Oxalate nephropathy: An important cause of renal failure after bariatric surgery
A 54-year-old male was seen in our nephrology clinic for progressive increase in his serum creatinine from 1.38 to 3.66 mg/dl over 9 months. There was no history of fever, diarrhea, steatorrhea, urinary tract symptoms, renal stones, or use of nephrotoxic agents. His past medical history included hypertension for 15 years, type 2 diabetes for 11 years, obstructive sleep apnea, depression, and treated cellulitis. He had undergone a duodenal switch procedure for morbid obesity (body mass index >50 kg/m2) 20 months earlier. Subsequently, he had lost more than 100 kg of body weight, and there was significant improvement in the control of blood pressure, sleep apnea, and blood sugar. His serum creatinine was 1.38 mg/dl and urinalysis was normal at the time of surgery.\nHis clinical examination was unremarkable. Laboratory investigations showed hemoglobin of 9.9 g/dl, white cell count of 6.9 × 103/μl, blood urea nitrogen of 51.82 mg/dl, and serum creatinine of 3.66 mg/dl. Serum electrolytes, calcium, phosphate, and bicarbonate were within normal limits. Urinalysis showed 5-10 white cells/hpf and 1-2 white cell casts without any proteinuria or hematuria. Ultrasound of kidneys showed normal sized kidneys with a few small bilateral calculi without any evidence of obstruction. Doppler of renal arteries was normal.\nIn view of progressive unexplained increase in creatinine, a kidney biopsy was done. The kidney biopsy [Figures and ] demonstrated 13 glomeruli of which six were globally sclerosed. The remaining glomeruli were histologically normal. The tubular interstitial compartment showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal with few intracellular and focal interstitial distributions. Under polarized light, the deposits appeared strongly birefringent forming fan-like, sheaf-like, or irregular shapes consistent with calcium oxalate crystals. There was an associated mild interstitial inflammation with moderate interstitial fibrosis and tubular atrophy. Blood vessels exhibited moderate arteriosclerosis and arteriolar hyalinosis. The immunofluorescence was negative and electron microscopy did not show any electron dense deposits but did reveal tubular damage with intratubular crystal deposition. His 24-h urinary oxalate level was found to be significantly elevated at 98.7 mg/day (normal range upto 40 mg/day). Urinary calcium and citrate were undetectable.\nA diagnosis of oxalate nephropathy secondary to enteric hyperoxaluria post-duodenal switch operation was made and he was started on low-oxalate, low-fat diet, with high-fluid intake (>3 liters per day). In addition, he was prescribed calcium citrate 1000 mg tid with meals as an oxalate binder. He was also started on cholestyramine 4 g twice daily and repeat urine oxalate improved markedly to 63 mg/day and his serum creatinine stabilized.