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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2013  |  Volume : 24  |  Issue : 3  |  Page : 571-575
Acute renal failure by ingestion of Euphorbia paralias

1 Department of Internal Medicine A, Charles Nicole Hospital, Tunis, Bab Saadoun, Tunisia
2 Urgent Reanimation Department, Montfleury (CAMU), Tunis, Bab Saadoun, Tunisia
3 Laboratory of Renal Pathology Research LR00SP01, Charles Nicole Hospital, Tunis, Bab Saadoun, Tunisia

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Date of Web Publication24-Apr-2013


Euphorbia paralias is known in traditional medicine as an anti-inflammatory agent, a purgative and for its local anesthetic property. To the best our knowledge, renal toxicity of this substance has not been previously reported. In this paper, we report the case of a 29-year-old male who developed renal damage following ingestion of Euphorbia paralias. He had been on follow-up for nephrotic syndrome since 1986, although irregularly, with several relapses but each responding well to steroid therapy. A kidney biopsy had not been performed earlier due to refusal by the patient. He was off steroids since April 2008 because the patient developed osteoporosis. He was admitted with general malaise and oliguria to our department in May 2009, following repeated vomiting and watery diarrhea for three days. On examination, he was edematous but had normal vital signs except for a pulse rate of 120/min. Hemoglobin was only 5.5 g/dL but with normal white cell and platelet counts. Blood biochemistry showed evidence of advanced renal failure with a serum creatinine level of 1835 μmol/L and urea at 44.6 mmol/L, sodium of 132 μmol/L and potassium at 4.3 mmol/L. He had features of nephrotic syndrome with severe hypoproteinamia and 24-h urinary protein of 10.45 g. Ultrasonography revealed enlarged kidneys with a reduced echogenecity of the medulla and the papillae. Subsequently, after hemodialysis with blood transfusion, a kidney biopsy was performed that showed focal segmental glomerulosclerosis associated with an acute tubular injury. On intensive interrogation, the patient gave a history of ingesting boiled Euphorbia paralias as a native treatment for edema, ten days prior to the onset of the current illness. A diagnosis of acute renal failure (ARF) resulting from the possible nephrotoxic effect of Euphorbia paralias poisoning was made. He was treated with intermittent hemodialysis and corticosteroids. Serum creatinine values improved after 48 days. At six months following the intoxication, serum creatinine of the patient was 240 μmol/L. In cases of unexplained ARF, a toxic mechanism should always be considered and acute renal failure caused by Euphorbia paralias should be included as a cause if renal toxicity is suspected in those places where it is being used as a native medicine.

How to cite this article:
Boubaker K, Ounissi M, Brahmi N, Goucha R, Hedri H, Abdellah TB, El Younsi F, Maiz HB, Kheder A. Acute renal failure by ingestion of Euphorbia paralias. Saudi J Kidney Dis Transpl 2013;24:571-5

How to cite this URL:
Boubaker K, Ounissi M, Brahmi N, Goucha R, Hedri H, Abdellah TB, El Younsi F, Maiz HB, Kheder A. Acute renal failure by ingestion of Euphorbia paralias. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2021 Sep 23];24:571-5. Available from: https://www.sjkdt.org/text.asp?2013/24/3/571/111069

   Introduction Top

Renal failure from acute tubular injury and/or tubulo-interstitial damage is usually caused by ischemia due to renal hypoperfusion in trau­matic or surgical cases or due to toxicity induced by chemical substances such as drugs as well as biological and chemical toxins. A large number of herbal and biological nephrotoxins can cause renal failure with transient or chro­nic requirement for dialysis. [1],[2] Plants of the genus Euphorbia are prolific producers of diterpenes of great biomedical interest. Among them, the sap, petty spurge from Euphorbia paralias [Figure 1], is known in traditional medicine as a purgative and local anesthetic. [3] To the best of our knowledge, renal toxicity by this compound had not been previously des­cribed. In this paper, we report a case of renal damage in a young man caused by ingestion of Euphorbia paralias.
Figure 1. Euphorbia paralias.

