function, proteinuria, and ultrasound findings in 62 pediatric patients who underwent surgery for obstructive uropathy were examined. Patients were younger than 12 months, normocreatininemic at the time of surgery, and examined at a mean age of 6.3+/-0.9 years. Out of the markers tested, serum concentration of cystatin C was significantly higher in patients when compared with the control group (p<0.001), and serum creatinine concentration was within reference interval in all patients. With respect to tubular function, 26% of patients had decreased concentration ability. Proteinuria was detected in 4.8% of patients. On ultrasound, 66.7% of kidneys after surgery had residual dilatation of the renal pelvis. The patients thrive well, and their somatic parameters do not differ from their peers. Half of the patients had one or more urinary tract infections from the date of surgery to the date of examination. Study results support the need for long-term nephrologic follow-up in patients after surgery for obstructive uropathy. The hypothesis that renal function in patients undergoing surgery aged younger than 3 or 6 months is better when compared with those aged 6 to 12 months has not been confirmed.

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Section: Tubular Functionsupporting

confidence: 43%

Long-term follow-up of renal function in patients after surgery for obstructive uropathy

et al. 2008

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“…It is now apparent that the range in the number of nephrons in the normal human population can vary by eightfold (between 227,327 and 1,825,380 per kidney) [94], and there is increasing evidence that the deteriorating renal function in later life is correlated with a lower nephron number at birth [95,96]. A number of reports of clinical UPJ obstruction demonstrate obsolescent and sclerotic glomeruli, presumably representing ongoing nephron destruction [51, [97][98][99][100]. The outcome for patients with posterior urethral valves is much less favorable due to the evolution of the lesions earlier in gestation, bilateral renal involvement, and acceleration of renal injury resulting from persistent bladder dysfunction.…”

Section: Progression and Recovery Following Release Of The Obstructionmentioning

confidence: 99%

Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy

et al. 2009

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Congenital obstructive nephropathy accounts for the greatest fraction of chronic kidney disease in children. Genetic and nongenetic factors responsible for the lesions are largely unidentified, and attention has been focused on minimizing obstructive renal injury and optimizing long-term outcomes. The cellular and molecular events responsible for obstructive injury to the developing kidney have been elucidated from animal models. These have revealed nephron loss through cellular phenotypic transition and cell death, leading to the formation of atubular glomeruli and tubular atrophy. Altered renal expression of growth factors and cytokines, including angiotensin, transforming growth factor-beta, and adhesion molecules, modulate cell death by apoptosis or phenotypic transition of glomerular, tubular, and vascular cells. Mediators of cellular injury include hypoxia, ischemia, and reactive oxygen species, while fibroblasts undergo myofibroblast transformation with increased deposition of extracellular matrix. Progression of the lesions involves interstitial inflammation and interstitial fibrosis, both of which impair growth of the obstructed kidney and result in compensatory growth of the contralateral kidney. The long-term outcome depends on timing and severity of the obstruction and its relief, minimizing ongoing injury, and enhancing remodeling. Advances will depend on new biomarkers to evaluate the severity of obstruction, to determine therapy, and to follow the evolution of lesions.

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“…This suggests that species differences determine the singlenephron compensation by the contralateral kidney. Children with ureteropelvic junction obstruction have been found to have significant glomerular sclerosis [33,34], and this can be associated with proteinuria [35]. Although we did not measure the number of glomeruli in the present study, we have reported that, following 14 or 28 days of severe partial UUO or complete UUO in the neonatal rat, there is no compensatory increase in the number of nephrons in the contralateral kidney [5].…”

Section: Discussionmentioning

confidence: 60%

Compensatory renal growth due to neonatal ureteral obstruction: implications for clinical studies

et al. 2005

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In response to unilateral ureteral obstruction (UUO), the contralateral kidney undergoes compensatory renal growth, which is enhanced in early development. We investigated the renal growth response to UUO in the neonatal rat. Within 2 days of birth, animals were subjected to sham-operation, complete UUO, or variable partial UUO, and kidneys were harvested 3-60 days later. Contralateral kidney weight increased after only 7 days of complete UUO. Increase in contralateral kidney weight was not significant for partial UUO until 45 days, but kidney/body weight ratio increased after only 14 days of 0.3 mm partial UUO. The rate of contralateral renal growth increased with age and with increasing severity of UUO. In rats subjected to 45 days UUO, glomerular area was proportional to kidney/body weight ratio (r =0.61, p <0.01). We conclude that the rate of compensatory renal growth is dependent on the severity and duration of obstruction, and takes place at the single nephron level. The results suggest that biologic variability limits the early detection of compensatory renal growth, which is compounded by limitations in measuring renal size by clinical imaging. Factoring kidney length (or volume) by intervertebral length (or body surface area) should improve the precision of tracking renal growth.

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Renal Histology in Ureteropelvic Junction Obstruction: Are Histological Changes a Consequence of Hyperfiltration?

Cited by 30 publications

References 13 publications

Long-term follow-up of renal function in patients after surgery for obstructive uropathy

Long-term follow-up of renal function in patients after surgery for obstructive uropathy

Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy

Compensatory renal growth due to neonatal ureteral obstruction: implications for clinical studies

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