Nephrology 1998; 4, 313-319

Review Article

Tropical plantcassociated nephropathy

SOMCHAI
EIAM-ONG AND VISITHSITPRIJA

Nephrobgy Unit, Department of Medicine, Faculty of Medicine, Chulalongkorn University Hospital, Bangkok,
Thailand

Summary: In the tropical area, nephrotoxicity can be caused by certain plants or plant materials. These
include djenkol bean, mushroom, Cullikpis laureola, Semicurpus unucurdium, Securidaca longipe dunculata and
Vicis fuvus. Djenkol beans consumed by people in South-east Asia can cause toxicity or djenkolism. Renal
manifestrations of djenkolism include dysuria, hematuria, proteinuria, urolithiasis, and acute renal failure.
Djenkolic acid in the bean can cause renal dysfunction by mechanical irritation of djenkolic acid crystals
and by direct toxicity. Renal involvement in mushroom poisoning is generally caused by certain species of
Amanita and Galerina. Amanita toxins produced by such mushrooms could exhibit their toxic effects on
several metabolic pathways of all eukaryotic cells including hepatocytes and renal cells. Renal failure is
severe with a high mortality rate. Phenolic compounds in the sap of Semecurpus unacurdium, the marking-
nut tree of India, can cause renal failure following prolonged exposure to the sap. Atractyloside, an alkaloid
found in the tuber of Cullikpis laureola, can cause hypoglycemia and nephrotoxicity. Gaultherin, an amorphous
steroid glucoside found in Securidaca longipe dunculatu, can cause extensive damage to the kidney. Divicine
and isouramil found in Vicis fuvus, broad bean, can trigger hemolysis in certain subjects with G-6PD
deficiency, resulting in reversible acute renal failure. Gossypol, the principal ingredient of cotton seed oil,
could cause distal renal tubular acidosis.

Keywords: Amanita toxins, Atractyloside, Divicine, Djenkolic acid, Gaultherin, Gossypol, Isouramil,
Phenolic compound.

