Herbo-Mineral Medicine, Lithom Exhibits Anti-Nephrolithiasis Activity in Rat Model of Hyperoxaluria by Attenuating Calcium Oxalate Crystal Formation and Oxidative Stress.

BACKGROUND: Calcium oxalate monohydrate (COM) forms the most common type of kidney stones observed in clinics, elevated levels of urinary oxalate being the principal risk factor for such an etiology. The objective of the present study was to evaluate the anti-nephrolithiatic effect of herbo-mineral formulation, Lithom. METHODS: The in vitro biochemical synthesis of COM crystals in the presence of Lithom was performed and observations were made by microscopy and Scanning Electron Microscope (SEM) based analysis for the detection of crystal size and morphology. The phytochemical composition of Lithom was evaluated by Ultra-High-Performance Liquid Chromatography (UHPLC). The in vivo model of Ethylene glycol-induced hyperoxaluria in Sprague-Dawley rats was used for the evaluation of Lithom. The animals were randomly allocated to 5 different groups namely Normal control, Disease control (ethylene glycol (EG), 0.75%, 28 days), Allopurinol (50 mg/kg, q.d.), Lithom (43 mg/kg, b.i.d.), and Lithom (129 mg/kg, b.i.d.). Analysis of crystalluria, oxalate, and citrate levels, oxidative stress parameters (malondialdehyde (MDA), catalase, myeloperoxidase (MPO)), and histopathology by hematoxylin and eosin (H&E) and Von Kossa staining was performed for evaluation of Lithom. RESULTS: The presence of Lithom during COM crystals synthesis significantly reduced the average crystal area, feret's diameter, and area-perimeter ratio, in a dose-dependent manner. SEM analysis revealed that COM crystals synthesized in the presence of 100 and 300 µg/mL of Lithom exhibited a veritable morphological transition from irregular polygons with sharp edges to smoothened smaller cuboid polygons. UHPLC analysis of Lithom revealed the presence of Trigonelline, Bergenin, Xanthosine, Adenosine, Bohoervinone B, Vanillic acid, and Ellagic acid as key phytoconstituents. In EG-induced SD rats, the Lithom-treated group showed a decrease in elevated urinary oxalate levels, oxidative stress, and renal inflammation. Von Kossa staining of kidney tissue also exhibited a marked reduction in crystal depositions in Lithom-treated groups. CONCLUSION: Taken together, Lithom could be a potential clinical-therapeutic alternative for management of nephrolithiasis.

Oxalate nephropathy and chronic turmeric supplementation: a case report.

We present a case of a 69-year-old man who presented for routine check-up and was incidentally found to have kidney failure with an initially unrevealing history and bland urinary sediment. He was diagnosed with oxalate nephropathy in the setting of chronic turmeric supplementation and chronic antibiotic therapy with associated diarrhea. Our case provides several key insights into oxalate nephropathy. First, the diagnosis requires a high index of clinical suspicion. It is uncommonly suspected clinically unless there is an obvious clue in the history such as Roux-en-Y gastric bypass or ethylene glycol poisoning. Diagnosis can be confirmed by histopathologic findings and corroborated by serum levels of oxalate and 24-hour urinary excretion. Second, the diagnosis can often be missed by the pathologist because of the characteristics of the crystals unless the renal pathologist has made it a rule to examine routinely all H&E sections under polarized light. This must be done on H&E, as the other stains dissolve the crystals. Third, one oxalate crystal in a routine needle biopsy is considered pathologic and potentially contributing to the AKI or to the CKD in an important way. Fourth, secondary oxalosis can be largely mitigated or prevented in many cases, especially iatrogenic cases. This can come through the surgeon or the gastroenterologist providing proper instructions to patients on an oxalate-restricted diet or other specific dietary measures. Lastly, this case highlights the success that results from cooperation and communication between the pathologist and the treating physician.

Oxalate nephropathy after pancreaticoduodenectomy: a case report.

