There has been a parallel rise in the need for bariatric surgery as the prevalence of obesity has increased by leaps and bounds over the last 2 decades. Certain procedures like Roux-en-Y gastric bypass are associated with nephrolithiasis, hyperoxaluria, and, rarely, oxalate nephropathy. We report an interesting case of a patient who had relentless progression of his kidney disease post-bariatric surgery.

© 2022 The Author(s). Published by S. Karger AG, Basel

The prevalence of obesity is staggering and shocking. As per the World Health Organization global estimates, almost 11% of adult population in 2016 was obese. Bariatric surgery is increasingly gaining popularity in the developing countries likewise the west for the management of extreme obesity. Bariatric surgery comes with its own sets of advantages and caveats. Surgeons need to be fully aware of all the possible outcomes of bariatric surgery enabling them to take a rationale call after discussing with a nephrologist. We report a case of 60-year-old diabetic and hypertensive gentleman who had progressive worsening of renal disease post-bariatric surgery.

Mr. JBR, 60-year-old diabetic and hypertensive man, came to the emergency room with complaints of fever, loss of appetite, and significant weight loss. He denied a history of flank pain, consumption of nephrotoxic drugs, diarrhea, or a history of renal stones. On examination, he appeared dehydrated and malnourished, body mass index (BMI) = 17.3 kg/m2. He had glossitis, angular cheilosis, and half-and-half nails. Systemic examination revealed tenderness in the left renal angle. He had been hypertensive and diabetic for the last 15 years, had clinically severe obesity (BMI = 42 kg/m2) for which he underwent sleeve gastrectomy in 2009 followed by abdominoplasty or tummy tuck in 2010. Postoperatively, he achieved a new BMI of 29 kg/m2 and had a significant improvement in his metabolic profile. In 2016, he resumed to gain weight and during this time underwent cholecystectomy for cholelithiasis. For worsening BMI, he underwent a revision of sleeve gastrectomy followed by nonbanded Roux-en-Y gastric bypass (RYGB) surgery in 2018. Postoperatively, his weight reduced by 42% and a significant change in the sugar profile was observed. His serum creatinine was 1.4 mg/dL and urinalysis was normal at the time of the discharge. During the next 6 months, he had multiple admissions for acute gastroenteritis, poor appetite, and malnutrition. In June 2019, he had multiple episodes of vomiting for which a computed tomography scan of the abdomen was done which showed a narrow fistulous tract from the gastric pouch to the left hemidiaphragm suggestive of an abscess. Endoscopic irrigation of the abscess was performed with placement of two internal drains and broad-spectrum intravenous antibiotics were administered. On the scan, left nephrolithiasis with left hydroureteronephrosis was observed and a double J stent was placed by the urologist. His serum creatinine was 2.2 mg/dL at the time of discharge. He now came for further treatment to our hospital. His routine laboratory investigations revealed serum creatinine 7 mg/dL, blood urea nitrogen 78 mg/dL, urine routine showed full-field pus cells and 8–10 rbc/hpf, hemoglobin 8 g/dL. Immunological tests such as antinuclear antibodies and anticytoplasmic antibodies were negative and complement levels were within the normal range. Ultrasound examination of the kidneys showed their normal size without any evidence of obstruction. Abdominal CT scan repeated showed left perirenal fat stranding with left nonobstructive calculi. The double J stent was removed and broad-spectrum antibiotics were continued with presumptive diagnosis of the left pyelonephritis. The patient initially showed improvement, but renal function began to deteriorate again and he underwent a percutaneous native kidney biopsy. Light microscopy revealed white crystalline tubular deposits suggestive of oxalate crystals with underlying glomerular tufts showing thickening of the basement membrane with mesangial expansion suggestive of diabetic nephropathy class 2b (shown in Fig. 1). The deposits appeared strongly birefringent, forming a fan-like shape in polarized microscopy (shown in Fig. 2). His urinary oxalate levels were 78 mg/dL (normal <40 mg/dL). He was managed with a low-fat and low-oxalate diet, high-fluid intake, and potassium citrate. He was also given calcium supplements and cholestyramine to reduce the oxalate absorption from the colon, but none helped and he finally had to be instituted on hemodialysis from January 2021. Currently, he is on maintenance hemodialysis 2/week and is currently doing well.

Light microscopy (PAS, ×40) reveals white crystalline tubular deposits suggestive of oxalate crystals (black arrow) with underlying glomerular tufts showing basement membrane thickening (black arrow heads) with mesangial expansion suggestive of diabetic nephropathy class 2b.

Oxalate crystals showing birefringence under polarized microscopy (arrow heads).

The global prevalence of obesity is soaring and this trend has paralleled even in patients with chronic kidney disease [1]. According to one study, obesity has been associated with a higher risk of nephrolithiasis, renal cell cancers, incident CKD, and end-stage renal disease [2]. The pathogenesis postulated for obesity-related renal injury is obesity-mediated hypertension, glomerular hyperfiltration, lower urinary ph, activation of the sympathetic nervous system, and insulin resistance [3, 4]. Considering the magnitude of patients with morbid obesity, bariatric surgery offers more than a ray of hope to these patients. The most commonly performed bariatric surgery RYGB, on the one hand, offers a better metabolic profile, long-term cardio- and renoprotection, mortality and morbidity benefits, but on the other hand, it is associated with renal complications such as nephrolithiasis and hyperoxaluria and, albeit rare, oxalate nephropathy that can lead to irreversible loss of kidney function [1, 5]. This was seen similarly in our case.

Post-RYGB surgery, elevated free fatty acids bind to the calcium in the intestinal lumen inhibiting the formation of calcium oxalate indirectly leading to increased availability of soluble-free oxalate in the intestinal lumen. This free oxalate is then absorbed by the colonic mucosa, gets excreted only to get deposited within the renal parenchyma [6].

Oxalate nephropathy post-RYGB is associated with a dismal prognosis, with 72.7% progressing to end stage renal disease within 3 months [6, 7]. In our case, patient presented 6 months post-surgery which is similar to a case reported by Yaghoubi et al. [8]. Other renal lesions such as hypertensive glomerulosclerosis, diabetic nephropathy, or obesity-associated focal segmental glomerulosclerosis can coexist in these patients because of underlying coexisting multiple comorbidities [7].

Oxalate nephropathy is managed with combination of dietary modification and luminal oxalate binders. Dietary changes include high fluid intake combined with low-fat and low-oxalate diet. Citric salts such as potassium citrate are usually given as urinary hypocitraturia usually coexists. Our patient was managed on same principles. Cholestyramine was also tried in our patient as there is little support for the same in literature [9]. RYGB reversal is the last option available if all available medical therapies fail, but it is unclear whether reversal of RYGB can improve long-term outcomes.

Renal injuries are dark side of the bariatric surgery, but it remains to be the only therapy which has shown the promise to improve long-term patient and kidney outcomes. It is important that the clinician and surgeon are aware of post-procedure renal complications associated with bariatric surgery.

This retrospective review of patient data did not require ethical approval in accordance with local/national guidelines. Informed written consent for publication including images was obtained from the patient. All procedures were conducted in accordance with the World Medical Association Declaration of Helsinki.

The authors declare that they have no conflict of interest.

No funding received.

Sahil Bagai wrote the manuscript and did final editing, Dinesh Khullar was physician in charge and did help in revising manuscript, Bhavna Bansal was reporting pathologist and helped in data collection, Pallavi Prasad helped in managing case and did editing, and Vipra Malik helped in writing of the manuscript.

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author/first author.

This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.