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   Case Report Top

A 29-year-old Tunisian male without any familial history of nephropathy was on follow-up since 1986 in the pediatric department and later in our department for nephrotic syn­drome. He had a normal blood pressure at 120/80 mmHg and therefore (ACEI), Ramipril, was only being given as an anti-proteinuric at the dose of 5 mg/day because of a tendency of the patient to develop hypotension. He did not receive any other anti-hypertensive drug or statins. Biochemistry showed protidemia at 48 g/L, albuminemia at 21 g/L and 24-h urinary protein of 12 g/day. Earlier, ultrasound of the kidneys had revealed normal-sized kidneys with good cortico-medullary differentiation. During follow-up, he was rather irregular and inferquent, but it is documented that between 1986 and 1998, he had eight relapses, all responding well to steroid therapy. The patient had refused a kidney biopsy. Since September 1998, he was lost to follow-up while he was on prednisone 30 mg every second day. He was re­viewed in February 2000 with relapse of nephrotic syndrome and was treated using prednisone at the dose of 1 mg/kg/day, with prompt response and reduction of the 24-h urinary protein from 12 to 1.5 g/day. All these changes were noted while he had maintained a normal renal function. Steroids were tapered and stopped in April 2008 because the patient had developed osteoporosis and the nephrotic syndrome was in remission And the patient was on treatment with ACEI only.

He was admitted to our department in May 2009 with oliguria and general malaise follo­wing repeated vomiting and watery diarrhea for three days. On examination, he showed edema, a blood pressure of 110/70 mmHg, heart rate 120/min, respiratory rate 18/min and temperature 37.2°C. Cardiac and pulmonary auscultations were normal. The patient had no other significant systemic symptoms or signs such as arthritis or skin lesions. The abdomen was soft and not distended and there was no hepato-splenomegaly. Laboratory findings re­vealed a serum creatinine level of 1835 μmol/L, urea at 44.6 mmol/L, uric acid at 499 μmol/L, a low sodium at 132 μmol/L, potassium at 4.3 mmol/ L, C-reactive protein at 23.4 mg/dL, AP at 84 U/L (normal range: 40-150 U/L), GGT 11 U/L (normal range: 10-45 U/L) and TB 5.3 μmol/L (normal range: 3.4-20 μmol/L). Blood examination showed a hemoglobin of 5.5 g/dL, total WBC at 6100/mm 3 with absolute eosinophil count at 1200/mL and platelets at 209,000/mm 3 . He had nephrotic syndrome with protidemia at 43 g/L, albuminemia at 21.3 g/L and a 24-h urinary protein of 10.45 g. Urine showed neither leukocyturia nor erythrocyturia, and he had no casts. Ultrasonography revealed enlarged kidneys with a decreased echogenecity of the medulla and the papillae. Subsequently, a kidney biopsy was performed after hemodialysis with blood trans­fusion. It revealed four of 17 glomeruli with global sclerosis; two of the remaining 13 glo­meruli exhibited segmental glomerular scle­rosis with mild expansion of the mesangial matrix and increased epithelial cells. There were signs of fibrosis and cellular infiltration in the interstitial tissue. Kidney biopsy also showed a loss of tubular cells and denuded proximal and distal tubules [Figure 2]. In part, there was an exfoliation of the tubular cells into the lumina with casts and debris obs­tructing the tubular lumen. Immunofluore­scence analysis demonstrated IgM segmentary deposits; IgG, IgA, C3, C4, C1q, fibrinogen, λ and k, however, were all negative. Electron microscopy was not performed because it is not available in our department. The histolo­gical diagnosis was focal segmental glome­rulosclerosis and associated acute tubular nec­rosis probably caused by a nephrotoxic agent.
Figure 2. Kidney biopsy: Tubulorrhexis and acute tubular acute epithelial cell necrosis, capillaritis and slight interstitial nephritis with neutrophils, lymphocytes in the interstitium.

