Acute kidney injury associated with ingestion of star fruit: Acute oxalate nephropathy: a report of two cases

2019 ◽  
Vol 8 (2) ◽  
pp. 47-51
Author(s):  
Mahmud Javed Hasan ◽  
Nitai Chandra Ray ◽  
Shaikh Shariful Islam ◽  
Shakil Azam Nahid ◽  
Tumpa Shom ◽  
...  

There are few case reports regarding star fruit's nephrotoxicity and neurotoxicity in chronic kidney disease patients. Star fruit (Averrhoa carambola) is commonly consumed as a herbal remedy for various ailments in tropical countries. However, the dangers associated with consumption of star fruit are not commonly known. Although star fruit induced oxalate nephrotoxicity in those with existing renal impairment is well documented, reports on its effect on those with normal renal function are infrequent. We report two unique clinical presentation patterns of star fruit nephrotoxicity following consumption of the fruit. The first patient is a 52 year-old male diabetic patient who had normal renal function prior to developing acute kidney injury (AKI) after consuming large amount of star fruit juice at once for remedy of diabetes. The second patient, a 27 years old young male who developed acute kidney injury following star fruit ingestion in empty stomach. One case needed 4 sessions of hemodialysis another case recovered over 2 weeks without the need for haemodialysis. Consumption of star fruit, especially on an empty stomach or in a state of dehydration may precipitate acute kidney injury. A history of star fruit ingestion must be actively looked for in patients presenting with unexplained acute kidney injury. The use of star fruit as a therapy for diabetes should be discouraged. CBMJ 2019 July: Vol. 08 No. 02 P: 47-51

2016 ◽  
Vol 48 (1-2) ◽  
pp. 37-39 ◽  
Author(s):  
Md Arshad Ul Azim ◽  
Abdus Salam

There are few case reports regarding star fruit's nephrotoxicity and neurotoxicity in chronic kidney disease patients. Recently cases are found in people with normal renal function Star fruit nephrotoxicity is believed to be due to its high oxalate content which causes acute obstructive oxalate nephropathy. A neurotoxin (caramboxin) present in the fruit is responsible for neurotoxic features. Here we present a young male who developed acute kidney injury following star fruit ingestion in empty stomach. After admission, patient was treated conservatively and recovered completely.Bang Med J (Khulna) 2015; 48 : 37-39


2017 ◽  
Vol 19 (1) ◽  
pp. 63-65 ◽  
Author(s):  
Abdul Mumith Ruhan ◽  
Parash Ullah ◽  
Md Moyeen Uddin ◽  
MM Jahangir Alam ◽  
Md Shafiqul Bari ◽  
...  

Star fruit (Averrhoa carambola) is a commonly available and popular fruit in many tropical and subtropical countries. Although star fruit induced oxalate nephropathy in patients with pre-existing renal impairment is well documented, reports on its effect on those with normal renal function are infrequent. Hereby we report a case where a young man with previously normal renal function presented with AKI that was attributable to consumption of star fruit. This write up illustrates the importance of obtaining the patient’s history with respect to ingestion of star fruit in case of sudden and unexplained development of renal impairment.J MEDICINE Jan 2018; 19 (1) : 63-65


2019 ◽  
pp. 089719001988288 ◽  
Author(s):  
Cucnhat P. Walker ◽  
Subrata Deb

Valproic acid (VPA) has been widely used more frequently as its approved indications have been expanded. More and more case reports on rare toxicities have been published in the literature (ie, hepatotoxicities, hyperammonemic encephalopathy, coagulation disorders, pancreatitis, thrombocytopenia). In spite of the long history of VPA, there is a lack of awareness of VPA toxicities among clinicians. We present two cases of a 44-year-old African American female and a 60-year-old Hispanic male taking chronic VPA therapy for psychiatric disorders admitted to the hospital with a combination of hepatotoxicities and acute kidney injury–associated rhabdomyolysis. In both cases, home VPA therapy was continued during hospitalization. Consequently, the female patient deceased and the male patient survived and discharged with continuation of his chronic VPA therapy. In cases of surviving patients, resumption of maintenance VPA upon discharge should be held and alternative therapy should be considered.


