Sage Journals: Discover world-class research

Abstract

Introduction

The outbreak of acute kidney injury (AKI) due to mushroom poisoning is not a frequently encountered medical challenge. Herein, we present 13 mushroom poisoning cases associated with AKI related to Amanita Proxima (A. Proxima) causing poisoning reported in a short time period in Turkey.

Methods

A total of 13 patients with AKI due to mushroom poisoning admitted to Usak Research and Training Hospital between November and December 2020 were included. Under morphological and microscopical investigations of mushroom specimens (from three patients), the species of the mushrooms were identified.

Results

The median age of 13 patients presenting with AKI due to mushroom poisoning was 55 (ranging between 19 and 72 years), and 60.4% were males. Nausea and vomiting were the first symptoms in most patients and appeared at a mean time of 12.8 ± 7.6 h after ingesting mushrooms. Mean serum creatinine on admission was 7.2 ± 3.8 mg/dL. Kidney replacement therapy (KRT) was administered to all patients, and mortality occurred in two due to sepsis and heart failure (HF). Species of the mushroom specimens obtained from three patients were identified as A. Proxima, a rarely encountered type of mushroom. A. Proxima has a considerable similarity to a common and edible species specific to the Mediterranean Basin, known as A. Ovoidea.

Discussion

Based on our findings, we emphasize the consideration of nephrotoxic mushrooms of the genus Amanita in the evaluation of mushroom poisoning cases, as well as the efforts needed to increase public awareness regarding the risk of fatal outcomes of consuming wild mushrooms.

Keywords

acute kidney injury chronic kidney disease hemodialysis mushroom poisoning

Introduction

Overall, at least 100 species, among the 100,000 mushroom species defined in the world, have been reported to be toxic to humans.¹ Cortinarius family (i.e., Cortinarius Orellanes), the Amanita family (i.e. Amanita Proxima [A. Proxima], A. Smithiana, A. Pseudoporphi, A. phalloides and Russula Subnugricans) have been considered responsible for the nephrotoxicity due to mushroom poisoning. For the Amanita family of mushrooms, A. Smithiana in North America, A. Proxima around the Mediterranean Basin, and the species of A. Pseudoporphia and A. Punctata in the Far East have also been reported to cause kidney failure.^2–6 A. phalloides can also produce mild to moderate AKI characterized by tubular necrosis particularly of the proximal renal tubules or because of prerenal factors and renal replacement therapy is occasionally required.¹ The clinical manifestation of A. Smithiana or A. Proxima is characterized by nausea and vomiting, the development of severe acute renal failure, and mild hepatitis 10–12 h after ingestion. However, in the case of Orellanus syndrome, a different clinical picture involving severe and usually irreversible delayed-onset renal failure arises.^1,7,8

The cases related to mushroom poisoning are frequently witnessed in spring and fall in Turkey each year; on the other hand, most cases of mushroom intoxication related to gastrointestinal (GI) toxicity, hepatotoxicity, and neurotoxicity are less frequent, and nephrotoxicity is rarely encountered.⁹ Based on the literature acute kidney injuries (AKI) due to mushroom poisoning have so far been reported as case reports; even so, the present study is the first to include such a large number of mushroom poisoning cases with AKI described in a single month.

Methods

A total of 13 patients with AKI due to mushroom poisoning admitted to Usak Research and Training Hospital between November and December 2020 were included in the study, aiming to present the clinical findings, clinical course, and outcomes of 13 patients admitted to a tertiary care center with AKI due to mushroom poisoning. The data of thirteen patients included in the study were obtained by scanning the hospital automation system and the registered files of the patients. The patients’ complaints on hospital admission, vital signs on admission, and laboratory findings such as biochemistry, blood gas, complete urinalysis, and hemogram were recorded. The patients were evaluated in terms of age, gender, the existence of accompanying comorbid diseases, the type and color of the mushroom consumed, and the time between the ingestion of the mushrooms and the onset of symptoms was also noted. The patients’ follow-up and treatment data were also acquired from the electronic files. According to morphological and microscopical investigations of mushroom specimens (from three patients), the species of the mushrooms were identified. The study was approved by the Ethics Committee of the Faculty of Medicine at Usak University (Date of Approval: 05/01/2023, Protocol No.: 40-40-15).

