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ObjectivesThe survival of pediatric patients with short bowel syndrome has improved in recent years. Enteric hyperoxaluria as a pathophysiological consequence has been hardly addressed so far. It can be associated with nephrolithiasis, nephrocalcinosis or even renal insufficiency. We assessed the prevalence of hyperoxaluria and its pathogenic consequences in a retrospective single centre study over the last 12 years.MethodsWe conducted an internal database search for all pediatric patients suffering from short bowel syndrome treated from 2010 to 2022 in the department of pediatric gastroenterology as well as the pediatric nephrology and dialysis unit. Out of 56 patients identified, 26 patients were analysed for etiology of short bowel syndrome, renal excretion of oxalate (24/26), remaining short bowel and large intestinal length as well as further clinical parameters such as eGFR, nephrocalcinosis/urinary stone formation or stool frequency.ResultsHyperoxaluria was detected in 14/26 patients (54%). Nephrocalcinosis was present in four patients. Out of these four patients, hyperoxaluria could be proven (21% of all hyperoxaluric patients) in three cases, one hyperoxaluric patient had nephrolithiasis (7%). In one patient hyperoxaluria lead to end stage renal disease. We found that 80% of patients with volvulus developed enteric hyperoxaluria. None of the investigated factors had an effect on oxalate excretion.ConclusionEnteric hyperoxaluria is a relevant pathophysiological finding in patients with short bowel syndrome occurring in about 50% of our cohort with multiple pathogenic complications. Regular screening for hyperoxaluria may be implemented in medical care for patients with short bowel syndrome. If necessary, prophylaxis, e.g., dietary advice or metaphylaxis should be initiated.

Abstract Enteric hyperoxaluria (EH) is a metabolic disease caused by excessive absorption of dietary oxalate leading to the formation of chronic kidney stones and kidney failure. There are no approved pharmaceutical treatments for EH. SYNB8802 is an engineered bacterial therapeutic designed to consume oxalate in the gut and lower urinary oxalate as a potential treatment for EH. Oral administration of SYNB8802 leads to significantly decreased urinary oxalate excretion in healthy mice and non‐human primates, demonstrating the strain's ability to consume oxalate in vivo. A mathematical modeling framework was constructed that combines in vitro and in vivo preclinical data to predict the effects of SYNB8802 administration on urinary oxalate excretion in humans. Simulations of SYNB8802 administration predict a clinically meaningful lowering of urinary oxalate excretion in healthy volunteers and EH patients. Together, these findings suggest that SYNB8802 is a promising treatment for EH.

Enteric hyperoxaluria is a secondary hyperoxaluria characterized by excessive absorption of intestinal oxalate and increased urinary oxalate. Enteric hyperoxaluria is closely related to the occurrence of urinary calcium oxalate stones. It is of great significance to effectively reduce the absorption of intestinal oxalate and urinary oxalate to prevent the occurrence of urinary calcium oxalate stones. This article reviews the pathogenesis and treatment of enteric hyperoxaluria. [ABSTRACT FROM AUTHOR]

Enteric hyperoxaluria (EH) is a metabolic disease caused by excessive absorption of dietary oxalate leading to the formation of chronic kidney stones and kidney failure. There are no approved pharmaceutical treatments for EH. SYNB8802 is an engineered bacterial therapeutic designed to consume oxalate in the gut and lower urinary oxalate as a potential treatment for EH. Oral administration of SYNB8802 leads to significantly decreased urinary oxalate excretion in healthy mice and non‐human primates, demonstrating the strain's ability to consume oxalate in vivo. A mathematical modeling framework was constructed that combines in vitro and in vivo preclinical data to predict the effects of SYNB8802 administration on urinary oxalate excretion in humans. Simulations of SYNB8802 administration predict a clinically meaningful lowering of urinary oxalate excretion in healthy volunteers and EH patients. Together, these findings suggest that SYNB8802 is a promising treatment for EH. SYNOPSIS: SYNB8802 is an engineered probiotic designed to metabolize oxalate in patients with enteric hyperoxaluria. The strain shows significant oxalate degradation in vitro and in vivo, and in silico modeling predicts that it can lower urinary oxalate in patients. Enteric hyperoxaluria is a metabolic disorder where oxalate overabsorption can lead to chronic kidney stones and ultimately kidney failure.SYNB8802 is an engineered probiotic, derived from Escherichia coli Nissle capable of degrading oxalate.SYNB8802 lowers urinary oxalate, a disease biomarker, as shown in preclinical data from mice and non‐human primates.In silico modeling predicts that SYNB8802 lowers urinary oxalate up to 71% in patients. [ABSTRACT FROM AUTHOR]

