• Acute kidney injury
• Dialysis
• Oxalate nephropathy
• Vitamin C

• Humans
• Male
• Middle Aged
• Acute Kidney Injury/etiology
• Acute Kidney Injury/chemically induced
• Ascorbic Acid/administration & dosage
• Ascorbic Acid/therapeutic use
• Diet/adverse effects
• Fatal Outcome
• Kidney/pathology
• Oxalates/adverse effects
• Oxalates/metabolism
• Renal Dialysis
• Adult

• chronic kidney disease
• dietary guidelines
• disease progression
• nutrition
• polycystic kidney disease

• Humans
• Polycystic Kidney, Autosomal Dominant/etiology
• Disease Progression
• Life Style
• Diet/adverse effects
• Renal Insufficiency, Chronic/etiology
• Diabetes Mellitus, Type 2/etiology
• Risk Factors

• Humans
• Kidney Transplantation/adverse effects
• Calcium Oxalate
• Kidney/pathology
• Hyperoxaluria/etiology
• Hyperoxaluria/complications
• Renal Insufficiency
• Oxalates

• National Natural Science Foundation of China

Short gut syndrome can lead to type 3 intestinal failure, and nutrition and hydration can only be achieved with parenteral nutrition (PN). While this is a lifesaving intervention, it carries short- and long-term complications leading to complex comorbidities, including chronic kidney disease. Through a patient with devastating inflammatory bowel disease’s journey, this review article illustrates the effect of short gut and PN on kidney function, focusing on secondary hyperoxaluria and acute precipitants of glomerular filtration. In extensive small bowel resections colon in continuity promotes fluid reabsorption and hydration but predisposes to hyperoxaluria and stone disease through the impaired gut permeability and fat absorption. It is fundamental, therefore, for dietary intervention to maintain nutrition and prevent clinical deterioration (i.e., sarcopenia) but also to limit the progression of renal stone disease. Adaptation of both enteral and parenteral nutrition needs to be individualised, keeping in consideration not only patient comorbidities (short gut and jejunostomy, cirrhosis secondary to PN) but also patients’ wishes and lifestyle. A balanced multidisciplinary team (renal physician, gastroenterologist, dietician, clinical biochemist, pharmacist, etc.) plays a core role in managing complex patients, such as the one described in this review, to improve care and overall outcomes.

• Crohn’s disease
• hyperoxaluria
• intestinal failure
• parenteral nutrition
• renal failure

• acute kidney injury
• oxalate nephropathy
• pathology
• primary hyperoxaluria
• secondary hyperoxaluria

• deep ultraviolet microscopy
• kidney biopsies
• oxalate
• oxalosis
• synchrotron diagnosis

• Calcium Oxalate
• Case-Control Studies
• Humans
• Kidney/diagnostic imaging
• Microscopy, Fluorescence
• Synchrotrons

• Acute kidney injury
• Acute tubulointerstitial nephritis
• Etiology
• Prognosis
• Secondary oxalate nephropathy

• dietary patterns
• intermittent fasting
• ketogenic diets
• kidney transplantation
• nutrition trends
• plant-based diets

This study aimed to analyze the clinicopathological features of acute kidney disease (AKD) with renal oxalosis.

Data for biopsy-proven AKD with oxalosis diagnosed from Jan 2011 to Oct 2018 was collected. The underlying diseases, dietary habits, clinical and pathological characteristics of newly emerging kidney disease were analyzed. The long-term renal prognosis was observed.