A 75-year-old male developed acute kidney injury KDIGO stage 3 a few weeks after Whipple surgery was performed for a distal cholangiocarcinoma. Kidney biopsy revealed oxalate nephropathy. This was attributed to post-Whipple malabsorption, poor compliance with pancreatic enzyme replacement therapy, and daily intake of vitamin C supplements. Pancreatic enzyme replacement therapy was resumed and calcium carbonate initiated, with an improvement in glomerular filtration rate. Unfortunately, due to oncological progression, best supportive care was initiated.We review the pathophysiology and conditions predisposing to secondary hyperoxaluria and oxalate nephropathy. This diagnosis should be considered among the main causes of acute kidney injury following pancreatectomy, with important therapeutic implications.

Intestinal Oxalate Absorption, Enteric Hyperoxaluria, and Risk of Urinary Stone Formation in Patients with Crohn's Disease.

Nephrolithiasis is a common urologic manifestation of Crohn's disease. The purpose of this study was to investigate the clinical characteristics, intestinal oxalate absorption, and risk factors for urinary stone formation in these patients. In total, 27 patients with Crohn's disease and 27 healthy subjects were included in the present study. Anthropometric, clinical, and 24 h urinary parameters were determined, and the [13C2]oxalate absorption test was performed. Among all patients, 18 had undergone ileal resection, 9 of whom had a history of urinary stones. Compared to healthy controls, the urinary excretion values of calcium, magnesium, potassium, sulfate, creatinine, and citrate were significantly lower in patients with Crohn's disease. Intestinal oxalate absorption, the fractional and 24 h urinary oxalate excretion, and the risk of calcium oxalate stone formation were significantly higher in patients with urolithiasis than in patients without urolithiasis or in healthy controls. Regardless of the group, between 83% and 96% of the [13C2]oxalate was detected in the urine within the first 12 h after ingestion. The length of ileum resection correlated significantly with the intestinal absorption and urinary excretion of oxalate. These findings suggest that enteric hyperoxaluria can be attributed to the hyperabsorption of oxalate following extensive ileal resection. Oral supplementation of calcium and magnesium, as well as alkali citrate therapy, should be considered as treatment options for urolithiasis.

The preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria.

OBJECTIVE: Kidney stones are a common complication of hyperoxaluria. The aim of this study is to investigate the protective and preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria. MATERIALS AND METHODS: Male Wistar rats between 110 and 145 g in weight were used in the study, Ulva lactuca aqueous extract and polysaccharides were prepared. The male albino rats were supplemented with 0.75 percent ethylene glycol (v/v) in their drinking water for six weeks to induce hyperoxaluria. Ulvan infusions (100 mg/kg body weight), ulvan polysaccharides (100 mg/kg body weight), and atorvastatin (two milligrams/kg body weight) to treat hyperoxaluric rats for four weeks (every other day) were used. Weight loss, serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation and kidney histopathological studies were done. RESULTS: Weight loss, rise of serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation were all shown to be prevented by the addition of atorvastatin, polysaccharides, or aqueous extract, respectively. Catalase (CAT) activity, glutathione peroxidase (GPX) activity, glutathione-S-transferase (GST) activity, and histopathological perturbations were all significantly reduced by the medicines that were studied. CONCLUSIONS: Hyperoxaluria caused by ethylene glycol may be prevented by a combination of Ulva lactuca aqueous extract, ulvan polysaccharides, and atorvastatin. A reduction in renal oxidative stress and an improvement of the antioxidant defense system may be responsible for these protective benefits. However, Ulva lactuca infusion and ulvan polysaccharides need to be studied further in humans, in order to determine their efficacy and safety.

Megadose Vitamin C Prescription Through Alternative Medicine Leading to End-Stage Renal Disease: Case Study and Literature Review.

