Acute tubulointerstitial nephritis due to large amount of sorrel (Rumex acetosa) intake

To the Editor:

Drugs and herbal remedies are important causes of acute tubulointerstitial nephritis (TIN) in children. In addition, nephrotoxic agents in foods may also cause acute TIN. Oxalate is one of the nephrotoxic agents found in plants like sorrel, chickweed, and common lamb's quarters.¹ Poisoning with oxalate-containing plants has been reported in humans and animals, even with fatal outcome.^2–4

We report a case of 12-year-old boy with acute TIN secondary to the consumption of sorrel. Eighteen days before admission to our hospital, the patient had been evaluated in a state hospital as an outpatient due to vomiting. At that time, he did not have oliguria or anuria. Laboratory examinations revealed mild proteinuria (++, dipstick), microscopic hematuria, microscopic pyuria, and calcium oxalate crystals on urinalysis; and increased alanine transaminase (ALT) (456 U/L), aspartate transaminase (AST) (79 U/L), creatinine (1.17 mg/dL, 103.43 μmol/L), and urea (51 mg/dL, 8.5 mmol/L) levels. The patient's symptoms subsided within 3 days and he was referred to our center to be investigated for the etiology. On admission, his sole symptom was polyuria; the medical histories of the patient and his family were not remarkable. Physical examination was normal. Blood biochemistry for liver and renal function tests was normal except hypophosphatemia (1.91 mg/dL, 0.62 mmol/L), and mildly elevated serum transaminase levels (ALT: 91 U/L and AST: 58 U/L). Complete blood count, lipid profile, and coagulation tests were normal. Urinalysis revealed phosphaturia, glucosuria, and generalized aminoaciduria. Tubular phosphate reabsorption was 23%; the patient had mild proteinuria (950 mg/day; 19.8 mg/m²/hour). Renal ultrasonography confirmed increased echogenicity of both kidneys. These findings suggested proximal tubulopathy and we learned that a couple of hours before he started vomiting, he had eaten a large amount of sorrel when he was playing in the meadow. He could not describe the exact amount of sorrel but he told that he ate until he was full and suffered from mouth soreness. Urine oxalate level was found to be increased (116 mg/1.73 m²/day; normal: < 45 mg/1.73 m²/day). Oral rehydration and electrolyte replacement treatment for hypophosphatemia were instituted; polyuria, proteinuria, glucosuria, and hyperoxaluria were resolved within few weeks; and ALT and AST levels were within normal ranges. Since the clinical response after cessation of the nephrotoxic agent was excellent and he exhibited a quick and complete recovery, renal biopsy would be very invasive and thus was not performed.

Sorrel (Rumex acetosa) is a sour plant which is frequently used in Turkish cuisine as a salad and is also an ingredient in sauces and soups in many regions. The sour flavor originates from oxalate and the amount is estimated to be up to 150 mg/50 g of sorrel. Oxalate is acutely toxic at high intake levels and the LD₅₀ for pure oxalic acid is about 25 g for a 65-kg human.¹ The kidneys are the most damaged organs in high-dose oxalate ingestion. Formation of crystals of calcium oxalate leads to impairment of kidney function.⁵ Extensive tubular injury with epithelial necrosis and interstitial fibrosis are observed in hyperoxaluria. A kidney biopsy would be more definitive for oxalate and sorrel intoxication; however, we did not perform a renal biopsy due to the patient's speedy recovery with supportive treatment. Calcium oxalate crystals can be found in other organs like bone, skin, blood vessels, and joints.⁶ Kidney injury can be reversible or permanent, and it may result in renal transplantation or even death if the management is not appropriate. A detailed history is crucial in differential diagnosis of acute TIN. Sorrel ingestion may result in acute TIN due to its oxalate content when consumed in large amounts; however, in this case, elimination from the diet and supportive therapy resulted in a good response.

Declaration of interest

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.