INTRODUCTION
The tropical zone is defined as the region on earth
adjacent to the equator between the Tropics of Cancer,
23.5 degree North and Capricorn, 23.5 degree South. A
variety of plants or plant materials in the tropics could
cause various deleterious effects on the kidney.'" The
kidney, as major excretory organ of the body, is
particularly vulnerable to various toxins because of its
high perfusion rate per gram of This could result
in delivery of large amounts of the toxic substances per
unit of time. Renal tubular cells could enhance toxin
entry with generation of intracellular metabolites that
may induce cell injury. Furthermore, the capacity of the
kidneys to concentrate urine could result in higher
concentrations of the toxin in the lumen of individual
nephrons than those attainable in blood. In this review,
nephrotoxicity from djenkol bean, mushroom,
Semecurpus unucurdium, Cullikpis laureola, Securidacu
Correspondence: Professor Somchai Eiam-Ong, MD, Nephrology
Unit, Department of Medicine, Faculty of Medicine, Chulalongkom
University Hospital, Bangkok, Thailand 10330.
Accepted for publication 2 September 1998.
longipe dunculata, Vicis favus, and cotton seed oil will be
described and emphasis will be placed on the first two,
DJENKOL BEAN NEPHROTOXICITY2'3*7-9
The djenkol bean is derived from the djenkol tree,
the scientific name of which is Pithecellobium jiringu or
Pithocolobium lobutum. The tree belongs to the family
Leguminosue. The djenkol tree is grown in many South-
east Asia countries and thus many local names of the
tree are designated (Table 1). It is a tree of fair size
growing up to 80 feet in height. The djenkol bean is
broad and round with 3-3.5 cm in diameter and 1.5-2 cm
Table 1 Local names of djenkol tree in different countries
Country Djenkol tree (local name)
Indonesia jiring, jenkol, genkol, djenkol
Malaysia yiniking, yi-ring
Thailand ma-niang, cha-niang, niang kraniang, niang-yai
Cambodia krakos
Burma danyin-thee
314
Fig 1 Djenkol bean.
in thickness (Fig. 1).The bean, resembling the chestnut
in appearance, is reddish-brown in color and emits a
strong sulfurous odor, which can be detected on the
breath when the bean is eaten.2,"
Djenkol beans are widely consumed as food by local
inhibitants and are eaten in different ways including
raw, fried, boiled or roasted methods, and sometimes
served as a dessert in the form of boiled sliced bean with
coconut and sugar. Immature beans are eaten as well as
the ripe ones, Occasionally, they are burrowed and
allowed to germinate or after pounding the bean are
made into sun-dried cake.
The djenkol bean has been shown to have a very
high nutritive food value." T h e bean contains high
protein and carbohydrate with low fat content, a certain
amount of vitamin B1, B, and C, folic acid, and various
minerals including calcium, phosphorus and iron.
Eighteen amino acids including all eight essential amino
acids also have been detected in djenkol bean. Djenkol
bean has also been used to treat diabetes mellitus by
traditional medical practitioners. However, a recent
study has shown that 70% alcoholic extract of the
djenkol bean has no hypoglycemic effect on normal
healthy rabbits."
It has been known among natives that the djenkol
bean, sometimes, causes toxicity or djenkolism in some
persons who are susceptible to the bean. Djenkolism has
been reported sporadically in the literat~re."-'~
Djenkolism may occur after the very first meal and then
subsequent ingestions may not produce any symptoms.
On the other hand, the toxicity may occur after many
symptom-free meals.' Sometimes, when several persons
share the same meal, only one of them develops the
symptoms. Djenkolism is alarming within 2-12 h after
eating the beam8 Two forms of djenkolism are
recognized: (1) mild djenkolism; the patients present
with spasmodic pain in loin and suprapubic area.
Laboratory findings include proteinuria, hematuria,
pyuria, and crystalluria with characteristic needle-shaped
crystals (Fig. 2). All these features resolve in a day or
two. As such, most patients do not seek medical help.
(2) Severe djenkolism; the victims present with severe
colicky abdominal pain, hypertension, vomiting,
S Eiam-Ong and V Sitprija
-- ----- ll__l - ~am---
Fig 2 Characteristic needle-shaped crystals of djenkolic acid.
Table 2 Common clinical and laboratory features of patients
with dienkolism in Southern urovinces of Thailand
Number of cases (%)
Clinical features
Abdominal pain
Dysuria
Anuria
Hypertension
Laboratory features
Renal failure 12 (55)
Hematuria 15 (68)
Proteinuria 10 (45)
Total number of patients = 22. Modified from ref 9
diarrhea, dysuria, and oliguria which could progress to
anuria. Diagnosis can be confirmed by demonstration of
crystals of djenkolic acid. Recovery is the rule, although
death has occurred in some cases. Urolithiasis has been
reported with djenkolic acid as the n~c1eus.l~"'
Recently, the largest series of patients with djenkolism
have been reported? In a retrospective study of six
southern provinces of Thailand during a period of 2 years,
there were 22 patients with djenkolism. Fifteen were
male and seven were female. Their age ranged from 15
to 57years. By history, the amount of djenkol beans
consumed varied from 3 to 20 and were eaten either
raw, fried or roasted. T h e raw beans tended to cause
more symptoms than the others, and the mature beans
were apparently more toxic than the younger ones.
T h e common clinical manifestations included abdominal
pain, dysuria, anuria, and hypertension. Laboratory
findings revealed renal failure, hematuria, proteinuria,
leukocyturia (Table 2). The needle-shaped crystalluria
was found in only one patient. In concurrence with
this finding, only few previously reported patients with
djenkolism show djenkolic acid crystals in their urine."-I4
Treatment was supportive and consisted of forced fluid
intake, administration of sodium bicarbonate, and
diuretics. Dialysis was performed in only one patient.
All patients recovered.
It is believed that djenkolism is caused by djenkolic
acid in the bean. In 1933, Van Veen and Hyman isolated
Tropical Plant Toxins and The Kidney 315