2013 ◽  
Vol 6 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Amir H. Qureshi ◽  
Daniel J. Soberon ◽  
Arif Asif ◽  
Tushar Vachharajani ◽  
Ali Nayer

IntroductionMethemoglobinemia refers to the presence of increased levels of methemoglobin (Fe3+) in the blood. Methemoglobinemia can cause cyanosis, dyspnea, fatigue, seizure, arrhythmia, coma, and even death. Although methemoglobinemia is shown to cause acute kidney injury in experimental settings, human case reports are exceedingly rare. In addition, morphological features of methemoglobinemia-induced renal disease in humans remain undefined.Case PresentationA 76-year-old man with a history of chronic obstructive pulmonary disease underwent bronchoscopy following local anesthesia with a benzocaine spray. The patient developed benzocaine-induced methemoglobinemia and acute renal failure. Urinalysis disclosed numerous dysmorphic erythrocytes, erythrocyte casts, and granular casts. Urine protein excretion was approximately 1.1 g/day. Serologic tests were negative. Renal biopsy demonstrated minor glomerular abnormalities, severe acute tubular necrosis, and numerous erythrocyte casts in the tubules. Despite supportive care, renal function deteriorated necessitating hemodialysis. Four months later, the patient remained on hemodialysis. To exclude a superimposed pathology, renal biopsy was repeated and showed numerous erythrocyte casts in the tubules and severe tubular damage.ConclusionMethemoglobinemia can cause acute kidney injury in humans. Morphological features resemble those observed in methemoglobin-induced acute kidney injury in experimental settings. This case calls for a heightened awareness of potential adverse effects of methemoglobinemia on renal function.


2017 ◽  
Vol 6 (2) ◽  
pp. 30-33
Author(s):  
Nazneen Mahmood

Now a day Acute Kidney Injury and Chronic Kidney Disease are the two common problems worldwide with increased mortality and morbidity as well as health care cost. Nephrotoxicity and neurotoxicity by the Star fruit, sometimes fatal, is far more frequent than reported. Star fruit belongs to the Oxalidaceae family, species Averrhoea carambola, is a popular fruit among Orientals. The aim of the study is to create awareness among the population regarding star fruit intoxication, to reduce the development of Acute Kidney Injury in general population, to reduce the mortality and burden of morbidity from chronic renal failure, to reduce the mortality of the patients of End stage renal disease taking regular haemodialysis and to reduce the mortality and burden of morbidity of the people suffering from Diabetes mellitus and Hypertension. Star fruit juice produces acute renal injury not only through the obstructive effect of calcium oxalate crystals, but also inducing apoptosis of renal epithelial cells, which may be caused by the levels of oxalate in the fruit. There have been reports of hiccup, confusion and occasional fatal outcomes in uremic patients after ingestion of star fruit. An excitatory neurotoxin from star fruit has been implicated although the exact nature of this toxic substance has not been identified. High quantities of oxalate in empty stomach and dehydrated state may pose an additional risk for development of renal injury. To avoid acute oxalate nephropathy, pure sour carambola juice or mild diluted post pickled juice should not be consumed in large amounts, especially in an empty stomach and dehydrated state. It is recommended that uremic patients should totally abstain from star fruit due the rare but potentially fatal complications.Anwer Khan Modern Medical College Journal Vol. 6, No. 2: July 2015, P 30-33


2014 ◽  
Vol 63 (12) ◽  
pp. A1853
Author(s):  
Ester Canovas Rodriguez ◽  
Lorenzo Hernando Marrupe ◽  
Alfonso Freites Esteves ◽  
Adriana De La Rosa Riestra ◽  
Javier Alonso Bello ◽  
...  

2015 ◽  
Vol 3 (2) ◽  
pp. 71-73 ◽  
Author(s):  
Md Mostarshid Billah ◽  
Md Anisur Rahman ◽  
Muhammad Abdur Rahim ◽  
Ayesha Tabassum Swarna ◽  
Palash Mitra ◽  
...  