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Following these results, the patient was inten­sively interrogated and, finally, the patient gave a history of one time ingestion of boiled plant of Euphorbia paralias ten days before as treatment for edema as a part of native medical treatment Therefore, nephrotoxicity resulting from Euphorbia paralias poisoning was consi­dered as the cause of the acute kidney injury.

In our patient, intermittent hemodialysis was performed every other day. He received 1 g of intravenous methyprednisolone as pulse during the first three consecutive days, followed by prednisone at a dose of 1 mg/kg every day. Urinary volume returned to normal and serum creatinine values normalised after 48 days. Six months later, the serum creatinine of the patient was 240 μmol/L and the 24-h urinary protein was 1.88 g.

   Discussion Top

Our results suggest that the patient had a re­lapse of nephrotic syndrome along with Eu­phorbia paralias intoxication-associated acute renal failure. Kidney biopsy showed focal segmental glomerulosclerosis associated with severe tubular necrosis and interstitial neph­ritis. Most probably, this is the first report on a case of Euphorbia paralias ingestion resulting in renal toxicity. In this case, it did not affect any other organ. Our patient used this plant for treating edema.

In the course of the centuries, important con­tributions have been made to therapeutics by traditional medicine, which is still used with disputable or mild efficaciousness. [3],[4],[5] In the last few years, a progressive impoverishment of this patrimony of secular knowledge has occurred owing to the changes in society, which have been wrought by technological civilization. However, in Tunisia, traditional medicine is still largely used.

Mediterranean spurges have been investigated by several authors. [6],[7] Samples of sea spurge, Euphorbiaceae plants are well known to possess interesting biological activities. [1],[8] Eu­phorbia paralias is a hardy perennial that inhabits sandy coasts and shingle beaches and is native to the entire Mediterranean region. [9] Euphorbia paralias is also one of the most common Euphorbia species growing in Egypt. [9]

In traditional medicine, it is known that the latex of Euphorbia paralias is used by fisher­men for external application as a local anesthetic against sting of weever fish (Trachynus vipera). [5] This plant is also used in human me­dicine as a purgative. [3] However, animal studies have shown that Euphorbia paralias had an anti-diarrheal effect as well as dose-dependent effects on muscles described as transient muscle stimulation followed by muscle inhibition in small doses and severe muscle relaxation in higher concentrations. It also has a molluscicidal, anti-feedant, antiviral and anti-leishmanial activities. [4],[10],[11],[12],[13] Anti-inflammatory effect is due to inhibition of nitric oxide generation by LPS-stimulated J774 murine macrophages. [14],[15]

Our patient probably had focal segmental glomerulosclerosis with cell cycle abnorma­lities of podocytes responsible for mild proteinuria before intoxication. He developed massive proteinuria and acute renal failure after Euphorbia paralias intoxication. We can­not deny the possibility that massive proteinuria occurred coincidentally after Euphorbia paralias intoxication, but the possibility of aggravation of podocyte injury still remains. His acute renal failure was due to a severe tubular necrosis confirmed by kidney biopsy. The exact mechanism of the toxicity is not known. However, Euphorbiaceae plants are well known to contain irritant, cytotoxic and tumor-promoting constituents [1] such as ingenanes [2] found in the latex of Euphorbia para­lias. These compounds inhibit the 3H-thymidine uptake by TLX/5 mouse lymphoma cells and are known to produce a persistent ery­thema of the mouse ear in sub-microgram doses. [2] Therefore, the underlying mechanisms responsible for renal injury by this plant are probably toxic and immunoallergic in nature, which resulted in acute renal failure. Other than kidney impairment, our patient did not have any other organ toxicity.

The therapeutic procedure is mainly based upon the treatment of complications of renal failure, hemodialysis and supportive care. Our patient needed intensive hemodialysis for 48 days. In our case, steroids were used not only as the treatment of nephrotic syndrome but also for the treatment of the interstitial neph­ritis. Our patient is now on conservative med­ical management for his chronic kidney disease because of the incomplete recovery with moderately elevated serum creatinine observed after six months.