Modern medicine has made tremendous advancements and succeeded in increasing longevity through adequate screening and diagnosis and various new therapeutic approaches. However, alternative medicine is a branch of health care practicing different traditional and unconventional, potentially hazardous therapies to treat commonly known ailments. Standard low-dose vitamin C, ie, 500-1000 mg, is approved in medical conditions like methemoglobinemia, scurvy, burns and also helps iron absorption in anemia. However, toxic doses carry high nephrotoxicity potential like in our case. We present a 74-year-old Caucasian female falling victim to one such alternative therapy leading to acute kidney injury requiring lifelong hemodialysis. She had endometrial cancer and received 100 gm of intravenous vitamin C weekly through a provider for the last 6 weeks as part of this alternate approach to cure her cancer. Upon admission, the serum creatinine level was elevated at 8.2 mg/dl, which subsequently did not improve with conservative management. Renal biopsy revealed diffuse acute tubular injury with polarized microscopy demonstrating calcium oxalate crystals. While her blood vitamin C levels were high, the serum oxalate level was normal. She ended up requiring renal replacement therapy permanently. Alternative medicine continues to be a significant health care hazard with the potential to cause unwanted irreversible nephrotoxicity. Public attention is necessary at various social levels to counter the detrimental outcomes of alternative medicine.

Three Tesla magnetic resonance imaging detects oxalate osteopathy in patients with primary hyperoxaluria type I.

BACKGROUND: With declining kidney function and therefore increasing plasma oxalate, patients with primary hyperoxaluria type I (PHI) are at risk to systemically deposit calcium-oxalate crystals. This systemic oxalosis may occur even at early stages of chronic kidney failure (CKD) but is difficult to detect with non-invasive imaging procedures. METHODS: We tested if magnetic resonance imaging (MRI) is sensitive to detect oxalate deposition in bone. A 3 Tesla MRI of the left knee/tibial metaphysis was performed in 46 patients with PHI and in 12 healthy controls. In addition to the investigator's interpretation, signal intensities (SI) within a region of interest (ROI, transverse images below the level of the physis in the proximal tibial metaphysis) were measured pixelwise, and statistical parameters of their distribution were calculated. In addition, 52 parameters of texture analysis were evaluated. Plasma oxalate and CKD status were correlated to MRI findings. MRI was then implemented in routine practice. RESULTS: Independent interpretation by investigators was consistent in most cases and clearly differentiated patients from controls. Statistically significant differences were seen between patients and controls (p < 0.05). No correlation/relation between the MRI parameters and CKD stages or Pox levels was found. However, MR imaging of oxalate osteopathy revealed changes attributed to clinical status which differed clearly to that in secondary hyperparathyroidism. CONCLUSIONS: MRI is able to visually detect (early) oxalate osteopathy in PHI. It can be used for its monitoring and is distinguished from renal osteodystrophy. In the future, machine learning algorithms may aid in the objective assessment of oxalate deposition in bone. Graphical Abstract A higher resolution version of the Graphical abstract is available as Supplementary information.

Risk factors for developing hyperoxaluria in children with Crohn's disease.

BACKGROUND: For the purpose of a better understanding of enteric hyperoxaluria in Crohn's disease (CD) in children and adolescents, we investigated the occurrence and risk factors for development of hyperoxaluria in those patients. METHODS: Forty-five children with CD and another 45 controls were involved in this cross-sectional study. Urine samples were collected for measurement of spot urine calcium/creatinine (Ur Ca/Cr), oxalate/creatinine (Ur Ox/Cr), and citrate/creatinine (Ur Citr/Cr) ratios. Fecal samples were also collected to detect the oxalyl-CoA decarboxylase of Oxalobacter formigenes by PCR. Patients were classified into 2 groups: group A (with hyperoxaluria) and group B (with normal urine oxalate excretion). The disease extent was assessed, and the activity index was calculated. RESULTS: According to the activity index, 30 patients (66.7%) had mild disease and 13 patients (28.9%) had moderate disease. There was no significant difference in Ur Ox/Cr ratio regarding the disease activity index. O. formigenes was not detected in 91% of patients in group A while it was detected in all patients in group B (p < 0.001). By using logistic regression analysis, the overall model was statistically significant when compared to the null model, (χ2 (7) = 52.19, p < 0.001), steatorrhea (p = 0.004), frequent stools (p = 0.009), and O. formigenes (p < 0.001). CONCLUSION: Lack of intestinal colonization with O. formigenes, steatorrhea, and frequent stools are the main risk factors for development of enteric hyperoxaluria in CD patients. Identifying risk factors facilitates proper disease management in future studies. A higher resolution version of the Graphical abstract is available as Supplementary information.

What treatments reduce kidney stone risk in patients with bowel disease?

