title: Adaptation of renal function after unilateral nephrectomy in children with renal tumors.
abstract: Following treatment, survivors of unilateral Wilms tumor (WT) develop structural and functional changes in the remnant kidney. A disproportional increase in functional over structural changes results in hyperfiltration, a condition that may lead to renal damage. We studied adaptation of renal function after uninephrectomy in ten WT patients and a child with renal cell carcinoma. Glomerular filtration rate (GFR) (measured by inulin and creatinine clearances), renal plasma flow (RPF) by para-aminohippurate (PAH) clearances and segmental tubular Na+ transport were studied before and following a protein load (renal functional reserve). Nine patients showed a well-adapted kidney function with a GFR of 82.27 (+/- 5.6), an RPF of 429.71 (+/- 65.6) ml/min/1.73 m2 and a filtration fracton (FF) of 20%. Absolute proximal Na+ reabsorption was 65.2 (+/- 9.6) ml/min/1.73 m2, distal tubular delivery was 18.2 (+/- 3.9) ml/min/1.73 m2 and absolute distal Na+ reabsorption was 2146 (+/- 435) microM/min. A peculiar finding was the high baseline creatinine clearances (176.17 ml/min/1.73 m2) related to increased baseline tubular creatinine secretion. Over 120 min following the protein load, GFR increased by 20%, RPF by 6% and FF remained unchanged. Absolute proximal reabsorption increased by 20% and distal reabsorption by 22%. While most changes in renal function induced by a protein load are similar in healthy individuals and uninephrectomized patients, a more predominant contribution to Na+ reabsorption by the proximal tubule was noted. Postload fractional proximal reabsorption remained at 77% while in healthy persons a decrease from 77% to 62% was reported. Two patients showed dysfunctional changes following nephrectomy characterized by an increased GFR (130 ml/min/1.73 m2), increased filtration fraction (29%) and inability to increase glomerular and tubular functions following a protein load (loss of functional reserve). The significance of these abnormalities is not known and requires long-term follow-up to evaluate whether hyperfiltration will lead to renal damage.
authors.affiliation: Department of Pediatrics, University of Calgary, Alberta, Canada. rdo@skin.azm.nl
authors.forename: R M
authors.initials: RM
authors.lastname: Donckerwolcke
authors.forename: M J
authors.initials: MJ
authors.lastname: Coppes
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D003404:Creatinine / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007223:Infant; D007668:Kidney / Q000503:physiopathology*; D007677:Kidney Function Tests; D007680:Kidney Neoplasms / Q000503:physiopathology* / Q000601:surgery; D007684:Kidney Tubules / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009392:Nephrectomy; D017595:Renal Plasma Flow / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D009396:Wilms Tumor / Q000503:physiopathology* / Q000601:surgery
chemical_list: D012964:Sodium; D003404:Creatinine