A total of 23 patients were included, comprised of 18 men and 5 women with a mean age of 51.6 ± 15.9 years. The peak Scr was 669.9 ± 299.8 μmol/L, and 95.7% of patients had stage 3 acute kidney injury (AKI). Drug-induced tubulointerstitial nephritis (TIN) was the most common cause (65.2%) of AKD, followed by severe nephrotic syndrome (17.4%). All patients had pathological changes indicating TIN, and 11 patients were complicated with the newly emerging glomerular disease (GD). The risk of oxalosis caused by increased enterogenous oxalate absorption accounted for only 26.1%, and others came from new kidney diseases. The majority (75%) of abundant (medium to severe) oxalosis occurred in patients without GD. There were no significant differences in the score for tubular injury (T-IS) and interstitial inflammation with different severities of oxalosis. Rate of Scr decrease (ΔScr%) at 2 weeks was negatively correlated with the severity of oxalosis (R = −0.542, p = 0.037), score for T-IS (R = −0.553, p = 0.033), and age (R = −0.736, p = 0.002). The decrease in Scr at 4 weeks was correlated with T-IS (R = −0.433), but had no correlation with oxalosis.

The present findings revealed that 95.7% of AKD with secondary renal oxalosis occurred in critically ill patients. AKD from tubular injury was the prominent cause. Severe oxalosis contributed to delayed early recovery of AKD.

• Renal oxalosis
• acute kidney disease
• acute kidney injury
• drug-induced
• renal tubular injury

• Antioxidant
• Cancer research
• Cell biology
• Cell differentiation
• Cytoskeleton
• E-cadherin
• EMT
• Food science
• Natural product
• Oxalate
• Plant products
• Polyphenol
• Polyphenols
• Renal system
• Wine pomace

• Acute Kidney Injury
• Biopsy
• Casts
• Creatinine
• Hyperoxaluria
• Juicing
• Kidney
• Nephropathy
• Polarized

• Acute Kidney Injury/diagnosis
• Fruit and Vegetable Juices
• Humans
• Hyperoxaluria
• Vegetables

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.

• Calcium oxalate
• Enteric hyperoxaluria
• Oxalosis
• Primary hyperoxaluria

• Heterocyclic Compounds

• biopsy
• calcium oxalate
• graft survival
• kidney transplantation
• renal insufficiency

• Allografts
• Calcium Oxalate/metabolism
• Female
• Graft Rejection/etiology
• Graft Rejection/metabolism
• Graft Rejection/mortality
• Graft Survival
• Humans
• Kidney Diseases/metabolism
• Kidney Diseases/mortality
• Kidney Diseases/surgery
• Kidney Transplantation/adverse effects
• Kidney Transplantation/mortality
• Male
• Middle Aged
• Prognosis
• Retrospective Studies
• Risk Factors
• Survival Rate
• Time Factors

• R01 DK103784 NIDDK NIH HHS
• National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
• R01DK103784
• investigator-initiated
• Allena Pharmaceuticals
• NIH

• Calcium oxalate
• Calcium phosphate
• Crystalline nephropathies
• MGRS
• Urate

Despite new therapeutics, the prognosis for pancreatic cancer remains poor. Pancreatic surgery is a therapeutic option in non-metastatic forms. The consequences for renal function are poorly described.

Patients who underwent surgery for pancreatic cancer between 1 January 2010 and 1 January 2017 and who experienced kidney biopsy in the Pitié-Salpêtrière Hospital were analysed.

Two hundred and ninety-four patients had pancreatic surgery during the period of analysis and five of them had a kidney biopsy (mean ± SD 20 months ±13.6 months after surgery) during the post-operative follow-up. Among these patients, three exhibited oxalate nephropathy (ON), indicating that the prevalence of ON in patients with pancreatectomy is at least 1%. ON may be insidious, with chronic renal failure without urinary abnormalities. All patients had a high oxalate-to-creatinine ratio in urine sample. Renal function improved after specific management of ON in two patients. Pancreaticoduodenectomy may represent a higher risk of ON than left pancreatectomy.

Although rare and underestimated, ON appears to be a real risk after pancreatic resection. Early detection may preserve renal function.