We examined how physicians made therapeutic choices to decrease stone risk in patients with bowel disease without colon resection, many of whom have enteric hyperoxaluria (EH), at a single clinic. We analyzed clinic records and 24-h urine collections before and after the first clinic visit, among 100 stone formers with bowel disease. We used multivariate linear regression and t tests to compare effects of fluid intake, alkali supplementation, and oxalate-focused interventions on urine characteristics. Patients advised to increase fluid intake had lower initial urine volumes (L/day; 1.3 ± 0.5 vs. 1.7 ± 0.7) and increased volume more than those not so advised (0.7 ± 0.6 vs. 0.3 ± 0.6 p = 0.03; intervention vs. non-intervention). Calcium oxalate supersaturation (CaOx SS) fell (95% CI -4.3 to -0.8). Alkali supplementation increased urine pH (0.34 ± 0.53 vs. 0.22 ± 0.55, p = 0.26) and urine citrate (mg/d; 83 ± 256 vs. 98 ± 166, p = 0.74). Patients advised to reduce oxalate (mg/day) absorption had higher urine oxalate at baseline (88 ± 44 vs. 50 ± 26) which was unchanged on follow-up (88 (baseline) vs. 91 (follow-up), p = 0.90). Neither alkali (95% CI -1.4 to 2.1) nor oxalate-focused advice (95% CI -1.2 to 2.3) lowered CaOx SS. Physicians chose treatments based on baseline urine characteristics. Advice to increase fluid intake increased urine volume and decreased CaOx SS. Alkali and oxalate interventions were ineffective.

Pancreatic insufficiency as a complication of type 1 diabetes causing enteric hyperoxaluria in a transplant kidney.

A kidney transplant recipient with a medical history of type 1 diabetes mellitus (T1DM) presents to the clinic with an acute kidney injury (AKI) and diarrhoea. Kidney biopsy found deposition of focal oxalate crystals, and further investigation revealed a raised 24-hour urinary oxalate and reduced faecal elastase. Therefore, we present a case of acute oxalate nephropathy (AON) secondary to enteric hyperoxaluria as a result of pancreatic insufficiency caused by T1DM. T1DM is a common cause of end-stage renal failure and exocrine pancreatic insufficiency. Therefore, AON secondary to enteric hyperoxaluria should be considered in patients with a transplant AKI. Earlier testing of 24-hour urinary oxalate and faecal elastase could generate diagnosis before biopsy results and allow commencement of pancreatic replacement therapy earlier to avoid permanent loss of kidney function.

Chaga mushroom-induced oxalate nephropathy that clinically manifested as nephrotic syndrome: A case report.

RATIONALE: The Chaga mushroom (Hymenochaetaceae, Inonotus obliquus) is a fungus belonging to the Hymenochaetaceae family. It is parasitic on birch and other tree species. Chaga mushrooms are rich in various vitamins, minerals, and nutrients. Some people consider these mushrooms medicinal as they have been reported to suppress cancer progression through anti-inflammatory and antioxidant effects. However, recent studies have reported that excessive ingestion of Chaga mushrooms can cause acute oxalate nephropathy. PATIENT CONCERNS: A 69-year-old man who ingested Chaga mushroom powder (10-15 g per day) and vitamin C (500 mg per day) for the past 3 months developed acute kidney injury (AKI) with the clinical manifestations of nephrotic syndrome (NS). DIAGNOSIS: Pathological findings showed focal acute tubular injury and the deposition of calcium oxalate crystals in the tubules. Light microscopy showed interstitial fibrosis and tubular atrophy, and electron microscopy showed the effacement of the foot processes in podocytes. Based on these results, the diagnosis was acute oxalate nephropathy accompanied by minimal change disease (MCD). INTERVENTIONS: The patient's kidney function did not improve with supportive care, such as hydration and blood pressure control. Thus, we recommended hemodialysis and the administration of a high dose of steroids (intravenous hydrocortisone 500 mg twice a day for 3 days and oral prednisolone at 1 mg/kg). OUTCOMES: The patient's kidney function recovered just 1 month after the start of treatment, and the MCD was completely remitted. LESSONS: In cases of AKI with an unknown cause, it is important to closely observe the patient's medication history, and it is recommended to perform kidney biopsy. Furthermore, this study showed that active dialysis and high-dose steroid treatment can restore kidney function in patients with AKI caused by acute oxalate nephropathy with MCD.