The Statistical Package for Social Sciences (SPSS) for Windows, version 22.0, software package was used to perform the statistical analyses (SPSS Inc., Chicago, IL, USA). For continuous variables, the distributions within the normal limits were determined through the Kolmogorov-Smirnov and Shapiro-Wilk tests. The findings were expressed as mean ± standard deviation (SD) when normally distributed and median (minimum-maximum) for not normally distributed variables, and the categoric variables were expressed as frequencies and percentages.

Results

A total of 13 patients presented with AKI due to mushroom poisoning were included in the present case-series study conducted at a tertiary care nephrology center between November and December 2020. Of 13 patients, the median age was detected to be 55 years (ranging between 19 and 72 years), and 69% were males.

Comorbid diseases included hypertension (HT) in five cases, diabetes mellitus (DM) in two cases, heart failure (HF) in one case, and chronic kidney disease (CKD) in one case. Overall, two members of the same family, in three different families were poisoned by the same mushroom species. The mushrooms were reported to have been collected by patients themselves in the wild, and consumed in the cooked form. Nausea and vomiting were the first symptoms in most patients and appeared at a mean time interval of 12.8 ± 7.6 h after the ingestion of the mushrooms (>6 h after the ingestion in 10 of 13 patients). The median time from the onset of the symptoms to the hospital admission was 64.9 h (12–144 h). Abdominal pain and decreased urine output were the accompanying symptoms with nausea and vomiting. Mean blood pressure level was 119 ± 17.8/69.5 ± 13.2 mmHg (Table 1). There was no case with evident hypotension, hypovolemia or cardiogenic shock on hospital admission but one case with heath failure developed cardiogenic shock during hospitalization. The mean serum value for creatinine and blood urea nitrogen (BUN) on admission were measured as 7.2 ± 3.8 mg/dL and 54.7 ± 28.3 respectively, while the median value of alanine aminotransferase (ALT) and the median value for aspartate aminotransferase (AST) was found as 145 (51–757) U/L and 62 (23–678) U/L, respectively. The median serum potassium and bicarbonate values were detected as 4.6 (4.0–6.0) mmol/L and 19.7 (13.3–21.9) mEq/L on admission, respectively. While the median creatinine kinase (CK) value was 188.5 (57–1635) U/L on admission, the CK levels were found very high (1635 U/L) in one patient also having concomitant HF and pulmonary infection. The median troponin (Tn) levels on admission were 0.43 (0.09–2.63) ng/mL. One patient with significantly elevated Tn was followed up conservatively since no acute coronary syndrome was considered during the cardiology consultation. The international normalized ratio (INR) value was also found to be high in this patient due to the use of warfarin (Table 1).

Table 1.

Demographic characteristics and laboratory findings of patients.