• chronic kidney disease
• oxalate nephropathy
• pancreatectomy
• pancreatic adenocarcinoma
• pancreatic exocrine insufficiency

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic nephropathy, and tolvaptan is the only therapy available. However, tolvaptan slows but does not stop disease progression, is marred by polyuria, and most patients worldwide lack access. This and recent preclinical research findings on the glucose-dependency of cyst-lining cells have renewed interest in the dietary management of ADPKD. We now review the current dietary recommendations for ADPKD patients according to clinical guidelines, the evidence base for those, and the potential impact of preclinical studies addressing the impact of diet on ADPKD progression. The clinical efficacy of tolvaptan has put the focus on water intake and solute ingestion as modifiable factors that may impact tolvaptan tolerance and ADPKD progression. By contrast, dietary modifications suggested to ADPKD patients, such as avoiding caffeine, are not well supported and their impact is unknown. Recent studies have identified a chronic shift in energy production from mitochondrial oxidative phosphorylation to aerobic glycolysis (Warburg effect) as a contributor to cyst growth, rendering cyst cells exquisitely sensitive to glucose availability. Therefore, low calorie or ketogenic diets have delayed preclinical ADPKD progression. Additional preclinical data warn of potential negative impact of excess dietary phosphate or oxalate in ADPKD progression.

• autosomal dominant polycystic kidney disease
• diet
• glycolysis
• ketogenic
• phosphate
• water

• Antidiuretic Hormone Receptor Antagonists/therapeutic use
• Humans
• Polycystic Kidney, Autosomal Dominant/diet therapy
• Polycystic Kidney, Autosomal Dominant/drug therapy
• Polycystic Kidney, Autosomal Dominant/genetics
• Tolvaptan/therapeutic use

Acute oxalate nephropathy (AON) is an increasingly recognized cause of acute kidney injury (AKI). Herein, we present two cases of biopsy-proven acute oxalate nephropathy in patients with gastrointestinal malabsorption, coincidentally both stemming from cholangiocarcinoma. The first is a 73-year-old male who presented with syncope and was found to have severe, oliguric AKI in the setting of newly diagnosed, nonresectable cholangiocarcinoma. The second is a 64-year-old man with remote resection of cholangiocarcinoma who presented after routine laboratory monitoring showed significant AKI. Temporary dialysis was required in both cases before renal recovery occurred. Together, these cases should increase physicians' suspicion of AON in the presence of malabsorption. By doing so, the workup of oxalate nephropathy can be expedited with prompt initiation of treatment.

• calcium oxalate
• crystalluria
• kidney stones
• oxalate

Ingestion of vitamin C is generally regarded as harmless. Oxalate nephropathy is an infrequent condition and is characterized by oxalate deposition in the renal tubules, in some cases resulting in acute kidney injury. It can be caused by overproduction of oxalate in genetic disorders and, more frequently, as a secondary phenomenon provoked by ingestion of oxalate or substances that can be transformed into oxalate in the patient.

We present a case of acute oxalate nephropathy in a 59-year-old black male with type 2 diabetes mellitus, who received a kidney transplant 11 years prior. He ingested a large amount of cashew pseudofruit (“cashew apple”) during 1 month and developed acute kidney injury. His previous blood creatinine was 2.0 mg/dL, which increased to 7.2 mg/d; he required hemodialysis. He was subsequently discharged without need for dialysis; 3 months later his blood creatinine stabilized at 3.6 mg/dL.

This pseudofruit is rich in ascorbic acid (vitamin C) and poor in oxalate. Urinary oxalate excretion begins to increase when amounts of ascorbic acid above bodily requirements are ingested, and may provoke acute oxalate nephropathy. The patient’s oxalate acute nephropathy, in this case, was attributed to excessive vitamin C ingestion from the cashew pseudofruit associated with decreased renal function.

• Acute kidney injury
• Acute renal injury
• Ascorbic acid
• Cashew
• Cashew pseudofruit
• Dialysis
• Oxalate nephropathy
• Renal function
• Renal transplant
• Vitamin C

Oxalate nephropathy is a rare disease. Especially chronic oxalate nephropathy still has many unknown aspects as compared to acute oxalate nephropathy with relatively well-known causality.