Introduction: Current knowledge of risk factors and renal histologic patterns of oxalate nephropathy (ON) not due to primary hyperoxaluria (PH) has been limited to small case series and case reports. Thus, we analyzed and compared clinical risk factors, histologic characteristics, and renal outcomes of patients with biopsy-confirmed ON among a cohort of patients with enteric and nonenteric risk factors. Methods: A clinical data repository of native kidney pathology reports from 2009 to 2020 at all Mayo Clinic sites was used to identify 421 ON cases. Results: After excluding cases in transplanted kidneys or due to PH, 64 cases remained. Enteric risk factors were present in 30 and nonenteric in 34. Roux-en-Y gastric bypass (17) and pancreatic insufficiency (6) were most common in the enteric hyperoxaluria group. In the nonenteric group, vitamin C (7) and dietary oxalate (7) were common, while no apparent risk was noted in 16. Acute kidney injury (AKI) stage III at the time of diagnosis was present in 60%, and 40.6% required dialysis. Patients in the nonenteric group had more interstitial inflammation (p = 0.01), and a greater number of tubules contained intratubular calcium oxalate (CaOx) crystals (p = 0.001) than the nonenteric group. Patients in the enteric group were more likely to have baseline chronic kidney disease (CKD) (p = 0.02) and moderate-to-severe tubulointerstitial fibrosis and atrophy (IFTA) (OR 3.49, p = 0.02). After a median follow-up of 10 months, 39% were dialysis dependent, 11% received a kidney transplant, and 32% died. On univariate analysis, >10 tubules with CaOx crystals, baseline CKD, and AKI requiring dialysis correlated with the risk of dialysis, transplant, or death. On multivariate analysis, only AKI requiring dialysis correlated with adverse renal outcomes. Conclusion: This is the largest cohort study of ON not due to PH. Histologic features differ in patients with enteric versus nonenteric risks. Patients in the enteric group are more likely to have baseline CKD and significant IFTA, while patients in the nonenteric group were more likely to have a greater number of tubules with CaOx crystals and corresponding interstitial inflammation. AKI requiring dialysis at the time of diagnosis was the single most significant predictor of adverse renal outcome. [ABSTRACT FROM AUTHOR]