Cases	Age (yrs)	Gender (M/F)	Comorbid disease	Symptom onset (h)	ALT (U/L) (0-55)	AST (U/L) (5-34)	CK (U/L)	Creatinine (mg/dL) (0.6-1.3)	BUN (mg/dL)	Tn (ng/mL) (0-0.047)	INR	Survival (%)	Recovery time (day)	Hospital admission (h)	Initiation of KRT (h)	Dialysis session (n)	Creatinine at discharge (mg/dL)	Systolic/diastolic BP (mmHg)
Case 1	55	M	No	8	73	42	383	1.5	21		1.0	Yes	25	12	72	2	1.21	110/70
Case 2	64	M	No	24	168	30	250	13.0	72	0.496	1.0	Yes	39	120	24	2	1.62	120/70
Case 3	42	M	No	16	317	62	178	5.6	39	0.096	1.1	Yes	44	48	48	4	1.07	110/64
Case 4	62	F	No	8	249	70	179	3.5	32		0.9	Yes	14	48	120	2	1.09	110/70
Case 5	50	F	HF	6	351	169	1635	5.8	62	0.174	4.7	No		72	24	3		100/60
Case 6	64	F	HT	2	105	23	401	9.5	85	0.381	0.9	Yes	16	96	24	3	0.72	160/100
Case 7	72	M	HT	15	145	27	198	11.4	84	0.817	1.1	No	24	144	48	3		130/70
Case 8	59	M	DM/HT	12	133	67	298	9.7	104	2.639	0.9	Yes	36	48	24	3	1.19	130/90
Case 9	54	M	HT	24	78	23	84	10.8	46		1.0	Yes	45	72	48	2	1.05	120/60
Case 10	19	M	No	16	757	194	57	3.0	26		1.1	Yes	19	48	48	2	1.19	120/70
Case 11	49	F	No	5	252	77	61	3.1	27		0.9	Yes	35	16	72	3	0.62	110/60
Case 12	72	M	DM/HT/CKD	8	51	23		11.2	84	0.673	1.0	Yes	61	48	24	2	1.96	100/60
Case 13	52	M	No	24	655	287	155	6.5	39	0.189	0.9	Yes	61	72	24	2	1.11	130/70
Mean ± SD/Median (min-max)/%	55 (19-72)	69/31%		12.8 ± 7.6	145 (51–757)	62 (23–678)	188.5 (57–1635)	7.2 ± 3.8	54.7 ± 28.3	0.43 (0.09–2.63)	1.0 (0.9–4.7)	84.6/15.4%	34.9 ± 16.2	64.9 (12–144)	48 (12–120)	2.5 ± 0.6	1.16 ± 0.40	119 ± 17.8/69.5 ± 13.2

ALT: Alanine aminotransferase, AST: Aspartate aminotransferase, BP: Blood pressure, BUN: Blood Urea Nitrogen, CK: Creatinine kinase, CKD: Chronic kidney disease, DM: Diabetes mellitus, HF: Heart failure, HT:Hypertension, INR: International normalized ratio, KRT: Kidney replacement therapy, Tn: Troponin.

The applied treatments included activated charcoal (n = 6), N-acetyl cysteine (NAC) (n = 8), penicillin G (n = 5), and silymarin (n = 3). All patients had fluid resuscitation in terms of their urine output, volume status and electrolyte disorders. Additionally, kidney replacement therapy (KRT) was administered to all patients due to AKI. The median time interval between the hospital admission and initiation of KRT was 48 h (12–120 h). The mean peak serum creatinine level was 8.9 ± 2.6 mg/dL. Intermittent hemodialysis was performed in 12 patients, and continuous venous-venous hemodialysis (CVVHD) was performed in one patient, while intermittent hemodialysis and plasma exchange were carried out in two patients with elevated transaminase levels on admission. AKI resolved within a mean time of 34.9 ± 16.2 days in 11 cases. The mean serum creatinine level was 1.16 ± 0.40 mg/dL at discharge (Table 1). Mortality occurred in two patients; due to sepsis and HF in one case, and in the other patient, sepsis was the culprit of mortality during the stay in the intensive care unit after cardiopulmonary arrest despite the recovery of AKI. The two cases with mortality were both delayed to admit to the hospital after mushroom ingestion (72 h and 144 h, respectively). No KRT was required after the discharge in surviving patients; however, two of these cases had persistence of high creatinine levels and development of stage-3 CKD during the follow-up. One of these cases had pre-existing CKD, and both cases had co-morbid DM and HT.

According to morphological and microscopical investigations of mushroom specimens (from three patients), the species of the mushrooms were identified as A. Proxima. While macroscobic descriptions were based on the colored photographs of basidiomata, microscobic data were obtained from dried specimens after sectioning and rehydration in 3% potassium hydroxide (KOH) solution under a light microscope. The details of the mushrooms were as follows: The familial features, Amanitaceae E.-J. Gilbert 1940; species, A. Proxima Dumée (1916); the macroscopic and microscopic features, pileus 70–145 mm across, firstly ovoid then convex then planar, whitish-to-ivory coating, smooth, shiny, viscous and silky also with a smooth margin. The cap’s flesh was stable and always white. The stipe was 125–205 × 30–45 mm, white, full, firm, and clavate. This species has a white, thick, sub membranous ring, and the universal veil is membranous and colorful on the outer surface from orange-tawny to bright reddish (Figure 1(a)). Free lamellae are 8–12 mm wide, spaced, and thick with straight or obtusely truncated, and the spores are printed white. Basidia tetrasporic is with a few rare, bi- and trisporic, and uncurled spores in dimensions of 35–70 × 9–12 µm, with sterigmata, and the spores are smooth, hyaline, amyloid, generally ellipsoidal to oblong, more rarely broadly ellipsoidal or cylindrical, and sometimes slightly narrowed at one end and irregularly shaped in dimensions of 7.8–12.5 (14) × 5.5–7.5 (9) µm (Figures 1(b) and 1(c)).

