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Diagnosis: Hyperoxaluria (and Acute Kidney Injury) Secondary to Short Bowel Syndrome - or Acute Oxalate Nephropathy

Oxalate nephropathy is a severe condition resulting from deposition of calcium oxalate crystals in kidney tissue, which causes tubular-interstitial injury and fibrosis, acute kidney injury (AKI), and/or chronic kidney disease (CKD). Most investigators have used the following diagnostic criteria for oxalate nephropathy: (1) progressive kidney disease, (2) oxalate crystal deposition with tubular injury and interstitial nephritis, and (3) exclusion of other etiologies of kidney disease (aside from vascular and/or diabetes-associated nephropathy). A hyperoxaluria enabling condition should ideally also be identified. The prevalence of oxalate nephropathy is unknown. Upon presentation, most patients had hypertension, diabetes, and/or a history of CKD. The latter may result from past subclinical deposition of oxalate crystals or represent a predisposing factor because of reduced excretion of oxalate. Approximately two-thirds of the patients have malabsorption-associated hyperoxaluria. Chronic pancreatitis and gastric bypass are common causes of oxalate nephropathy. The combination of the hyperoxaluria-enabling condition with an additional factor or trigger may lead to crystal formation and kidney damage. Factors such as acute dehydration, diuretic use, inflammation, antibiotic use, or high dietary oxalate intake may increase the urinary oxalate concentration. Renin-angiotensin-aldosterone system (RAAS) blocker use is also highly prevalent in patients presenting with oxalate nephropathy and may favor oxalate crystal-associated kidney injury via the reduction of glomerular filtration fraction. Clinical presentation of oxalate nephropathy varies across the spectrum of AKI, AKI on CKD, and CKD (The above text taken from: Demoulin N, et al. Pathophysiology and Management of Hyperoxaluria and Oxalate Nephropathy: A Review. Am J Kidney Dis. 2022;79(5):717-727. [PubMed link]).

See the chapter: Tubulointerstitial Diseases of our Tutorial.

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References

  • Nasr SH, Valeri AM, Said SM, Sethi S, Nath KA, Lieske JC, Bu L. Clinicopathologic Characteristics, Etiologies, and Outcome of Secondary Oxalate Nephropathy. Mayo Clin Proc. 2024 Feb. Epub ahead of print. [PubMed link].
  • Llanos M, Kwon A, Herlitz L, Shafi T, Cohen S, Gebreselassie SK, Sawaf H, Bobart SA. The Clinical and Pathological Characteristics of Patients with Oxalate Nephropathy. Kidney360. 2024;5(1):65-72. [PubMed link]
  • Bao D, Wang Y, Zhao MH. Oxalate Nephropathy and the Mechanism of Oxalate-Induced Kidney Injury. Kidney Dis (Basel). 2023;9(6):459-468. [PubMed link]
  • Demoulin N, Aydin S, Gillion V, Morelle J, Jadoul M. Pathophysiology and Management of Hyperoxaluria and Oxalate Nephropathy: A Review. Am J Kidney Dis. 2022;79(5):717-727. [PubMed link]

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