Data directly demonstrating the relationship between urinary oxalate (UOx) excretion and stone events in those with enteric hyperoxaluria (EH) are limited. Therefore, we assessed the relationship between UOx excretion and risk of kidney stone events in a retrospective population-based EH cohort. In all, 297 patients from Olmsted County, Minnesota were identified with EH based upon having a 24-h UOx ≥40 mg/24 h preceded by a diagnosis or procedure associated with malabsorption. Diagnostic codes and urologic procedures consistent with kidney stones during follow-up after baseline UOx were considered a new stone event. Logistic regression and accelerated failure time modeling were performed as a function of UOx excretion to predict the probability of new stone event and the annual rate of stone events, respectively, with adjustment for urine calcium and citrate. Mean ± standard deviation age was 51.4 ± 11.4 years and 68% were female. Median (interquartile range) UOx was 55.4 (46.6–73.0) mg/24 h and 81 patients had one or more stone event during a median follow-up time of 4.9 (2.8–7.8) years. Higher UOx was associated with a higher probability of developing a stone event (P < 0.01) and predicted an increased annual risk of kidney stones (P = 0.001). Estimates derived from these analyses suggest that a 20% decrease in UOx is associated with 25% reduction in the annual odds of a future stone event. Thus, these data demonstrate an association between baseline UOx and stone events in EH patients and highlight the potential benefit of strategies to reduce UOx in this patient group. Background Data directly demonstrating the relationship between urinary oxalate (UOx) excretion and stone events in those with enteric hyperoxaluria (EH) are limited. Methods We assessed the relationship between UOx excretion and risk of kidney stone events in a retrospective population-based EH cohort. In all, 297 patients from Olmsted County, Minnesota were identified with EH based upon having a 24-h UOx ≥40 mg/24 h preceded by a diagnosis or procedure associated with malabsorption. Diagnostic codes and urologic procedures consistent with kidney stones during follow-up after baseline UOx were considered a new stone event. Logistic regression and accelerated failure time modeling were performed as a function of UOx excretion to predict the probability of new stone event and the annual rate of stone events, respectively, with adjustment for urine calcium and citrate. Results Mean ± SD age was 51.4 ± 11.4 years and 68% were female. Median (interquartile range) UOx was 55.4 (46.6–73.0) mg/24 h and 81 patients had ≥1 stone event during a median follow-up time of 4.9 (2.8–7.8) years. Higher UOx was associated with a higher probability of developing a stone event (P < 0.01) and predicted an increased annual risk of kidney stones (P = 0.001). Estimates derived from these analyses suggest that a 20% decrease in UOx is associated with 25% reduction in the annual odds of a future stone event. Conclusions These data demonstrate an association between baseline UOx and stone events in EH patients and highlight the potential benefit of strategies to reduce UOx in this patient group. [ABSTRACT FROM AUTHOR]

Enteric hyperoxaluria is a metabolic disorder resulting from conditions associated with fatty acid malabsorption and characterized by an increased urinary output of oxalate. Oxalate is excessively absorbed in the gut and then excreted in urine where it forms calcium oxalate crystals, inducing kidney stones formation and crystalline nephropathies. Enteric hyperoxaluria is probably underdiagnosed and may silently damage kidney function of patients affected by bowel diseases. Moreover, the prevalence of enteric hyperoxaluria has increased because of the development of bariatric surgical procedures. Therapeutic options are based on the treatment of the underlying disease, limitation of oxalate intakes, increase in calcium salts intakes but also increase in urine volume and correction of hypocitraturia. There are few data regarding the natural evolution of kidney stone events and chronic kidney disease in these patients, and there is a need for new treatments limiting kidney injury by calcium oxalate crystallization., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: EL and MD filed a patent relative to the use of Stiripentol against primary hyperoxaluria (WO2017140658A1). The authors declare no competing interest regarding this review., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Calcium oxalate (CaOx) crystal deposition within the tubules is often a perplexing finding on renal biopsy of both native and transplanted kidneys. Understanding the underlying causes may help diagnosis and future management. The most frequent cause of CaOx crystal deposition within the kidney is hyperoxaluria. When this is seen in native kidney biopsy, primary hyperoxaluria must be considered and investigated further with biochemical and genetic tests. Secondary hyperoxaluria, for example due to enteric hyperoxaluria following bariatric surgery, ingested ethylene glycol or vitamin C overdose may also cause CaOx deposition in native kidneys. CaOx deposition is a frequent finding in renal transplant biopsy, often as a consequence of acute tubular necrosis and is associated with poorer long-term graft outcomes. CaOx crystal deposition in the renal transplant may also be secondary to any of the causes associated with this phenotype in the native kidney. The pathophysiology underlying CaOx deposition is complex but this histological phenotype may indicate serious underlying pathology and should always warrant further investigation. [ABSTRACT FROM AUTHOR]

