Saudi Journal of Kidney Diseases and Transplantation

: 2021  |  Volume : 32  |  Issue : 2  |  Page : 564--567

Unusual cause of irreversible acute kidney injury postgastrectomy

Rashmi Yadav1, Urmila Anandh1, Swarnalata Gowrishankar2,  
1 Department of Nephrology, Yashoda Hospitals, Secunderabad, Telangana, India
2 Department of Pathology, Apollo Hospitals, Jubilee Hills, Hyderabad, Telangana, India

Correspondence Address:
Urmila Anandh
Department of Nephrology, Yashoda Hospitals, Secunderabad, Telangana


A 56-year-old male was diagnosed to have carcinoma stomach following evaluation of lack of appetite and weight loss. He underwent neoadjuvant chemotherapy and gastrectomy. Following surgery he developed progressive renal failure. A renal biopsy led to the diagnosis of oxalate nephropathy. Despite treatment his renal functions never recovered. Oxalate nephropathy is an underappreciated cause of renal failure postgastrectomy. It can cause irreversible renal failure unless detected and treated early.

How to cite this article:
Yadav R, Anandh U, Gowrishankar S. Unusual cause of irreversible acute kidney injury postgastrectomy.Saudi J Kidney Dis Transpl 2021;32:564-567

How to cite this URL:
Yadav R, Anandh U, Gowrishankar S. Unusual cause of irreversible acute kidney injury postgastrectomy. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 24 ];32:564-567
Available from:

Full Text

 Case Report

Mr. MP is a 56-year-old male, a known case of type 2 diabetes mellitus and hypertension was diagnosed with carcinoma stomach when he had presented with symptoms of lack of appetite and weight loss. He underwent a total gastrectomy with lymph node dissection in a different hospital three months back. He also received neoadjuvant chemotherapy (5-flourouracil, leucovorin, oxaliplatin and docetaxel). Four cycles were administered before surgery and three cycles afterwards. His renal parameters before the surgery were within normal limits. However, after the last chemotherapy cycle two months post gastrectomy, he developed febrile neutropenia. His further chemotherapy was discontinued.

Two weeks after the resolution of his neutropenia, he started developing pedal edema, shortness of breath and decreased appetite. His evaluation revealed renal failure (creatinine 2.8 mg/dL), normal urine examination (routine and microscopic) and normal sized kidneys on ultrasound. He was managed with diuretics with which his fluid overload improved. However his renal functions continued to worsen over the next two months [serum creatinine (SCr) 5.9 mg/dL] and subsequently he was referred to our center. At our hospital his SCr was 10.3 mg/dL. His other investigations are given in [Table 1]. He was initiated on hemodialysis through left internal jugular venous catheter. His urine examination was essentially unremarkable and urine protein creatinine ratio was 0.73. The 24-h urinary protein excretion was 185.38 mg/day. His fundus examination revealed early background diabetic retinopathy. Urine for eosinophils was negative. Dialysis was continued as required.{Table 1}

In view of rapid deterioration of renal functions, he underwent a renal biopsy. Light microscopic evaluation showed normal glomeruli. Evidence of tubular injury with significant grayish blue to semi translucent fan shaped to polygonal shaped crystals within the tubules and in the interstitium was noted [Figure 1]. The crystals were refringent under polarized light [Figure 2]. Patchy interstitial widening with mild to moderate lymphomononuclear infiltrate was also seen. About 10%–15% interstitial fibrosis and tubular atrophy was observed. One artery was sampled which was unremarkable. Immunoflourescence examination revealed no immune deposits. Based on these findings, a final diagnosis of acute tubule-interstitial nephritis with significant calcium oxalate deposits was made.{Figure 1}{Figure 2}

A 24-h oxalate excretion was done after renal biopsy which was 369 mg/24 h (Normal: 45 mg/day). He was started on oral calcium along with pyridoxine and magnesium supplementation. He became dialysis independent at the time of discharge, three months later his creatinine was 3.5 mg/dL and he remains dialysis independent with a urine output of approximately 1.5 L/day.