Figure 1.

Amanita Proxima (a) fruit bodies, (b and c) spores.

Ecology

A. Proxima Dumée (1916) is a rare species seen in fall under broad-leaved and sparse Pinus sp. The specimen with nearly broad-leaved and sparse Pinus sp. was examined in Usak by HB on November 7, 2020 (7501).

Discussion

Our findings detected in 13 patients with AKI due to wild mushroom poisoning demonstrate that for the first time in the literature, our series is the largest number of AKI cases due to mushroom poisoning developing in such a short time. Therefore, we consider that it will be appropriate to define our cases as an outbreak.

AKI due to mushroom poisoning has previously been reported in case reports and case series.^{2–8,10–18} In a previous study performed in 22 cases with acute GI symptoms due to mushroom poisoning in Turkey in 2016, all patients were reported to consume the same mushroom species together,¹⁹ whereas in our study the cases consumed mushroom at different times. Aydın et al. presented a case series of three patients diagnosed with Amanita nephrotoxic syndrome in the same period recently but the identification of the mushroom species was not carried out.²⁰ Retrospective studies on mushroom poisoning in our country revealed a high rate of GI symptoms and hepatotoxicity due to mushroom poisoning and do not provide sufficient information regarding nephrotoxicity.^21,22,23 However, two cases of AKI were previously seen and described due to the poisoning of A. Phalloides in Denizli, Turkey.²⁴ In a study carried out in Sweden, Hedman et al. also presented the findings of 39 nephrotoxicity cases of long-term followed-up due to the Cortinarius species of mushroom poisoning between 1979 and 2012.⁸ Although the study by Hedman et al. has been the largest case series of nephrotoxicity due to mushroom poisoning described in the literature so far, the cases were recruited in the study over approximately 33 years.⁸

In our country, cases of mushroom poisoning have been reported to occur mostly in spring and fall.^21–23 The cases described in our study were admitted to the hospital with AKI due to mushroom poisoning in November and December 2020. Although cases of mushroom poisoning also occurred during spring, none of them presented with AKI, possibly related to the differences in seasonal rainfall. In our study, the symptoms commenced at a later stage (>6 h) in the majority of the cases. In spite of late-onset symptoms have been stated to be more serious in previously published studies, the exact relation of symptom onset to disease severity remains unclear.^24,25 Also, in a study conducted in Turkey by Visneci et al., severe poisoning cases due to the ingestion of cultivated mushrooms were reported to reveal the symptoms at an earlier period.²⁶

Some mushroom species cause kidney injury through different pathophysiological mechanisms. Orellanine found in Cortinarius species (C. orellanus, C. rubellus and C. orellanosus), is concentrated in the kidney and oxidation of orellanine in renal tissue may produce cell damage. Orellanine also inhibits alkaline phosphatase in the proximal tubule cells, leading to disruption of ATP production and deplete glutathione in renal tissue and cause oxygen-free radical formation may contribute to the cytotoxic damage and the tubular epithelium is the toxin’s primary target⁸ (Hedman et al. 2017). Ingestions of T. equestre and R. subnigricans can cause rhabdomyolysis and renal injury¹⁷ (Cho and Han 2016). A. proxima (Mediterranean Amidella) and A. smithiana (North American Lepidella) ingestions cause “Amanita nephrotoxic syndrome”. A. smithiana contains A. smithiana toxin which is found to be responsible for Amanita nephrotoxic syndrome. A. proxima does not have A. smithiana toxin, but the presentation is similar. A. proxima with allenic norleucine (2-amino-4,5-hexadienoic acid) mycotoxin causes Amanita nephrotoxic syndrome defined as tubulointerstitial nephritis and tubular necrosis shown by renal biopsies¹ (Graeme 2014).