Introduction: Patients with short bowel syndrome (SBS) may exhibit enteric hyperoxaluria (EH), and the prevalence of oxalate nephropathy in SBS is likely underestimated. Plasma oxalate (POx) is a surrogate of systemic oxalate deposition and, consequently, may increase the risk of developing chronic kidney disease (CKD). The main objective of this study was to explore the distribution of POx levels in patients with SBS., Methods: Patients followed for SBS were recruited prospectively in the OXAGO study (NCT04119765) to assess POx during their annual renal follow-up including iohexol clearance. The inclusion criteria were age ≥18 years, and SBS type 2 and type 3 for more than 6 months., Results: A total of 47 patients were included but only 45 patients has a measured POx (55% males, 80% SBS type 2, 66% parenteral nutrition, 61% kidney stone history). POx levels were 6.8 ± 4.4 μmol/l, 29% of patients had POx ≥5 μmol/l. In the whole cohort, mean urinary oxalate (UOx) was 648±415 and 54% were >500 μmol/24h. In the group of patients with high POx levels (HPO), 24-hour urine oxalate was significantly higher than in the group with normal POx levels (NPO) (919 ± 566 vs. 526 ± 257 μmol/l; P  = 0.003). Glomerular filtration rate (GFR) was 66 ± 22 ml/min per 1.73 m 2 , and 91% had CKD. GFR was significantly lower in the HPO than in the NPO group (49 ± 23 vs. 73 ± 18 ml/min per 1.73 m 2 ; P  = 0.0005., Conclusion: Patients with SBS can display increased POx levels even with GFR >30 ml/min per 1.73 m 2 . POx may be an interesting biomarker to assess the severity of EH., (© 2024 International Society of Nephrology. Published by Elsevier Inc.)

Purpose: To evaluate the potential of ALLN-177, an orally administered, oxalate-specific enzyme therapy to reduce urine oxalate (UOx) excretion in patients with secondary hyperoxaluria. Methods: Sixteen male and female subjects with both hyperoxaluria and a kidney stone history were enrolled in an open-label study. Subjects continued their usual diets and therapies. During a 3-day baseline period, two 24-h (24-h) urines were collected, followed by a 4-day treatment period with ALLN-177 (7,500 units/meal, 3 × day) when three 24-h urines were collected. The primary endpoint was the change in mean 24-h UOx from baseline. Safety assessments and 24-h dietary recalls were performed throughout. Results: The study enrolled 5 subjects with enteric hyperoxaluria and 11 with idiopathic hyperoxaluria. ALLN-177 was well tolerated. Overall mean (SD) UOx decreased from 77.7 (55.9) at baseline to 63.7 (40.1) mg/24 h while on ALLN-177 therapy, with the mean reduction of 14 mg/24 h, (95% CI − 23.71, − 4.13). The calcium oxalate-relative urinary supersaturation ratio in the overall population decreased from a mean of 11.3 (5.7) to 8.8 (3.8) (− 2.8; 95% CI − 4.9, − 0.79). This difference was driven by oxalate reduction alone, but not any other urinary parameters. Mean daily dietary oxalate, calcium, and fluid intake recorded by frequent diet recall did not differ by study periods. Conclusion: ALLN-177 reduced 24-h UOx excretion, and was well tolerated. The results of this pilot study provided justification for further investigation of ALLN-177 in patients with secondary hyperoxaluria. Trial registration: Clinicaltrials.gov NCT02289755. [ABSTRACT FROM AUTHOR]

Hyperoxaluria and resultant oxalate nephropathy are infrequently reported causes of irreversible renal failure. A rapid decline in renal function in an otherwise insidiously progressive oxalate nephropathy may be triggered by various superimposed insults like the use of nephrotoxic drugs. We present the case of a patient with rapidly progressive renal failure due to oxalate nephropathy that lead to a retrospective diagnosis of chronic pancreatitis. This case highlights the importance of timely assessment for enteric hyperoxaluria in patients with unexplained renal failure of tubulointerstitial nature. [ABSTRACT FROM AUTHOR]