Djenkolic acid would cause renal dysfunction by

mechanical irritation of djenkolic acid crystals to the
renal tubules and/or to the urinary tract, and by direct
nephroto~icity.~'~ The solubility of djenkolic acid is
increased when pH becomes more alkaline. For example,
when pH of urine is elevated from 5 to 7.4, the solubility

"i' T'
of djenkolic acid increases 43% and at pH 8.1, the
solubility elevates to 92%.17In vitro study has shown
that after leaving the saturated solution of synthetic L-
djenkolic acid for overnight at room temperature, the
djenkolic acid will be easily ~ r y s t a l l i z e d .It
' ~is~ ~
proposed
~

I
I
COOH COOH
that djenkolic acid which is present in a soluble state
in the blood at pH 7.4 may crystallize in the urine due
to its acid reaction."
Isolated perfusion kidney method has been used to
Fig 3 Chemical formula of djenkolic acid (C7H1404NZS2).
examine the direct effect of djenkolic acid on the renal
tubule.23Rat kidneys perfused with djenkolic acid have
significantly lower inulin clearance than that of the
control group (240 & 80 vs 570 f80 pL/min, P< 0.05,
the needle-shaped crystals from the urine of a patient
n=5). In the same study, the addition of djenkolic acid,
who suffered from djenkolism and also succeeded in
at the concentration of 1 pg/mL, to the perfusion medium
isolating the same crystals from djenkol beans."
after a control period could cause a significant reduction
Djenkolic acid is an amino acid which is rich in sulfur
in inulin clearance (319 f70 vs 490 & 9 pL/min, P< 0.01,
(Fig. 3). Three years later, Vigneaud and Patterson
synthesized djenkolic acid from the cysteine thioacetal
n=5). This occurs without any significant changes in
renal plasma flow (RPF), urine flow or fractional
of formadehyde."
excretion of Na or K.
Studies have shown that the djenkol bean contains
djenkolic acid 1.6 g/lOO g or 1 2 % by ~ e i g h t . l ' , l This
~,~~
A recent study in male Wistar rats has shown that
djenkolic acid nephrotoxicity is dependent on duration
value is relatively high when compared with the other
of exposure to djenkolic acid as well as its dose (Eiam-
contents of 18 amino acids in djenkol beans. About
Ong et al. unpublished data). Djenkolic acid administered
93% of djenkolic acid is in the free form, and only 7%
as a single bolus dose at the concentrations varying from
is bound to pr~tein.''"~Since most of the djenkolic acid
is in the free form, elimination of this acid from djenkol
10, 20, 30, and 40pg has no effects on urinary and
renal hemodynamic parameters. However, intravenous
beans could be performed by boiling the bean in distilled
infusion of djenkolic acid, only at the dose of 40pg,
water, 5% HC1 or 5% NaHC0310*14. Either one of these
could cause significant decreases in urine volume and
methods, could reduce djenkolic acid to 30-32%.
impaired renal hemodynamic parameters.
Interestingly, if the beans is further boiled in 5%
From available data, djenkol bean nephrotoxicity
NaHC03 for another lOmin, only 14% of djenkolic
appears to be attributed to both djenkol bean and host
acid is left." Perhaps, this might be the easiest way to
factor. The events occurring in the urine phase are
remove djenkolic acid from djenkol bean.
more important in the pathogenesis of djenkol bean
Many studies on djenkolism in experimental animals
nephrotoxicity than those in the blood phase (Fig. 4).
including monkeys, rabbits, guinea-pigs, dogs, rats and
The crystals and direct nephrotoxicity from djenkolic
mice have been described with different
acid could occur in certain species of animals, at a
Crystalluria have been reported to be found only in
certain urine pH, under the control of some enzymes or
monkey and rat^.'^^'^^^'^'^ One study, however, have shown
there may be other unknown factors. Although the acute
only a decreased urinary output, increased red blood
nephrotoxicity from djenkolic acid is well characterized,
cells, white blood cells, epithelial cells and casts in the
the contributory role of djenkolic acid as the proximate
urine.7 Histological examination of experimental rats
cause of chronic renal failure in the tropical area would
and mice fed with extract of djenkol bean have revealed
require a long-term study.
acute tubular necrosis in the kidney.20'21Interestingly,
the pathological findings in the kidneys of mice fed with
the commercial L-djenkolic acid are identical to those
of mice fed with djenkol bean." There is only one report MUSHROOM POISONINGZ~3~'4
(Fig. 5 and 6)
on histological studies of renal tissues in humans. These
include edematous kidneys with cortical necrosis, Mushroom poisoning or mycetismus has been reported
swelling of the tubular epithelium, leukocytes in the world wide including the tropics, but may be more
glomeruli, and acute haemorrhagic inflammation in the prevalent in Europe.'" Renal involvement occurs most
perirenal tissue.l2 often from amanita p o i s ~ n i n g . ~Amanita
* ~ ? ~ ~ toxins are
 16 S Eiam-Ong and V Sitprija

