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Oxalate nephropathy with a granulomatous lesion due to excessive intake of peanuts

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Abstract

A 65-year-old Japanese male developed renal dysfunction, showing proteinuria and marked urinary excretion of β2-microglobulin. He had consumed approximately 100–200 g peanuts and 750–1,000 ml beer every day for two or three months. He had previously been treated for hypertension with an angiotensin-converting enzyme inhibitor, enalapril. He then visited his primary-care doctor with mild fever, and renal dysfunction with mild diabetes mellitus were diagnosed. He was referred to our hospital, and because no diabetic retinopathy was observed by ophthalmological tests, renal biopsy examination was performed to clarify renal dysfunction. Renal biopsy specimens showed intimal thickening in the small arteries and interstitial nephritis with a granulomatous lesion, accompanied by oxalate crystals under polarized light. Glomeruli were unremarkable without any immunoglobulin deposition, and nodular lesions. Because he daily consumed a large amount of peanuts, oxalate nephropathy due to excessive intake of peanuts was strongly suspected. This case revealed that unusual food habits, including nuts, can cause oxalate nephropathy, and that close examination by renal biopsy was useful for clarifying the etiology of the unknown renal damage.

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References

  1. Lorenzo V, Alvarez A, Torres A, Torregrosa V, Hernández D, Salido E. Presentation and role of transplantation in adult patients with type 1 primary hyperoxaluria and the I244T AGXT mutation: single-center experience. Kidney Int. 2006;70:1115–9.

    Article  CAS  Google Scholar 

  2. Hoppe B, Leumann E. Diagnostic and therapeutic strategies in hyperoxaluria: a plea for early intervention. Nephrol Dial Transplant. 2004;19:39–42.

    Article  Google Scholar 

  3. Hill GS. Calcium and the kidney, hydronephrosis. In: Jennette JC, Olson JL, Schwartz MM, Silva FG, editors. Heptinstall’s pathology of the kidney. Philadelphia: Lippincott–Raven; 1998. pp. 891–936.

    Google Scholar 

  4. Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol. 2007;177:565–9.

    Article  Google Scholar 

  5. Mandell I, Krauss E, Millan JC. Oxalate-induced acute renal failure in Crohn’s disease. Am J Med. 1980;69:628–32.

    Article  CAS  Google Scholar 

  6. Yoshida O, Terai A, Ohkawa T, Okada Y. National trend of the incidence of urolithiasis in Japan from 1965 to 1995. Kidney Int. 1999;56:1899–904.

    Article  CAS  Google Scholar 

  7. Isonokami M, Nishida K, Okada N, Yoshikawa K. Cutaneous oxalate granulomas in a haemodialysed patient: report of a case with unique clinical features. Br J Dermatol. 1993;128:690–2.

    Article  CAS  Google Scholar 

  8. Böör A, Jurkovic I, Friedmann I, Benický M, Kocan P. Calcium oxalate granuloma of the nose of a chronically dialysed nephritic patient. J Laryngol Otol. 2001;115:514–6.

    PubMed  Google Scholar 

  9. Khan SR. Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies. Clin Exp Nephrol. 2004;8:75–88.

    Article  CAS  Google Scholar 

  10. Yasui T, Fujita K, Asai K, Kohri K. Osteopontin regulates adhesion of calcium oxalate crystals to renal epithelial cells. Int J Urol. 2002;9:100–8.

    Article  CAS  Google Scholar 

  11. Taylor EN, Curhan GC. Oxalate intake and the risk for nephrolithiasis. J Am Soc Nephrol. 2007;18:2198–204.

    Article  CAS  Google Scholar 

  12. Stoller ML, Carroll PR. Urology. In: Tierney LM, McPhee SJ, Papadakis MA, editors. Current medical diagnosis and treatment. New York: McGraw–Hill; 2003. p. 903–45.

    Google Scholar 

  13. Churg J, Cotran RS, Sinniah R, Sakaguchi H, Sobin LH, editors. Tubular and tubulo-interstitial nephropathy caused by metabolic disturbances. In: Renal disease: classification and atlas of tubulo-interstitial diseases. 1st ed. New York, Igaku-Shoin, 1985. p. 157–60.

  14. Brinkley LJ, Gregory J, Pak CY. A further study of oxalate bioavailability in foods. J Urol. 1990;144:94–6.

    Article  CAS  Google Scholar 

  15. Ferraz RR, Tiselius HG, Heilberg IP. Fat malabsorption induced by gastrointestinal lipase inhibitor leads to an increase in urinary oxalate excretion. Kidney Int. 2004;66:676–82.

    Article  CAS  Google Scholar 

  16. Borghi L, Meschi T, Schianchi T, Briganti A, Guerra A, Allegri F, Novarini A. Urine volume: stone risk factor and preventive measure. Nephron. 1999;81 Suppl 1:31–7.

    Article  CAS  Google Scholar 

  17. Siener R, Schade N, Nicolay C, von Unruh GE, Hesse A. The efficacy of dietary intervention on urinary risk factors for stone formation in recurrent calcium oxalate stone patients. J Urol. 2005;173:1601–5.

    Article  CAS  Google Scholar 

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Correspondence to Noriko Mori.

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Sasaki, M., Murakami, M., Matsuo, K. et al. Oxalate nephropathy with a granulomatous lesion due to excessive intake of peanuts. Clin Exp Nephrol 12, 305–308 (2008). https://doi.org/10.1007/s10157-008-0046-5

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  • DOI: https://doi.org/10.1007/s10157-008-0046-5

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