title: Renal glomerular and tubular injury after gastric bypass in obese rats.
abstract: OBJECTIVE
  Roux-en-Y gastric bypass (RYGB) surgery is the most common surgical intervention for long-term weight loss in morbidly obese patients. By decreasing obesity-associated hyperfiltration, diabetes, and hypertension, RYGB is touted to stabilize, if not prevent, progression of chronic renal disease. To test this, the renal histology of diet-induced obese rats that underwent RYGB surgery was compared with that of pair-fed and sham obese controls.
  
  
  METHODS
  Sprague-Dawley rats, fed a high-fat, low-oxalate diet to induce gross obesity, were randomized to RYGB (n = 6), gastrointestinal-intact sham-operated obese controls (sham, n = 4), or gastrointestinal-intact sham-operated obese pair-fed controls (fed, n = 8). Daily body weight and food intake were recorded. On postoperative day 42, renal histology and immunohistochemistry were examined. Renal pathology was assessed by a categorical glomerular lesion score and a quantitative glomerular/tubular scoring system by experienced veterinary pathologists. Osteopontin and ED-1 (monocyte/macrophage cell) stainings were estimated by the percentage of stained area and the number of counted cells/high-power field, respectively.
  
  
  RESULTS
  Compared with sham and fed controls, RYGB rats had significant decreases in body weight (P < 0.001), more glomerular lesions (P = 0.02), and received higher glomerular and tubular lesion scores (P < 0.01). RYGB rodents had significantly stronger staining for osteopontin within the inner medullary region (P < 0.005) and ED-1 within the outer medullary region (P < 0.02) compared with sham and fed controls.
  
  
  CONCLUSIONS
  In this diet-induced obese rat model, RYGB is associated with chronic glomerulosclerosis and tubulointerstitial nephritis, confirmed by histology and immunohistochemistry. Prospective studies to better define the injurious mechanisms in this model are underway.
authors: Department of Urology, Center for the Study of Lithiasis and Pathological Calcification, University of Florida, Gainesville, Florida, USA. Benjamin.Canales@urology.ufl.edu
authors: Benjamin K
authors: BK
authors: Canales
authors: Leticia
authors: L
authors: Reyes
authors: Mary K
authors: MK
authors: Reinhard
authors: Saeed R
authors: SR
authors: Khan
authors: Carolina G
authors: CG
authors: Goncalves
authors: Michael M
authors: MM
authors: Meguid
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D059305:Diet, High-Fat / Q000009:adverse effects; D004195:Disease Models, Animal; D015390:Gastric Bypass / Q000009:adverse effects*; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007678:Kidney Glomerulus / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D007684:Kidney Tubules / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009395:Nephritis, Interstitial / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009767:Obesity, Morbid / Q000601:surgery*; D053495:Osteopontin / Q000378:metabolism; D010865:Pilot Projects; D011183:Postoperative Complications / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D015854:Up-Regulation; D015431:Weight Loss
chemical_list: C506897:Spp1 protein, rat; D053495:Osteopontin