The patient was a 70-year-old woman who had a history of small bowel resection 25 years before, cholecystectomy 10 years before, and renal stones (calcium oxalate stones) 7 years before. She had been suffering from chronic diarrhea and had been treated by a local physician. The patient was found to have renal dysfunction (creatinine 3.09 mg/dL, eGFR 12.3 mL/min/1.73 m², hemoglobin 7.8 g/dL) and was referred to our department. The patient was admitted to our hospital for further investigation. Renal ultrasound showed hepatorenal echo contrast in an opposite manner and clear contrast between the renal cortex and medullary pyramid. Renal biopsy was performed, and histological examination showed tubulointerstitial disorder due to deposition of calcium oxalate. Daily urinary excretion of calcium oxalate was significantly increased. The patient was encouraged to drink water and administered vitamin B₆, citric acid, K and Na hydrate. Thereafter, her symptoms improved.

Case reports of chronic oxalate neuropathy are rare in the literature, and its underlying mechanism has not been understood. Our patient had a history of small bowel resection and cholecystectomy. We considered that her short bowel syndrome had influenced the development of calcium oxalate nephropathy.

• Oxalate
• Renal failure
• Ultrasound

Little is known of the clinical outcomes of secondary oxalate nephropathy. To inform clinical practice, we performed a systematic review of case reports and case series to examine the clinical characteristics and outcomes of patients with secondary oxalate nephropathy.

Electronic databases were searched for case reports and case series of individual cases or cohorts of patients with biopsy-proven oxalate nephropathy in native or transplanted kidneys from 1950 until January 2018.

Fifty-seven case reports and 10 case series met the inclusion criteria, totaling 108 patients. The case series were meta-analyzed. Mean age was 56.4 years old, 59% were men, and 15% were kidney transplant recipients. Fat malabsorption (88%) was the most commonly attributed cause of oxalate nephropathy, followed by excessive dietary oxalate consumption (20%). The mean baseline serum creatinine was 1.3 mg/dl and peaked at 4.6 mg/dl. Proteinuria, hematuria, and urinary crystals was reported in 69%, 32%, and 26% of patients, respectively. Mean 24-hour urinary oxalate excretion was 85.4 mg/d. In addition to universal oxalate crystal deposition in tubules and/or interstitium, kidney biopsy findings included acute tubular injury (71%), tubular damage and atrophy (69%), and interstitial mononuclear cell infiltration (72%); 55% of patients required dialysis. None had complete recovery, 42% had partial recovery, and 58% remained dialysis-dependent. Thirty-three percent of patients died.

Secondary oxalate nephropathy is a rare but potentially devastating condition. Renal replacement therapy is required in >50% of patients, and most patients remain dialysis-dependent. Studies are needed for effective preventive and treatment strategies in high-risk patients with hyperoxaluria-enabling conditions.

• acute kidney injury
• chronic kidney disease
• nephrolithiasis
• oxalate nephropathy
• oxalosis
• secondary oxalosis

• Detox diets
• High intensity training
• Intermittent fasting
• Juicing
• Obesity management
• Paleo diet

• Caloric Restriction
• Diet, Paleolithic
• Diet, Reducing
• Exercise/physiology
• Fasting/physiology
• Humans
• Obesity/diet therapy
• Obesity/therapy
• Weight Loss/physiology

In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of death. Some uremic toxins are ingested with the diet, such as phosphate and star fruit-derived caramboxin. Others result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves. These nutrients include l-carnitine, choline/phosphatidylcholine, tryptophan and tyrosine, which are also sold over-the-counter as nutritional supplements. Physicians and patients alike should be aware that, in CKD patients, the use of these supplements may lead to potentially toxic effects. Unfortunately, most patients with CKD are not aware of their condition. Some of the dietary components may modify the gut microbiota, increasing the number of bacteria that process them to yield uremic toxins, such as trimethylamine N-Oxide (TMAO), p-cresyl sulfate, indoxyl sulfate and indole-3 acetic acid. Circulating levels of nutrient-derived uremic toxins are associated to increased risk of death and cardiovascular disease and there is evidence that this association may be causal. Future developments may include maneuvers to modify gut processing or absorption of these nutrients or derivatives to improve CKD patient outcomes.