Background Since plasma oxalate (POx) concentrations increase at lower glomerular filtration rate (GFR) levels, even among those without enteric (EH) or primary hyperoxaluria (PH), the appropriate thresholds for considering a disorder of oxalate metabolism are poorly defined. The current study was completed to establish relationships between POx, GFR, and urine oxalate excretion (UOx) among patients with PH, EH, and routine urinary stone disease (USD). Methods The most recent POx measurement on all Mayo Clinic patients between 2005 and 2015 were electronically pulled from the Lab Information System together with the closest serum creatinine within 14 days and 24 h urine study within 60 days. After exclusion of patients not in steady state at the time of blood draw, 270 patients were available for study. Records were reviewed for clinical diagnoses to categorize patients as PH, EH, or USD. Waste plasma for Pox was also obtained from controls without USD undergoing clinical GFR testing. Results In all 3 groups POx increased as eGFR fell. For any given eGFR, POx was highest in the PH group and lowest in the USD and control groups (p < 0.0001). POx was also influenced by UOx excretion (reflecting total body oxalate burden, absorption from diet and endogenous production). Generalized estimating equations of POx vs eGFR revealed higher average POx levels in PH compared to EH,USD or control, and for EH compared to USD or control. GEE prediction models were created that use POx, UOx, age, and serum creatinine to estimate the probability of a PH diagnosis. Conclusions New models were developed to help interpret POx when considering PH in clinical practice even when it was not previously suspected and/or eGFR is reduced. [ABSTRACT FROM AUTHOR]

Objectives: The survival of pediatric patients with short bowel syndrome has improved in recent years. Enteric hyperoxaluria as a pathophysiological consequence has been hardly addressed so far. It can be associated with nephrolithiasis, nephrocalcinosis or even renal insufficiency. We assessed the prevalence of hyperoxaluria and its pathogenic consequences in a retrospective single centre study over the last 12 years., Methods: We conducted an internal database search for all pediatric patients suffering from short bowel syndrome treated from 2010 to 2022 in the department of pediatric gastroenterology as well as the pediatric nephrology and dialysis unit. Out of 56 patients identified, 26 patients were analysed for etiology of short bowel syndrome, renal excretion of oxalate (24/26), remaining short bowel and large intestinal length as well as further clinical parameters such as eGFR, nephrocalcinosis/urinary stone formation or stool frequency., Results: Hyperoxaluria was detected in 14/26 patients (54%). Nephrocalcinosis was present in four patients. Out of these four patients, hyperoxaluria could be proven (21% of all hyperoxaluric patients) in three cases, one hyperoxaluric patient had nephrolithiasis (7%). In one patient hyperoxaluria lead to end stage renal disease. We found that 80% of patients with volvulus developed enteric hyperoxaluria. None of the investigated factors had an effect on oxalate excretion., Conclusion: Enteric hyperoxaluria is a relevant pathophysiological finding in patients with short bowel syndrome occurring in about 50% of our cohort with multiple pathogenic complications. Regular screening for hyperoxaluria may be implemented in medical care for patients with short bowel syndrome. If necessary, prophylaxis, e.g., dietary advice or metaphylaxis should be initiated., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Schaefer, Schulz-Heise, Rueckel, Rauh, Juengert, Galiano, Meier, Woelfle, Schiffer and Hoerning.)

Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis and/or chronic kidney disease. There are different diseases related to hyperoxaluria: (1) kidney stones, 50% of them being explained by intermittent hyperoxaluria, secondary to dietary mistakes such as low hydration, excess of oxalate consumption and/or low calcium consumption; (2) primary hyperoxaluria, a genetic orphan disease inducing a massive production of oxalate by the liver, leading to increased plasma oxalate increase and saturation, and further systemic oxalosis with oxalate deposition, nephrocalcinosis and ultimately kidney failure, the management of this disease being currently dramatically modified by the onset of new therapeutic tools such as RNA interference; and (3) enteric hyperoxaluria, resulting from increased intestinal oxalate absorption because of intestinal malabsorption (short bowel syndrome, bariatric surgery, exocrine pancreatic insufficiency, etc.). Diagnosis and therapeutic management of these diseases require a full understanding of oxalate physiology that we detail in this review.

