Clinical and molecular markers of chronic interstitial nephropathy in congenital unilateral ureteropelvic junction obstruction

Purpose: We evaluated clinical and biological variables, and their meaning as reliable markers of chronic interstitial nephropathy in a selected group of children with prenatally detected hydronephrosis who underwent pyeloplasty because of congenital unilateral ureteropelvic junction obstruction. Materials and Methods: We reviewed the clinical, prenatal and postnatal ultrasonographic, and scintigraphic records of children for whom intraoperative biopsy records were available. We performed histological analysis, and evaluated tubulointerstitial immunostaining for vimentin and a-smooth muscle actin, and the immunohistochemical and mRNA expression of the renin-angiotensin system peptides and transforming growth factor-01. Results: The children were divided in 2 groups according to the absence (group 1) or presence (group 2) of chronic interstitial nephropathy in the biopsy. Patients in group 2 were significantly younger at prenatal diagnosis (p = 0.031), and had decreased split renal function (p = 0.005) and worse drainage (p = 0.035) on preoperative diuretic renography. No differences were found in terms of degree of hydronephrosis, or its prenatal and postnatal variation. Group 2 biopsies exhibited greater immunostaining for a-smooth muscle actin and vimentin (p = 0.004 and p = 0.047, respectively), and transforming growth factor-01 mRNA levels (p = 0.06). Vimentin and a-smooth muscle actin positivity correlated with renin, angiotensin II receptors 1 and 2, and transforming growth factor-01 mRNA levels, and all correlated with preoperative split renal function and post-void washout. Conclusions: In congenital unilateral ureteropelvic junction obstruction chronic interstitial nephropathy and poor postoperative recovery seem to be associated with an earlier diagnosis of hydronephrosis, functional loss greater than 10% and worse scintigraphic drainage. Moreover, there is a strong correlation between molecular fibrogenic markers and histologically and scintigraphically demonstrated renal damage.