The Cortinarius family (i.e., Cortinarius Orellana) and the Amanita family (i.e., A. Proxima, A. Smithiana, A. Echinocephalia, and A. Punctata, etc.) are the two toxic mushroom species identified to be associated with the nephrotoxicity. Even so, these species differ in terms of clinical manifestations. The Cortinarius family is associated with late-onset and mostly irreversible kidney damage.⁸ In Cortinarius intoxication, AKI occurs later after the ingestion of the mushroom and GI symptoms; even so, in Amanita intoxication, AKI develops earlier with GI symptoms, an important feature in the differential diagnosis. A. Proxima is a species of white mushroom leading to a “proximian” syndrome, characterized by early digestive disorders, mild hepatic cytolysis, and end-stage renal failure.¹¹ A. Proxima has allenic-norleucine toxin which is considered to be responsible for the tubulointerstitial nephritis characterized by acute tubular necrosis and reversible kidney damage which differs from Orellanin due to the absence of alkaline phosphatase inhibition. Dehydration due to nausea and vomiting in patients may also contribute to the development of AKI. Creatinine levels of the patients increased despite of intravenous fluid resuscitation.

The first case report of A. Proxima poisoning leading to AKI was released in 1994 by a medical team from Montpellier, France.¹⁰ Based on the findings of the study performed by the Poison Center of Marseille, the time between the ingestion and occurrence of first symptoms was approximately 13 h in 26 out of 31 cases having accidentally consumed the A. Proxima species of mushrooms. All patients displayed GI symptoms, and oliguria or anuria developed in 14 of the cases a few days later. Temporary dialysis was required in 11 cases; of these 11 cases, 10 had moderate hepatic cytolysis. The severity of symptoms was considered to be dose-dependent since some individuals in the same family showed no symptoms despite consuming the same food.¹¹

In another study, the poisoning of an 11-year-old child was reported as the first and only pediatric case requiring dialysis, but achieving a full recovery.¹²

In our case series, although reversible in most of our patients, the kidney damage was clinically severe enough to require KRT in all cases. Our cases with A. Proxima poisoning had high creatinine levels, co-morbid DM and CKD or HT, and temporary mild-to-moderate elevation of liver transaminases (especially ALT), and all these findings were compatible with A. Proxima-induced poisoning. The complaints of nausea and vomiting started an average of 12.9 h (2–24 h) after ingesting mushrooms in our study. Kidney damage was clinically severe enough to require KRT in all cases but reversible in most cases.

Despite being a rarely encountered mushroom species, A. Proxima Dumée (1916) has similar properties to a common and edible species known as A. Ovoidea. Differentiating between those two species is difficult as the only distinguishing macroscopic feature is the volva with an orange-colored and membranous nature in A. Proxima, compared to the white color and friable nature in A. Ovoidea.

No case of poisoning due to A. Proxima has been reported in Turkey to date, whereas several cases have been reported in countries such as France, Spain, and Italy.^{2–6,10–16,18} In our study, the mushroom species obtained from three cases having mushroom poisoning were determined to be A. Proxima, emphasizing the consideration of nephrotoxic mushrooms of the genus Amanita in evaluating the cases of mushroom poisoning.

In a study on A. Proxima poisoning, where CK levels due to the possibility of rhabdomyolysis and related kidney damage were assessed, mild elevation of CK was revealed in some of the patients, while significant CK elevation was detected in only one patient with severe HF dying due to cardiac reasons during the follow-up period; therefore, the researchers stated that A. Proxima leads to serious cardiac toxicity.^11,13 Notably, one of our cases having significantly elevated troponin levels was followed up conservatively since electrocardiographic findings were not suggestive of acute coronary syndrome, and troponin levels were normalized in a short time during the follow-up. Very high levels of creatine kinase (CK) (69,121 U/L), hypocalcemia and cardiogenic shock was detected in patients who developed AKI due to rhabdomyolysis caused by Russula Subnugricans.¹⁷ In our patient group, the average CK level was 188.5 U/L, the highest value was 1635 U/L, the patient had heart failure and pulmonary infection.