Djenkol Bean Factor : Host Factor : at least five related toxins: two phallotoxins, phalloidin
- Number - Individual and phalloin and three amatoxins, a-, p-, and g-
- Maturity .Hydration amanitin,25’26 In 100 g of fresh A. phalloides, there may
- Season be 10 mg phalloidin, 8 mg a-amanitin, 5 mg fi-amanitin,
- Method of Intake
0.5 mg g-amanitin, and traces of phall~in.’~These
Blwd Phase :
compounds have an LD50 for the white mouse after
.Concentration intraperitoneal injection, of 1.9 mg/kg of phalloidin,
Acute Toxicity
.Hemodynamic Changes 8 1.4 mg/kg of phalloin, and 0.1, 0.4, and 0.8 mg/kg,
(Djenkolisrn) respectively, of the three amanitins.14 The LDS0for the
Urine Phase : dog and the guinea pig is about 0.1 mg amatoxins/kg. It
.Concentraliou is apparent that a-amanitin is the most important toxin
~ Local Environment
Chronic Toxicity in A. phalloides. It is 20 times more toxic than phalloidin,
* PH and its lethal activity extends over an interval 20 times
enzymes ?
L -Stone
- CRF ? that of phalloidin. Phalloidin and phalloin are
unknuwn factors ?
completely hydrolyzed in the stomach. Amanitin is an
indole, resistant to hydrolysis by gastric juice.
Fig 4 Proposed mechanism of djenkolic acid nephrotoxicity.
Pharmacologically, the initial effect of amanitin
poisoning is hepatic glycogen mobilization. Enzymes of
lipid, carbohydrate, and protein metabolism are
inhibited. One target effect known is the rupture of the
SS bridge within cyclopeptide-containing enzymes. In
w i ~ ostudies have shown that amanita toxins could
exhibit their toxic effects on eukaryotic cells of all
type^.'^,^' The toxin could be detected in minute
quantities using various methods including paper
chromatographic techniques, thin layer chromatography,
and radioimmun~assays.~~-~’
In man, the generally accepted lethal dose of the
mushroom is more than 50 g of fresh t i s s ~ e .Indeed,
~~,~~
such dose of the mushroom could kill not just one but
Fig 5 Amanita phalloides two or three victims. In one study, 5-8 mg of amatoxins,
determined by chromatographic and immunological
method, has been extracted from a single mushroom,
20-25 g in weight, and might represent the lethal
quantity for a man.30 After ingestion of mushroom
containing amanita toxins, delayed appearance of gastro-
intestinal distress and the severity of subsequent illness
presumably depend upon the a-amanitin content of the
fungus meal. Appearance of symptoms is
characteristically delayed for 6-12 or up to 24 h.24*35736
In
the primary acute phase, severe vomiting and continuous
diarrhea produce weakness, dehydration, hypotension,
and muscle cramps. Other important features include
increased blood urea nitrogen, potassium deficiency, and
leukocytosis. Children and adolescents may succumb
during this primary acute phase of poisoning. If the
patient survives the first phase, there is an apparent
improvement and this could be followed by relapse phase.
Fig 6 Amanita Prirosa This phase is caused by enterohepatic circulation of
amatoxins and is one of the most crucial mechanisms
leading to the fatal out~ome.””~ Clinical features in the
relapse phase are characterized by hepatomegaly, cramps,
found in Amnita phalloides (Death Cap), Amanita wirosa drowsiness, dilatation of the pupils, albuminuria,
(Destroying Angle), Amanita w e m (Spring Amanita), hemoglobinuria, oliguria or anuria. Coma and death may
other related snecies of Amnita, and Dossiblv in Galerim occur, usually within 3-5 days, The usual cause of death
Prenemtu and Lepiota c r e t a ~ e u . ~Chemically,
~-~~ there are is acute hepatic necrosis. Nearly one-third of patients
Tropical Plant Toxins and The Kidney
who die are jaundice, with deposition of fat in liver,
kidneys, and heart.
Pathologic lesions include serous membrane and
visceral hemorrhages and damage to the liver, kidneys,