Obesity alone is a known risk factor for nephrolithiasis, and bariatric surgery has been linked to a higher incidence of post-operative new-onset nephrolithiasis. The mean interval from bariatric surgery to diagnosis of nephrolithiasis, ranges from 1.5 to 3.6 years. The stone risk is greatest for purely malabsorptive procedures, intermediate for Roux-en-Y gastric bypass and lowest for purely restrictive procedures (laparoscopic adjustable gastric banding, laparoscopic sleeve gastrectomy) where it approaches or is reduced below that of non-operative obese controls. A history of nephrolithiasis and increasing age at the time of surgery are both associated with an increased risk of new stone formation post-operatively. The underlying pathophysiologic changes following bariatric surgery include increased colonic absorption of oxalate leading to hyperoxaluria, hypocitraturia and increased urinary calcium oxalate supersaturation, which predispose to stone formation. The majority of incident stones are medically managed, with some requiring interventions in the form of lithotripsy or ureteroscopy. [ABSTRACT FROM AUTHOR]

Background: Enteric hyperoxaluria (EH) occurs with a rate of 5-24% in patients with inflammatory bowel disease, ileal resection and modern bariatric surgery. The excessive absorption of calcium oxalate causes chronic kidney disease (CKD) in patients with EH. In the literature, a single experience was reported in combined intestine-kidney transplantation (CIKTx) in patients with CKD due to EH.Methods: After a report of 2 successful cases of CIKTx in patients with EH and CKD, one was performed at our center in a 59-year-old Caucasian female who developed intestinal failure with total parenteral nutrition (TPN) dependence after a complication post-bariatric surgery. Before CIKTx, she underwent kidney transplantation alone (KTA) twice, which failed due to oxalate nephropathy.Results: In July 2014, the patient underwent CIKTx and bilateral allograft nephrectomy to avoid EH and oxalate stone burden. The postoperative course was complicated with acute tubular necrosis due to the use of high pressors related to perioperative bleeding. The patient was discharged 79 days after CIKTx with a serum creatinine (sCr) of 1.2 mg/dl and free of TPN. Her sCr increased at 7 months and a renal biopsy showed oxalate nephropathy. SLC26A6 (oxalate transporter) staining was significantly diminished in native duodenum/rectum as well as in intestinal allograft compared to control.Conclusions: KTA in patients with CKD secondary to EH should not be recommended due to high risk of recurrence. Although other centers showed good long-term outcomes in CIKTx, our patient experienced recurrence of EH due to oxalate transporter defect, early kidney allograft dysfunction and prolonged antibiotic use. [ABSTRACT FROM AUTHOR]

The article provides answers to a question concerning pre-renal acute kidney injury (AKI) including hyperphosphatemia.

Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid. This condition typically occurs in patients with underlying primary or secondary hyperoxaluria. Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate, whereas secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate. In both conditions, oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis. Affected organs can include bones, joints, heart, eyes, and skin. Since patients can present with renal failure and oxalosis before the underlying diagnosis of hyperoxaluria has been made, it is important to consider hyperoxaluria in patients who present with unexplained soft tissue crystal deposition. The best treatment of oxalosis is prevention. If patients present with advanced disease, treatment of oxalate arthritis consists of symptom management and control of the underlying disease process. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: To give a comprehensive and focused overview on the current knowledge of the causal relations of metabolic syndrome and/or central obesity with kidney stone formation. Methods: Previous reports were reviewed using PubMed, with a strict focus on the keywords (single or combinations thereof): urolithiasis, nephrolithiasis, kidney stones, obesity, metabolic syndrome, bariatric surgery, calcium oxalate stones, hyperoxaluria, insulin resistance, uric acid stones, acid–base metabolism. Results: Obesity (a body mass index, BMI, of >30kg/m2) affects 10–27% of men and up to 38% of women in European countries. Worldwide, >300 million people are estimated to be obese. Epidemiologically, a greater BMI, greater weight, larger waist circumference and major weight gain are independently associated with an increased risk of renal stone formation, both for calcium oxalate and uric acid stone disease. Conclusions: There are two distinct metabolic conditions accounting for kidney stone formation in patients with metabolic syndrome/central obesity. (i) Abdominal obesity predisposes to insulin resistance, which at the renal level causes reduced urinary ammonium excretion and thus a low urinary pH; the consequence is a greater risk of uric acid stone formation. (ii) Bariatric surgery, the only intervention that facilitates significant weight loss in morbidly obese people, carries a greater risk of calcium oxalate nephrolithiasis. The underlying pathophysiological mechanisms are profound enteric hyperoxaluria due to intestinal binding of calcium by malabsorbed fatty acids, and severe hypocitraturia due to soft or watery stools, which lead to chronic bicarbonate losses and intracellular metabolic acidosis. [Copyright &y& Elsevier]