• caramboxin
• carnitine
• choline
• chronic kidney disease
• gut–kidney axis
• indoxyl sulfate
• microbiota
• p-cresyl sulfate
• trimethylamine N-Oxide (TMAO)
• tryptophan
• tyrosine

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

• Calcium salts
• Soluble oxalate
• Spinach
• pH

Hyperoxaluria is characterized by an increased urinary excretion of oxalate. Primary and secondary hyperoxaluria are two distinct clinical expressions of hyperoxaluria. Primary hyperoxaluria is an inherited error of metabolism due to defective enzyme activity. In contrast, secondary hyperoxaluria is caused by increased dietary ingestion of oxalate, precursors of oxalate or alteration in intestinal microflora. The disease spectrum extends from recurrent kidney stones, nephrocalcinosis and urinary tract infections to chronic kidney disease and end stage renal disease. When calcium oxalate burden exceeds the renal excretory ability, calcium oxalate starts to deposit in various organ systems in a process called systemic oxalosis. Increased urinary oxalate levels help to make the diagnosis while plasma oxalate levels are likely to be more accurate when patients develop chronic kidney disease. Definitive diagnosis of primary hyperoxaluria is achieved by genetic studies and if genetic studies prove inconclusive, liver biopsy is undertaken to establish diagnosis. Diagnostic clues pointing towards secondary hyperoxaluria are a supportive dietary history and tests to detect increased intestinal absorption of oxalate. Conservative treatment for both types of hyperoxaluria includes vigorous hydration and crystallization inhibitors to decrease calcium oxalate precipitation. Pyridoxine is also found to be helpful in approximately 30% patients with primary hyperoxaluria type 1. Liver-kidney and isolated kidney transplantation are the treatment of choice in primary hyperoxaluria type 1 and type 2 respectively. Data is scarce on role of transplantation in primary hyperoxaluria type 3 where there are no reports of end stage renal disease so far. There are ongoing investigations into newer modalities of diagnosis and treatment of hyperoxaluria. Clinical differentiation between primary and secondary hyperoxaluria and further between the types of primary hyperoxaluria is very important because of implications in treatment and diagnosis. Hyperoxaluria continues to be a challenging disease and a high index of clinical suspicion is often the first step on the path to accurate diagnosis and management.

• Primary hyperoxaluria
• Transplantation
• Renal stones
• Secondary hyperoxaluria
• Renal failure

A 49-year-old woman visited the clinic because of acute hepatitis and acute kidney injury with decreased urine output presenting microscopic hematuria and proteinuria. An abdominal computed tomography revealed a localized, hypoattenuated lesion in a hepatic lateral segment, and kidney biopsy showed oxalate crystal deposition with tubular necrosis. In addition, the patient׳s 24-hour urinary excretion of oxalate was increased. Her kidney and liver injury improved after sessions of hemodialysis, and urinary oxalate excretion was normalized. Major mutations in primary hyperoxaluria have not been proven. A full sequencing of target genes may be helpful to diagnose a rare form of primary hyperoxaluria.

• Acute kidney injury
• Acute liver injury
• 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

• acute kidney injury
• chronic kidney disease
• crystalline nephropathy
• end-stage renal disease
• nephrolithiasis
• urolithiasis

• Acute Kidney Injury/etiology
• Adult
• Calcium Oxalate/immunology
• Humans
• Immunity, Innate
• Inflammasomes
• Nephrolithiasis/complications
• Nephrolithiasis/surgery
• Renal Insufficiency, Chronic/etiology

• U54 DK083908 NIDDK NIH HHS
• U54 DK100227 NIDDK NIH HHS
• U54KD083908 PHS HHS

Oxalate nephropathy is commonly caused by ethylene glycol, vitamin C, and foods like star fruit that contain a lot of oxalate. Peanuts also have high oxalate contents. However, case reports of peanut-induced oxalate nephropathy are not common. Here, we describe a case of peanut-induced acute oxalate nephropathy with acute kidney injury and intend to demonstrate the conditions under which peanut-induced oxalate nephropathy is likely to occur.

• Acute kidney injury
• Arechis hypogaea
• Oxalates