heart, and central nervous Severe oliguria can
progress to total anuria with azotemia. Concomitant
jaundice from liver damage aggravates the renal injury.
Treatment of severe amanita poisoning should be
directed toward removal of the fungus meal from the
gastrointestinal tract by emetics, cathartics, and gastric
and colonic lavage. To reduce the effect of enterohepatic
circulation, elimination of biliary fluid via a duodenal
tube has been reported to be benefit in severe poisoning.29
Forced diuresis and early charcoal hemoperfusion have
been reported to be effective in removing toxin from the
Treatment subsequent to gastric lavage includes
replacement of body fluids and correction of salts
imbalance as indicated by clinical course and laboratory
estimation of sugar, potassium, sodium, chloride, alkali
reserve, and urea content of the blood. Intravenous
administration of fluid up to 3Lfday may be required.
While collapse should be treated by stimulants, the
severe decrease in blood pressure could be managed
by administration of whole blood, plasma or plasma
expander. No proven specific antidote for the Amanita
toxins is available, although an ‘antiphalloid serum’
prepared in Europe is reported to be useful.40From animal
studies, there are many effective agents for the treatment
of amatoxin poisoning. Silybin, a mixture of flavones
of Silybium marianium, could suppress the uptake of
amatoxin into hepatocytes.4l Similar activities but with
doses 10 times higher, have been reported for penicillin
and prednisolone. The therapeutic regimen consisting
of penicillin in combination with chloramphenicol and
sulphamethoxazole is suggested to enhance excretion of
u-amanitin by displacing it from its plasma albumin
binding Some authors recommend insufion of
thioctic (lipoic) acid in adequate amounts of 300mgl
day (500mg/day for comatose patient).4345Thioctic acid
does not decrease the uptake of amatoxin by liver cells.
Administration of vitamin K may be helpful if the
prothrombin time is prolonged. Oral administration of
neomycin appears to help the victims by suppressing
intestinal bacterial growth and ammonia production.
SEMECARPUS ANACARDIUM POISONING‘~2
The sap of the marking-nut tree of India is used in
dyeing and printing cloth. Occasionally, it is also used
in the preparation of indigenous medicine in India.
Besides India, it is used elsewhere in the tropics and
subtropics. The bark and husk contain an extremely
irritating, black, caustic juice that causes severe
dermatitis. Prolong exposure to the sap can cause
abdominal pain, vomiting, fever, and renal If
the juice is taken internally, it also can cause renal
317
damage with dysuria, hematuria, proteinuria, and acute
renal failure. Nephrotoxicity is possibly due to the
phenolic constituents of this sap.
Renal biopsy shows cytoplasmic necrosis of glomerular
cells, extensive damage to the tubules and interstitium,
and necrolysis of intertubular arterioles. The basement
membrane usually escapes damage.
CALLILEPIS LAUREOLA POISONING’.2
Callikpis laureola (Impila), a member of the family
Compositae, is a perennial herb widespread in the
grasslands of southern Africa. The plant has a tuberous
rootstock that emits a characteristic odor similar to that
of peaches. Callikpis laureola has been used as infusions
for a wide variety of illness including coughs difficult
breathing, constipation, intestinal worms, impotence,
sterility, other gynecological complaints. Local people
also use the plant for disinfectant purpose. Chewing and
ingesting parts of the plant result in impila poisoning,
which is caused by atracty-loside, a microcrystalline
compound with hypoglycemic and nephrotoxic
effe~ts.4~”’Hypoglycemia is believed to occur by
inhibition of oxidative pho~phorylation.~~ Patients who
