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Star fruit intoxications have been reported mainly in uremic patients, leading to various
degrees of neurological symptoms and potentially fatal outcomes. Nephrotoxicity has been
reported in few patients with normal renal function or moderate chronic renal impairment
(CRI). The present report describes clinical course, management, and outcome of six patients
with moderate CRI admitted to ICU for severe star fruit intoxication.

Over a 1-year period we observed six cases of star fruit intoxication. All but two patients
were prospectively monitored. For each case we collected clinical characteristics,
management, and outcome.

On admission, all patients presented acute renal failure with underlying moderate CRI and
required intubation for coma. The most common symptoms were hiccups, mental confusion,
seizures, and coma. Status epilepticus was authenticated in three patients. Management
consisted of several methods of renal replacement therapy (RRT) and supportive measures.
Four patients survived without sequelae and two patients died.

Severe star fruit intoxication can occur in patients with moderate CRI with a potentially fatal
outcome. Prompt continuous RRT should be instituted
We have previously discovered that star fruit can induce oliguric acute renal failure. To
investigate the mechanisms of star fruit-associated acute oxalate nephropathy, the
nephrotoxic effect of star fruit was examined in both cellular experiments and animal models.
We evaluated renal function, pathological changes in kidney tissues and apoptotic effects
using terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay in four groups
of rats a control group (CG), fed with tap water (1); a star fruit group (SG), fed with star
fruit juice naturally containing 0.2 M oxalate (2); and oxalate groups (OxG), fed with 0.2 M
(3) or 0.4 M (4) oxalate solution. The effects of both star fruit juice and oxalate on MDCK
cells were also analyzed by flow cytometry. We found that the mean creatinine clearance was
significantly lower in the SG, 0.2 M OxG and 0.4 M OxG. Dose-dependent apoptotic effects
were evident from the TUNEL assay, and flow cytometry analysis of treated MDCK cells
showed dose- and time-dependent effects. Our findings suggest that star fruit juice produces
acute renal injury, not only through the obstructive effect of calcium oxalate crystals, but also
by inducing apoptosis of renal epithelial cells, which may be caused by the levels of oxalate
in the fruit.


CG, control group;

-MEM, essential medium alpha medium;

FBS, fetal calf serum;

MDCK cells, MadinDarby Canine kidney cells;

OxG, oxalate groups;

PBS, phosphate-buffered saline;

SG, star fruit group;

LDH, lactate dehydrogenase;

GGT, glutamyl transpeptidase;

ALP, alkaline phosphatase;

TUNEL, terminal deoxynucleotidyl transferase nick-end labeling


The present study was designed to evaluate the effect of Diyarbakr watermelon (Citrullus
lanatus cv. Srme) juice on lipid peroxidation states in rat liver, kidney and brain. In vivo
administration of carbon tetrachloride (CCl4) once a week for 28 days caused a significant
elevation of serum markers of liver damage, aspartate aminotransferase (AST), alanine
aminotransferase (ALT), total bilirubin (TB) and decrease in albumin when compared to the
control group. However, administration of carbon tetrachloride along with watermelon juice
or ursodeoxycolic acid (UDCA) significantly reduces these changes. Increased lipid peroxide
(LPO) level was observed in the liver, kidney and brain tissues after CCl4 administration.
However, watermelon juice and UDCA treatment prevented the increase in LPO. The results
indicated that watermelon juice protects the liver, kidney and brain tissues from experimental
CCl4 toxicity in rats and that the protective effect of watermelon juice may be due to its
antioxidant activity and inhibition of lipid peroxide formation. In conclusion, present study
reveals biological evidence that supports the use of watermelon juice in the treatment of
chemical-induced hepatotoxicity.


Juice, extracted from Diyarbakr watermelon, displays antioxidant activity. Watermelon

juice used daily protected an animal model from CCl4 toxicity. Watermelon juice alleviates
pathological changes caused by CCl4.


Watermelon juice;


Ursodeoxycolic acid;

Carbon tetrachloride;

Lipid peroxidation;


Background. Nonimmune renal injury plays an important role in acute and chronic rejection
by triggering an injury response through cytokine and chemokine release. Bioflavonoids are

agents with potential immunosuppressive and renoprotective properties. We studied the

effects of quercetin and curcumin, two bioflavonoids, on ischemia-reperfusion in the rat.
Methods. Rats underwent 30 min of left renal pedicle occlusion with simultaneous right
nephrectomy and were pretreated with quercetin or curcumin. Serial serum creatinine was
measured, and renal expression of the chemokines regulated upon activation, normal T-cell
expressed and secreted (RANTES), monocyte chemoattractant protein-1 (MCP-1), and
allograft inflammatory factor(AIF) was quantified by polymerase chain reaction.
Results. Pretreatment with quercetin or curcumin resulted in preservation of histological
integrity, with a decrease in tubular damage and interstitial inflammation. On day 2 after
ischemia-reperfusion, quercetin pretreatment decreased the mean serum creatinine level from
6.51.4 to 3.30.5 mg/dl (P=0.06). On day 7, the creatinine level for control animals was
7.51.5 mg/dl, which was significantly decreased by pretreatment with quercetin, curcumin,
or both together (creatinine levels: 1.61.3, 1.80.2, and 2.00.4 mg/dl, respectively; all
P<0.05 vs. untreated). By semiquantitative polymerase chain reaction, RANTES, MCP-1,
and AIF were detected at high levels in kidneys on day 2 but not in normal kidneys.
Pretreatment with quercetin or curcumin strongly attenuated this expression.
Conclusion. Quercetin and curcumin reduce ischemia-reperfusion injury and its inflammatory
sequelae. The bioflavonoids hold promise as agents that can reduce immune and nonimmune
renal injury, the key risk factors in chronic graft loss.