Supportive treatment modalities are more commonly used in treating patients with mushroom poisoning. In our study, some patients were treated with activated charcoal, NAC, penicillin G, and silymarin. However, no significant difference was seen in terms of the clinical course and the outcomes between the treated and untreated patients.

There are some limitations of the present study. First, no kidney biopsies were performed due to the rapid recovery of AKI, and therefore we could document no kidney pathology. Second, the specimens of mushrooms were not provided for all patients.

Conclusions

In conclusion, our study performed in a tertiary care nephrology center indicated that it is likely to encounter 13 cases of AKI due to mushroom poisoning in a very short time, which can be defined as an outbreak. The identification of A. Proxima as the culprit in three patients also seems notable, given that A. Proxima is a rarely encountered mushroom specimen and also a considerable similarity to a common and edible species specific to the Mediterranean region known as A. Ovoidea. Accordingly, our findings emphasize that nephrotoxic mushrooms of the genus Amanita should be considered in evaluating the cases of mushroom poisoning, as well as increasing public awareness regarding the risk of fatal outcomes of consuming wild mushrooms and that the collecting and consuming mushrooms require expertise.

Footnotes

Author contributions

Conceptualization: ZA, HBS; Methodology: ZA, HBS; Formal analysis and investigation: ZA, HBS; Writing–original draft preparation: ZA; Writing–review and editing: ZA, HBS. All authors have read and accepted the final version of the manuscript.

Declaration of conflicting interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical statement

ORCID iD

Zelal Adibelli

References

Graeme

. Mycetism: a review of the recent literature. J Med Toxicol 2014; 10: 173–189. DOI: 10.1007/s13181-013-0355-2.

Yang

Lin

Huang

, et al. Acute renal failure caused by mushroom poisoning. Journal of the Formosan Medical Association = Taiwan yi zhi 2006; 105: 263–267. DOI: 10.1016/S0929-6646(09)60317-X.

Courtin

Gallardo

Berrouba

, et al. Renal failure after ingestion of Amanita proxima. Clin Toxicol 2009; 47: 906–908. DOI: 10.3109/15563650903289485.

Lee

Kim

Seok

, et al. Acute kidney injury resulting from amanita neoovoidea intoxication. J Kor Med Sci 2018; 33: e230. DOI: 10.3346/jkms.2018.33.e230.

Barman

Warjri

Lynrah

, et al. Amanita nephrotoxic syndrome: presumptive first case report on the Indian subcontinent. Indian J Nephrol 2018; 28: 170–172. DOI: 10.4103/ijn.IJN_353_16.

Beaumier

Rioult

Georges

, et al. Mushroom poisoning presenting with acute kidney injury and elevated transaminases. Kidney Int Rep 2019; 4: 877–881. DOI: 10.1016/j.ekir.2019.02.016.

Kirchmair

Carrilho

Pfab

, et al. Amanita poisonings resulting in acute, reversible renal failure: new cases, new toxic Amanita mushrooms. Nephrol Dial Transplant 2012; 27: 1380–1386. DOI: 10.1093/ndt/gfr511.

Hedman

Holmdahl

Molne

, et al. Long-term clinical outcome for patients poisoned by the fungal nephrotoxin orellanine. BMC Nephrol 2017; 18: 121. DOI: 10.1186/s12882-017-0533-6.

Anon. Ministry of Health General Directorate of Public Health (2021) National poison consulting center (UZEM) reports 2014-2020., https://hsgm.saglik.gov.tr/depo/kurumsal/yayinlarimiz/Raporlar/Uzem/uzem_raporlari_2014-2020.pdf (2022, accessed 26 July 2022).

10.

Leray

Canaud

Andary

, et al. Amanita proxima poisoning: a new cause of acute renal insufficiency. Nephrologie 1994; 15: 197–199.

11.

de Haro

Jouglard

Arditti

, et al. Acute renal insufficiency caused by Amanita proxima poisoning: experience of the Poison Center of Marseille. Nephrologie 1998; 19: 21–24.

12.

