A Case of Oxalate Nephropathy in a Known Diabetic Patient following Acute Alcoholic Pancreatitis

This was a case of a 39-year-old gentleman known to have diabetes mellitus since February 2021 on insulin glargine (Lantus) 16 units nocte and sitagliptin/metformin 50/500 mg once a day who presented to a tertiary teaching hospital in Kenya in May 2021 with a three-week history of vomiting and diarrhea. He had been previously admitted to a different facility with acute alcoholic pancreatitis. His examination was nonremarkable except for mild dehydration and pallor. He had moderate metabolic acidosis and deranged renal function. Prior to this, his creatinine was normal. As part of the evaluation for the rapid deterioration of renal function, a kidney biopsy performed revealed oxalate nephropathy. He was started on renal replacement therapy with hemodialysis.


Background
Oxalate nephropathy is a rare condition associated with excess oxalate in the system. is can be either from increased absorption from the gastrointestinal tract or endogenously from the liver because of glyoxylate metabolism. ese are referred to as secondary and primary hyperoxaluria, respectively. Primary hyperoxaluria ensues in the background of reduced or absent activity of enzymes involved in the glyoxylate metabolism [1,2]. In secondary hyperoxaluria, there is either increased exposure to dietary sources of oxalate or any pathological conditions that increase intestinal absorption of oxalic acid.
ese conditions are associated with fat malabsorption. Excess oxalate results in hyperoxaluria since it is primarily excreted by the kidneys [3]. is causes renal dysfunction, which is diagnosed primarily on kidney biopsy [4].

Case Presentation
is is a case of a 39-year-old male known to have diabetes mellitus since February 2021 on Lantus 16 units nocte and sitagliptin/metformin 50/500 mg once daily. He presented to the hospital in May 2021 with a three-week history of postprandial, nonbilious vomiting and a four-day history of watery, nonbloody diarrhea, associated with reduced appetite, progressive generalized body malaise, and reduced urine output. He had also noted decreasing insulin requirements with the last injection 2 weeks prior to presentation. e past medical history was remarkable for an admission 3 months prior to presentation and managed for acute alcoholic pancreatitis. At presentation, he was moderately pale and dehydrated, with a PR at -87 bpm and raised BP at 157/90 mmHg. Systemic examination was nonremarkable.
e initial laboratory parameters are highlighted in Tables 1 and 2. An impression of acute kidney injury likely due to rapidly progressive glomerulonephritis with high anion gap metabolic acidosis, symptomatic uremia, and microcytic hypochromic anemia in the diabetic patient was made.

Initial Management.
He was admitted to a high dependency unit where he underwent urgent hemodialysis, transfusion with two units of packed red blood cells, intravenous fluid resuscitation, and insulin therapy.
He also underwent lower and upper gastrointestinal endoscopy as evaluation for the anemia, which revealed gastric erosions and hemorrhoids. Table 3 shows the results of the additional tests carried out.

Imaging.
Kidney ureter and bladder ultrasound showed bilateral renal parenchymal disease. Contrast-enhanced computed tomography revealed features consistent with chronic pancreatitis; moderately edematous kidneys with moderate periphrenic stranding. e impression was revised to nondiabetic kidney disease with possibility of oxalosis because of chronic pancreatitis seen on the contrast-enhanced CT abdomen. Figures 1 and 2 show the images of the CT scans.

Histopathology.
Kidney biopsy was performed in view of the above results. is showed 1 core with 28 glomeruli, one of which was globally sclerosed.
ere were no segmental scars. e mesangium showed normal cellularity with a marked increase in the matrix and focal nodule formation. ere was no endocapillary hypercellularity. e capillary walls showed mild thickening without spikes or double contours on silver stain. e tubules showed diffuse acute on chronic tubular injury and numerous oxalate casts on polarized light microscopy.
ere were severe (50%) interstitial fibrosis and tubular atrophy with chronic inflammation present in fibrotic areas. ere were moderate hyaline arteriolosclerosis and arteriosclerosis. Immunofluorescence microscopy, referred out, was reported as follows: 8 glomeruli negative for immunoglobulin and complement deposits. Electron microscopy was not performed. e diagnosis was severe acute on chronic tubular injury with calcium oxalate deposits and nodular diabetic glomerulosclerosis (see Figures 3 and 4).

Discussion and Conclusion
At presentation, the aforementioned patient's renal dysfunction would have been attributed to diabetes that had been diagnosed three months before presentation. However, everything else pointed towards a possibility of nondiabetic kidney disease. He had no proteinuria, no hematuria, or any     2 Case Reports in Nephrology other microvascular complications and had a rapid decline of renal function, therefore, meeting the criteria for renal biopsy [5]. ese, together with a previous history of acute pancreatitis and abdominal CT scan findings, raised a possibility of secondary hyperoxaluria with oxalate nephropathy. is diagnosis was confirmed on histology.
Oxalate nephropathy results from excess oxalate in the system. is can be because of increased absorption from the gastrointestinal tract, ascorbic acid administration (intravenously or orally), or increased endogenous production from defects in the enzymes involved in the glyoxylate metabolism.
Normally, oxalate present in the gastrointestinal tract is bound to calcium preventing its absorption and increasing its excretion. However, impaired exocrine function, in acute or chronic pancreatitis, leads to reduced digestion of fatty acids, hence resulting in fat malabsorption. e free fatty acids bind calcium instead, leaving the oxalate unbound and increasing its absorption into the bloodstream from the colon [4]. e excess oxalate is excreted via the kidneys causing renal damage. Mechanisms of renal damage include recurrent nephrolithiasis from calcium oxalate complexes and crystals, nephrocalcinosis, and interstitial fibrosis [6].
A systemic review on secondary nephropathy showed that 35% of the patients present with acute kidney injury followed by 29% presenting with acute on chronic kidney disease [7]. e aforementioned patient presented with acute kidney injury.
In conclusion, one needs to have a high index of suspicion for possibility of nondiabetic kidney disease in diabetic patients with rapidly deteriorating renal function, especially in the absence of other microvascular complications of diabetes.

Conflicts of Interest
e authors declare that they have no conflicts of interest.