This study aims to highlight the potential serious complications of acute kidney injury (AKI) resulting from the consumption of excessive amounts of starfruit, a common traditional remedy.

A 78-year-old male with a past medical history of hypertension, diabetes mellitus and hyperlipidemia without prior nephropathy presented to the emergency department (ED) with hiccups, nausea, vomiting and generalized weakness. In the preceding 1 wk, he had consumed 3 bottles of concentrated juice self-prepared from 1 kg of small sour starfruits. His serum creatinine was noted to be 1101 μmol/L from baseline normal prior to his ED visit. He was diagnosed with AKI secondary to excessive starfruit consumption.

Consumption of starfruit can cause acute renal failure, with a good outcome when promptly identified and treated.

• Acute kidney injury
• Acute renal failure
• Starfruit
• Hemodialysis
• Case report

Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Regardless of the cause, the increased load of dietary oxalate presented to the kidneys has been linked to different kidney-related conditions and injuries, including calcium oxalate nephrolithiasis, acute and chronic kidney disease. In this paper, we review the current literature on the association between dietary oxalate intake and kidney outcomes.

• acute kidney injury
• chronic kidney disease
• diet
• nephrocalcinosis
• nephrolithiasis
• oxalate

Star fruit (Averrhoa carambola) is a well-known product in tropical countries. There are few reports published in literature with acute kidney injury due to oxalate induced nephropathy. However, none of them have an important neurological feature. We present a case of a 51-year-old male with paresis and altered mental status. Screening for neurological diseases such as stroke, Guillain-Barre, meningitis and encephalitis were negative. In the evolution, he developed acute kidney failure and was submitted to 4 dialysis sessions. After talking to the family, we discovered he had ingested over 50 star fruits prior to the acute neurologic deficits. He recovered renal function so a renal biopsy was not required. Physicians should actively look for star fruit ingestion history in patients presenting with unexplained acute kidney injury with or without neurological features. Besides, taking star fruit in a large amount, accompanied by an empty stomach and dehydrated state, is a risk factor for neurotoxicity.

• Acute kidney injury
• Averrhoa
• calcium oxalate
• dialysis

Star fruit is a popular medicinal fruit in the tropics. Its hypoglycaemic properties are considered useful in achieving glycaemic control in diabetes. Star fruit induced nephrotoxicity is a rare cause of acute kidney injury in individuals with both normal and reduced baseline renal function. We present three cases of acute kidney injury due to star fruit nephrotoxicity from Sri Lanka, and discuss the published literature on this topic.

Three Sri Lankan patients, all with a background of diabetes, presented to us with acute nausea and anorexia following recent consumption of star fruit. Two patients complained of diarrhoea and one patient complained of intractable hiccoughs. They all had elevated serum creatinine on admission. Two were known to have normal baseline serum creatinine levels. On renal biopsy two had evidence of oxalate crystal deposition. One did not show crystal deposition but had acute interstitial nephritis for which no alternate cause could be identified. Two were treated with short courses of prednisolone and two required acute haemodialysis. All recovered renal function, with both patients with known baselines approaching their premorbid serum creatinine levels.

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.

• Acute kidney injury
• Oxalate
• Star fruit

A 56-year-old man with stable chronic kidney disease (CKD) for two years following a single episode of calcium oxalate urolithiasis developed progressive elevation of his serum creatinine concentration. Urinalysis revealed pyuria and white cell casts, a few red blood cells, minimal proteinuria, and no crystals. Urine culture was sterile. Gallium scintigraphy was consistent with interstitial nephritis. Proton pump inhibitor intake was discontinued, and a short course of oral corticosteroids was initiated. Percutaneous kidney biopsy, performed because of the continued deterioration of renal function to a minimum estimated glomerular filtration rate (eGFR) value of 15 mL/min per 1.73 m² and persistent pyuria, revealed deposition of oxalate crystals in the tubules and interstitium, pronounced tubular changes, and interstitial nephritis and fibrosis. Urinary oxalate excretion was very high, in the range usually associated with primary hyperoxaluria. However, investigations for primary or enteric hyperoxaluria were negative. He reported a diet based on various nuts high in oxalate content. Estimated oxalate content in the diet was, for years, approximately four times higher than that in the average American diet. The institution of a diet low in oxalates resulted in the rapid normalization of urinary oxalate excretion and urinary sediment and in the slow, continuous improvement of renal function to near normal levels (eGFR 59 mL/min/1.73 m²) before his death from a brain malignancy 3.5 years later. The manifestations of nephropathy secondary to dietary hyperoxaluria, including the urine findings, can be indistinguishable from other types of interstitial nephritis. The diagnosis of dietary hyperoxaluria requires careful dietary history and a kidney biopsy. Identifying dietary hyperoxaluria as the cause of CKD is important because the decrease in dietary oxalate intake without any other measures can lead to sustained improvement in renal function.

• chronic kidney disease
• dietary hyperoxaluria
• oxalate nephropathy

Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis, but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma, profound tubular damage and interstitial inflammation and fibrosis. Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to end-stage renal disease (ESRD). This sequence of events, well recognized in the past in primary and enteric hyperoxalurias, has also been documented in a few cases of dietary hyperoxaluria. Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide, thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions. Studies addressing this question have the potential of improving population health and should be undertaken, alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate, and into the mechanisms of development of oxalate-induced renal parenchymal disease. Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.

• Dietary hyperoxaluria
• Chronic oxalate nephropathy
• Acute oxalate nephropathy
• Acute tubular necrosis
• Interstitial nephritis
• Nephrocalcinosis
• Calcium oxalate nephrolithiasis
• Oxalate transporters
• Inflammasomes