The authors obtained all appropriate consent forms from the patient for the publication of this case report.


Acute kidney injury (AKI) is common in patients with cancer and can affect almost 17.5% of patients within one year of diagnosis of cancer.[1] Cancer associated AKI often have a higher requirement of renal replacement therapy (8%–60%), longer hospital stay and a higher mortality.[2],[3],[4] The malignancies with the highest risk of developing AKI are renal cell carcinoma, hematological malignancies and liver cancer.[4] However, in a large nationwide survey from China, AKI was seen most in gastrointestinal malignancies.[5]

Multiple medical risk factors (volume depletion, chemotherapy nephrotoxicity, hypercalcemia, etc.,) are responsible for the development of AKI.[6] These patients also have a higher risk of postoperative AKI especially following gastrointestinal and lung cancer surgery.[6],[7],[8]

Our case illustrates a rare form of AKI (oxalate nephropathy) following gastric surgery. Oxalate nephropathy following jejuno-ileal bypass for obesity (abandoned in 1979) has been reported in literature.[9] However other forms of surgery (Roux-en-Y gastric bypass [RYGB]) for morbid obesity has been introduced in practice. RYGB is being recognized as a cause for the development of irreversible oxalate nephropathy.[10] Our case underwent total gastrectomy and esophago-ileal anastomosis. This surgical procedure has been rarely reported to cause oxalate nephropathy, however physiologically increased colonic oxalate absorption is a possibility in this form of surgery also. This is underscored in a series of 11 patients undergoing gastric surgeries, three of whom who underwent gastrectomy subsequently went on to develop oxalate nephropathy.[11]


Gastric surgery either in patients with obesity or in malignancies carry a high risk of developing oxalate nephropathy. This can lead to irreversible renal failure if not detected and treated early.

Conflict of interest: None declared.


1Christiansen CF, Johansen MB, Langeberg WJ, Fryzek JP, Sørensen HT. Incidence of acute kidney injury in cancer patients: A Danish population-based cohort study. Eur J Intern Med 2011;22:399-406.
2Darmon M, Ciroldi M, Thiery G, Schlemmer B, Azoulay E. Clinical review: Specific aspects of acute renal failure in cancer patients. Crit Care 2006;10:211.
3Candrilli S, Bell T, Irish W, Morris E, Goldman S, Cairo MS. A comparison of inpatient length of stay and costs among patients with hematologic malignancies (excluding Hodgkin disease) associated with and without acute renal failure. Clin Lymphoma Myeloma2008;8:44-51.
4Benoit DD, Hoste EA. Acute kidney injury in critically ill patients with cancer. Crit Care Clin 2009;26:151-79.
5Jin J, Wang Y, Shen Q, Gong J, Zhao L, He Q. Acute kidney injury in cancer patients: A nationwide survey in China. Sci Rep 2019;9: 3540.
6Perazella MA. Renal vulnerability to drug toxicity. Clin J Am Soc Nephrol 2009;4:1275- 83.
7Kim CS, Oak CY, Kim HY, et al. Incidence, predictive factors and clinical outcomes of acute kidney injury after gastric surgery for gastric cancer. PloS One 2013;8:e82289.
8Licker M, Cartier V, Robert J, et al. Risk factors of acute kidney injury according to RIFLE criteria after lung cancer surgery. Ann Thorac Surg 2011;91:844-50.
9Requarth JA, Burchard KW, Colacchio TA, et al. Long-term morbidity following jejunoileal bypass. The continuing potential need for surgical reversal. Arch Surg 1995;130:318-25.
10Nelson WK, Houghton SG, Milliner DS, Lieske JC, Sarr MG. Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: Potentially serious and unappreciated complications of Roux-en-Y gastric bypass. Surg Obes Relat Dis 2005;1:481-5.
11Nasr SH, D’Agati VD, Said SM, et al. Oxalate nephropathy complicating Roux-en-Y gastric bypass: An underrecognized cause of irreversible renal failure. Clin J Am Soc Nephrol 2008;3:1676-83.