In cases of unexplained acute renal failure, a toxic mechanism should always be considered. Diagnosis of renal toxicity of Euphorbia pa­ralias was possible only when the patient was intensively interrogated about ingestion of any nephrotoxic substance. Raising the awareness among medical practitioners about the possi­bility of Euphorbia paralias producing renal toxicity is needed for recognising this condi­tion early and for possible prevention and early medical intervention.

   References Top

1.Hecker E. New toxic, irritant and cocarcinogenic diterpenoids esters from Euphorbiaceae and from Thymelaeaceae. Pure Appl Chem 1977;49:1423-31.  Back to cited text no. 1
2.Sayed MD, Rizk A, Hammouda FM, El-Missiry MM, Williamson EM, Evans FJ. Constituents of Egyptian Euphorbiaceae. IX. Irritant and cytotoxic ingenane esters from Euphorbia paralias L. Experientia 1980;36: 1206-7.  Back to cited text no. 2
3.Pliny the Elder. Naturalis historia, 26:45. published by Harvard University Press, Massachusetts and William Heinemann, London; 1949-54.  Back to cited text no. 3
4.Atta AH, Mouneir SM. Evaluation of some medicinal plant extracts for antidiarrhoeal activity. Phytother Res 2005;19:481-5.  Back to cited text no. 4
5.Guarrera PM. Traditional phytotherapy in Central Italy (Marche, Abruzzo, and Latium). Fitoterapia 2005;76:1-25.  Back to cited text no. 5
6.Corea G, Fattorusso E, Lanzotti V, et al. Jatrophane diterpenes as Pglycoprotein inhi­bitors. First insights of structure-activity rela­tionships and discovery of a new, powerful lead. J Med Chem 2003;46:3395-402.  Back to cited text no. 6
7.Di Giorgio C, Delmas F, Tueni M, Cheble E, Khalil T, Balansard G. Alternative and com­plementary antileishmanial treatments: Assess­ment of the antileishmanial activity of 27 Lebanese plants, including 11 endemic species. J Altern Complement Med 2008;14:157-62.  Back to cited text no. 7
8.Evans FJ, Soper CJ. The tigliane, daphnane and ingenane diterpenes, their chemistry, dis­tribution and biological activities. Lloydia 1978; 41:193-233.  Back to cited text no. 8
9.Tackholm V. Student Flora of Egypt, 2 nd ed. Beirut: Cairo University Press; 1974  Back to cited text no. 9
10.Abdelgaleil SA, el-Aswad AF, Nakatani M. Molluscicidal and antifeedant activities of diterpenes from Euphorbia paralias L. Pest Manag Sci 2002;58:479-82.  Back to cited text no. 10
11.Abdelgaleil SA, Kassem SM, Doe M, Baba M, Nakatani M. Diterpenoids from Euphorbia paralias. Phytochemistry 2001;58:1135-9.  Back to cited text no. 11
12.Barile E, Fattorusso E, Ialenti A, Ianaro A, Lanzotti V. Paraliane and pepluane diterpenes as anti-inflammatory agents: First insights in structure-activity relationships. Bioorg Med Chem Lett 2007;17:4196-200.  Back to cited text no. 12
13.Jakupovic J, Morgenstern T, Marco JA, Berendsohn W. Diterpenes from Euphorbia paralias. Phytochemistry 1977.47;1611-9.  Back to cited text no. 13
14.Corea G, Fattorusso C, Fattorusso E, Lanzotti V.Amygdaloidins A_L twelve new 13alpha-OH jatrophane diterpines from Euphorbia amygdaloidesL. Tetrahedron 2005;61:4485-94.  Back to cited text no. 14
15.Oksüz S, Gürek F, Lin LZ, Gil RR, Pezzuto JM, Cordell GA. Aleppicatines A and B from Euphorbia aleppica. Phytochemistry 1996;42: 473-814.  Back to cited text no. 15

Correspondence Address:
Karima Boubaker
Department of Internal Medicine A, Charles Nicole Hospital, Tunis
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DOI: 10.4103/1319-2442.111069

PMID: 23640634

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