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The incidence of secondary hyperoxaluria in post-bariatric surgery patients is well documented. the roux en and bypass and gastric band techniques are the most closely related. a frequent complication is renal ureteral lithiasis with progressive loss of glomerular filtration rate.
Present the case of a 63-year-old female, history of gastric bypass, due to morbid obesity n(150 to 90 kg), DM 2 difficult to control. He was admitted to the nephrology department due to anasarca and rapidly progressive deterioration of renal function, baseline creatinine 1.12 mg/dl, at admission 4.5 mg/dl, complement C3 49 mg/dl, C4 17 mg/dl (low) ANA 1:80, lupus nephritis is suspected against diabetic nephropathy. Renal biopsy: 2 acellular nodules pas and silver + are observed. the interstitium with patches of fibrosis with tubular atrophy, thyroidization type, infiltrated with lymphocytes, polymorphonuclear cells, and eosinophils. Birefringent intratubular calcifications causing diffuse tubular damage, cytoplasmic dephascellation, loss of brush borders. negative direct IF.
Lithogenicity from bariatric surgery is multifactorial, and includes at least 3 mechanisms: (1) calcium saponification as a result of fat malabsorption reduces calcium-oxalate binding. (2) in addition, the increase in bile salts in the colon (as a result of their decreased absorption in proximal portions of the intestine) increases the permeability of the mucosa to oxalate (3) a reduction in colonization by oxalobacter formigenes, especially with repeated use of beta-lactams.
Serum and urinary metabolic screening of patients after bariatric surgery would allow an increase in the early detection of patients at high risk of enteric hyperoxaluria. once the lithiasic disease is detected, dietary adjustments and avoiding the indiscriminate use of antibiotics are essential to prevent the progressive deterioration of renal function.