Abstract: The formation of renal calculi secondary to enteric hyperoxaluria is rare in the paediatric population. We present the case of an 8-year-old boy who had short bowel syndrome resulting in enteric hyperoxaluria which led to the development of urolithiasis and bilateral ureteric strictures, both of which resolved with medical management. We also review the literature on enteric hyperoxaluria. [Copyright &y& Elsevier]

Summary: Surgical intervention has become an accepted therapeutic alternative for the patient with medically complicated obesity. Multiple investigators have reported significant and sustained weight loss after bariatric surgery that is associated with improvement of many weight-related medical comorbidities, and statistically significant decreased overall mortality for surgically treated as compared with medically treated subjects. Although the Roux-en-Y gastric bypass (RYGB) is considered an acceptably safe treatment, an increasing number of patients are being recognized with nephrolithiasis after this, the most common bariatric surgery currently performed. The main risk factor appears to be hyperoxaluria, although low urine volume and citrate concentrations may contribute. The incidence of these urinary risk factors among the total post-RYGB population is unknown, but may be more than previously suspected based on small pilot studies. The etiology of the hyperoxaluria is unknown, but may be related to subtle and seemingly subclinical fat malabsorption. Clearly, further study is needed, especially to define better treatment options than the standard advice for a low-fat, low-oxalate diet, and use of calcium as an oxalate binder. [Copyright &y& Elsevier]

Roux-en-Y bypass surgery is the most common bariatric procedure currently performed in the United States for medically complicated obesity. Although this leads to a marked and sustained weight loss, we have identified an increasing number of patients with episodes of nephrolithiasis afterwards. We describe a case series of 60 patients seen at Mayo Clinic-Rochester that developed nephrolithiasis after Roux-en-Y gastric bypass (RYGB), including a subset of 31 patients who had undergone metabolic evaluation in the Mayo Stone Clinic. The mean body mass index of the patients before procedure was 57 kg/m2 with a mean decrease of 20 kg/m2 at the time of the stone event, which averaged 2.2 years post-procedure. When analyzed, calcium oxalate stones were found in 19 and mixed calcium oxalate/uric acid stones in two patients. Hyperoxaluria was a prevalent factor even in patients without a prior history of nephrolithiasis, and usually presented more than 6 months after the procedure. Calcium oxalate supersaturation, however, was equally high in patients less than 6 months post-procedure due to lower urine volumes. In a small random sampling of patients undergoing this bypass procedure, hyperoxaluria was rare preoperatively but common 12 months after surgery. We conclude that hyperoxaluria is a potential complicating factor of RYGB surgery manifested as a risk for calcium oxalate stones.Kidney International (2007) 72, 100–107; doi:10.1038/sj.ki.5002194; published online 21 March 2007 [ABSTRACT FROM AUTHOR]

Kidney stones are the result of a complex interaction of hereditary and environmental factors. They are an increasingly common affliction of industrialized societies. In nearly all cases, kidney stone formation can be drastically reduced or prevented if the patient adheres closely to a carefully designed prevention program. We emphasize an approach oriented around stone composition and targeted at specific risk factors. Our approach begins with fluid and dietary modifications and progresses to pharmacological treatment in nonresponders. [ABSTRACT FROM AUTHOR]

We studied the effect of oral calcium supplementation in patients with enteric hyperoxaluria. Three patients with renal stone events following ileal resection were given oral calcium supplement. One of the three patients was put on a low-fat diet. The treatment reduced urinary oxalate excretion to the normal range. Subsequently, 2 patients reduced the dose of calcium supplementation at their own discretion and consequently developed renal stones again together with hyperoxaluria. Based on these observations, we believe that an adequate dose of calcium can normalize urinary oxalate excretion. [ABSTRACT FROM AUTHOR]