Marquant

Rousset-Rouviere

Bosdure

, et al. Amanita proxima poisoning in a child. Arch Pediatr 2011; 18: 1290–1293. DOI: 10.1016/j.arcped.2011.08.029.

13.

Besancon

Schmitt

Glaizal

, et al. Occurrence of severe cardiac alterations in Amanita proxima poisoning: two original observations. Ann Fr Anesth Reanim 2012; 31: 466–468. DOI: 10.1016/j.annfar.2012.01.021.

14.

Chávez

EBS

Arrobas

Bayo

, et al. Fracaso renal agudo secundario a intoxicación por setas en la provincia de Badajoz en el ano 2013. Diálisis Traspl 2015; 36: 62. DOI: 10.1016/j.dialis.2015.04.034.

15.

Kang

Cheong

Lee

, et al. Severe but reversible acute kidney injury resulting from Amanita punctata poisoning. Kidney Res Clin Pract 2015; 34: 233–236. DOI: 10.1016/j.krcp.2015.05.007.

16.

Mancini

Assisi

Balestreri

, et al. A rare case of acute renal failure related to amanita proxima ingestion. G Ital Nefrol: organo ufficiale della Societa italiana di nefrologia 2015; 32.

17.

Cho

Han

. A case of mushroom poisoning with Russula subnigricans: development of rhabdomyolysis, acute kidney injury, cardiogenic shock, and death. J Kor Med Sci 2016; 31: 1164–1167. DOI: 10.3346/jkms.2016.31.7.1164.

18.

Gioacchino

Luisa

Onofrio

, et al. Acute renal failure after amanita ovoidea eating. Indian J Nephrol 2019; 29: 73–74. DOI: 10.4103/ijn.IJN_33_18.

19.

Bal

AAM

Anil

Yilmaz

, et al. An outbreak of non-fatal mushroom poisoning with Omphalotus olearius among Syrian refugees in Izmir, Turkey. Toxin Rev 2016; 35: 1–3. DOI: 10.3109/15569543.2016.1169548.

20.

Mehmet Fethullah Aydın

Oruç

Yıldız

, et al. Alparslan Ersoy Three cases of mushroom poisoning with an unexpected initial presentation: acute kidney injury with Amanita proxima poisoning. Ren Replace Ther 2023; 9. DOI: 10.1186/s41100-023-00515-x.

21.

Eren

Demirel

Ugurlu

, et al. Mushroom poisoning: retrospective analysis of 294 cases. Clinics 2010; 65: 491–496. DOI: 10.1590/S1807-59322010000500006.

22.

Cevik

Unluoglu

. Factors affecting mortality and complications in mushroom poisonings over a 20 year period: a report from central anatolia. Turk J Emerg Med 2014; 14: 104–110. DOI: 10.5505/1304.7361.2014.36024.

23.

Acar

NCM

Canakci

. Evaluation of mushroom poisoning cases in emergency department in the early and late period, 10-year observational study. Ankara Med J 2020; 20: 531–540. DOI: 10.5505/amj.2020.48091.

24.

Yardan

Baydin

Eden

, et al. Wild mushroom poisonings in the Middle Black Sea region in Turkey: analyses of 6 years. Hum Exp Toxicol 2010; 29: 767–771. DOI: 10.1177/0960327110361758.

25.

Kaygusuz

OGK

Celik

Dursun

. Denizli’den Türkiye köygöçüren mantarı Amanita phalloides zehirlenmesi. Biyolojik Çeşitlilik ve Koruma 2013; 6: 22–25. Available at: https://dergipark.org.tr/tr/pub/biodicon/issue/55883/765692

26.

Visneci

EFAD

Acar

Özdamar

, et al. Mushroom poisoning cases from an emergency department in central anatolia: comparison and evaluation of wild and cultivated mushroom poisoning. Eur J Emerg Med 2019; 18: 28–33. DOI: 10.4274/eajem.35220.

Outbreaks of mushroom poisoning associated with acute kidney injury

Abstract

Introduction

Methods

Results

Discussion

Keywords

Introduction

Methods

Results

Ecology

Discussion

Conclusions

Footnotes

Author contributions

Declaration of conflicting interest

Funding

Ethical statement

ORCID iD

References