survive the hypoglycemic renal failure invariably develop
centrilobular hepatocellular necrosis. Hepatotoxicity is
not caused by atractyloside but by another unidentified
compound. Jaundice occurs, especially in children, and
may aggravate renal dysfunction. Hypoglycemia,
metabolic acidosis, hyperkalemia, and azotemia are very
common. Renal damage occurs in the majority of severe
cases.
The kidneys are enlarged and heavy, with a pale,
swollen cortex. Tubular necrosis affects both the
convoluted tubules and the loops of Henle. Tubules
contain casts and may rupture, with extravasation into
the interstitium. Edema and intense cellular reaction
follow. Tubular cell regeneration may be seen in those
who survive the first few days.
SECURIDACA LONGIPE DUNCULATA
POISONING’*2
A wild bush in the grasslands of eastern and southern
Africa is extensively used in traditional infusions and
medications for a wide variety of complaints. Its toxin, an
amorphous steroid glucoside, gaultherin, causes extensive
local tissue d e ~ t r u c t i o n . ~A
” ~cupful
~ of the infusion
causes death in 12-24 h, with extensive damage to the
gut, liver, and kidneys. Acute renal failure may be
encountered in severe cases.
318
VICIS FAVUS
The broad bean is a very potent trigger of hemolysis in
people with hereditary deficiency of the red cell enzyme,
glucose-6-phosphate dehydrogenase. The enzyme is
involved in the smaller pathway which handles 10% of
glucose metabolism in the red cell. Divicine and
isouramil in Vicis fuvw cause hemolysis through iron-
catalyzed formation of reactive hydroxyl intermediates.
Reversible acute renal failure occurs occasionally but
does not necessarily correlate with severity of hemolysis.
Histopathologic studies show degeneration and
regeneration of tubular epithelial cells.
COTTON SEED OIL (Bossuprm
ARBOREUM)
Cotton seed oil has been reported to cause distal renal
tubular acidosis in Chinese patients who use it for
cooking.53The mechanism of acidification defect is not
understood. Gossypol, the principle ingredient of cotton
seed oil, has been used by Chinese scientists as a method
of female fertilization regulation.54 The antifertility
efficacy as determined by sperm concentration is close to
100%.Yet, gossypol can cause kaliuresis and hypokalemia
especially with low potassium intake.55 Hypokalemic
paralysis usually occurs in summer when people have
excessive sweating. Na-K ATPase activity is suppressed
and prostaglandin E, is increased. Nephrotoxic effects
of gossypol could be similar to amphotericin by increasing
membrane ~ermeability.~~ Further scientific study is
required.
CONCLUSION
Tropical diseases reflect the interaction of the human
body with various external environmental factors
including the tropical climate, socio-economy, nutrition,
access to medical care, and genetic variations. Available
data to date have suggested that tropical plants could
cause a variety of renal disorders depending on the
substances the plants contain. Prevention of tropical
plant-associated nephropathy is crucial and should be
emphasized. This could be accomplished by avoiding
any exposure to such plants. Appropriate treatment
strategies should be immediately planned when the
specific plant has been identified. ARF, the main
pathology of which is acute tubular necrosis, is one of
the most common and most serious conditions of tropical
plant-induced renal involvement. The treatment of
severe ARF in these patients is basically similar to those
caused other etiologies.
S Eiam-Ong and V Sitprija
ACKNOWLEDGEMENT
A portion of this review article was presented at the
XIVth International Congress of Nephrology, 25-29 May
1997 Sydney Australia. The authors would like to thank
you Miss Tipwan Tongthamrongrat for her excellent
typographical assistance.
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