Bilimbi/belembu fruit belongs to the family of Oxalidacae, species Averrhoa bilimbi. Freshly prepared concentrated juice of bilimbi has very high oxalic acid content and consumption carries a high risk of developing acute kidney injury (AKI) by deposition of calcium oxalate crystals in renal tubules. AKI due to Averrhoa bilimbi juice injestion is very rare. We report the case history of a 60-year-old hypertensive, dyslipidemic patient, with normal renal function, who ingested around 600ml of juice in fasting state for treating dyslipidemia. The patient developed AKI and required three sessions of hemodialysis. Her renal function returned to normal after five weeks.Bangladesh Crit Care J September 2015; 3 (2): 71-73


2019 ◽  
Vol 317 (3) ◽  
pp. F695-F704 ◽  
Author(s):  
Karl A. Nath ◽  
Vesna D. Garovic ◽  
Joseph P. Grande ◽  
Anthony J. Croatt ◽  
Allan W. Ackerman ◽  
...  

Heme oxygenase (HO) activity is exhibited by inducible (HO-1) and constitutive (HO-2) proteins. HO-1 protects against ischemic and nephrotoxic acute kidney injury (AKI). We have previously demonstrated that HO-2 protects against heme protein-induced AKI. The present study examined whether HO-2 is protective in ischemic AKI. Renal ischemia was imposed on young and aged HO-2+/+ and HO-2−/− mice. On days 1 and 2 after renal ischemia, there were no significant differences in renal function between young male HO-2+/+ and HO-2−/− mice, between young female HO-2+/+ and HO-2−/− mice, or between aged female HO-2+/+ and HO-2−/− mice. However, in aged male mice, HO-2 deficiency worsened renal function on days 1 and 2 after ischemic AKI, and, on day 2 after ischemia, such deficiency augmented upregulation of injury-related genes and worsened histological injury. Renal HO activity was markedly decreased in unstressed aged male HO-2−/− mice and remained so after ischemia, despite exaggerated HO-1 induction in HO-2−/− mice after ischemia. Such exacerbation of deficiency of HO-2 protein and HO activity may reflect phosphorylated STAT3, as activation of this proinflammatory transcription factor was accentuated early after ischemia in aged male HO-2−/− mice. This exacerbation may not reflect impaired induction of nephroprotectant genes, since the induction of HO-1, sirtuin 1, and β-catenin was accentuated in aged male HO-2−/− mice after ischemia. We conclude that aged male mice are hypersensitive to ischemic AKI and that HO-2 mitigates such sensitivity. We speculate that this protective effect of HO-2 may be mediated, at least in part, by suppression of phosphorylated STAT3-dependent signaling.


2017 ◽  
Vol 32 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Sokratis Stoumpos ◽  
Patrick B. Mark ◽  
Emily P. McQuarrie ◽  
Jamie P. Traynor ◽  
Colin C. Geddes

Background. Severe acute kidney injury (AKI) among hospitalized patients often necessitates initiation of short-term dialysis. Little is known about the long-term outcome of those who recover to normal renal function. The aim of this study was to determine the long-term renal outcome of patients experiencing AKI requiring dialysis secondary to hypoperfusion injury and/or sepsis who recovered to apparently normal renal function. Methods. All adult patients with AKI requiring dialysis in our centre between 1 January 1980 and 31 December 2010 were identified. We included patients who had estimated glomerular filtration rate (eGFR) >60 mL/min/1.73 m2 12 months or later after the episode of AKI. Patients were followed up until 3 March 2015. The primary outcome was time to chronic kidney disease (CKD) (defined as eGFR persistently <60 mL/min/1.73 m2) from first dialysis for AKI. Results. Among 2922 patients with a single episode of dialysis-requiring AKI, 396 patients met the study inclusion criteria. The mean age was 49.8 (standard deviation 16.5) years and median follow-up was 7.9 [interquartile range (IQR) 4.8–12.7] years. Thirty-five (8.8%) of the patients ultimately developed CKD after a median of 5.3 (IQR 2.8–8.0) years from first dialysis for AKI giving an incidence rate of 1 per 100 person-years. Increasing age, diabetes and vascular disease were associated with higher risk of progression to CKD [adjusted hazard ratios (95% confidence interval): 1.06 (1.03, 1.09), 3.05 (1.41, 6.57) and 3.56 (1.80, 7.03), respectively]. Conclusions. Recovery from AKI necessitating in-hospital dialysis was associated with a very low risk of progression to CKD. Most of the patients who progressed to CKD had concurrent medical conditions meriting monitoring of renal function. Therefore, it seems unlikely that regular follow-up of renal function is beneficial in patients who recover to eGFR >60 mL/min/1.73 m2 by 12 months after an episode of AKI.


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