Pathophysiology and Management of Hyperoxaluria and Oxalate Nephropathy: A Review.

Hyperoxaluria results from either inherited disorders of glyoxylate metabolism leading to hepatic oxalate overproduction (primary hyperoxaluria), or increased intestinal oxalate absorption (secondary hyperoxaluria). Hyperoxaluria may lead to urinary supersaturation of calcium oxalate and crystal formation, causing urolithiasis and deposition of calcium oxalate crystals in the kidney parenchyma, a condition termed oxalate nephropathy. Considerable progress has been made in the understanding of pathophysiological mechanisms leading to hyperoxaluria and oxalate nephropathy, whose diagnosis is frequently delayed and prognosis too often poor. Fortunately, novel promising targeted therapeutic approaches are on the horizon in patients with primary hyperoxaluria. Patients with secondary hyperoxaluria frequently have long-standing hyperoxaluria-enabling conditions, a fact suggesting the role of triggers of acute kidney injury such as dehydration. Current standard of care in these patients includes management of the underlying cause, high fluid intake, and use of calcium supplements. Overall, prompt recognition of hyperoxaluria and associated oxalate nephropathy is crucial because optimal management may improve outcomes.

Secondary oxalate nephropathy in a patient with exocrine pancreatic insufficiency successfully treated, with complete kidney recovery.

INTRODUCTION: Oxalate nephropathy is a relatively rare and under-recognized condition that commonly presents as acute kidney injury (AKI) and often leads to end-stage renal disease. Complete recovery of kidney function is extremely rare even when treatment is instituted early on. CASE PRESENTATION: We present the case of a 68-year-old man with known type 2 diabetes mellitus and an asymptomatic unrecognized exocrine pancreatic insufficiency, who was admitted due to dialysis-dependent AKI. Kidney biopsy revealed oxalate nephropathy. A wide diagnostic assessment and a multi-factorial treatment plan that included a change of diet, therapy for exocrine pancreatic insufficiency and fat malabsorption, sodium bicarbonate and potassium citrate, calcium supplements with meals, and methylprednisolone, resulted in complete recovery of kidney function. CONCLUSION: It is important for physicians to be aware of oxalate nephropathy in cases of prolonged AKI. After confirmation of diagnosis, a wide diagnostic approach is imperative to identify all the causes that have led to oxalosis. A multi-factorial therapeutic approach can lead to complete kidney recovery.

Prospective Randomized Evaluation of Idiopathic Hyperoxaluria Treatments.

Purpose: Calcium oxalate (CaOx) stone formation is influenced by urinary oxalate excretion. Stone formers with elevated urinary oxalate are commonly prescribed a low-oxalate diet or oral supplementation with vitamin B6 and magnesium to reduce urinary oxalate excretion. This study aims to compare the effects of dietary modification vs supplementation vs a combination of both on urinary oxalate. Materials and Methods: We enrolled patients with a documented history of CaOx stones and newly diagnosed idiopathic hyperoxaluria. Patients were randomized into three treatment groups: low oxalate diet (D), supplementation with 25 mg vitamin B6 and 400 mg magnesium oxide (S), or both low oxalate diet and B6/magnesium supplementation (DS). Baseline and 3-month postintervention 24-hour urine tests were obtained. The primary endpoint was change in 24-hour urinary oxalate (Ox24) at 12 weeks. Secondary endpoints included changes in other 24-hour urine parameters, compliance rates, and adverse effect rates. Results: In total, 164 patients were recruited and 62, 47, and 55 were enrolled into the D, S, and DS groups, respectively. Of these, 99 patients completed the study (56.5% of the D, 72.3% of the S, and 54.6% of the DS groups, respectively). Significant differences were noted in median percent reduction in Ox24 values (-31.1% vs -16.0% vs -23.9%, p = 0.007) in the D, S, and DS groups, respectively. Furthermore, the percentages of patients within each treatment arm who realized a decrease in Ox24 were also found to be significantly different: D = 91.4% vs. S = 67.6% vs DS = 86.7%, p = 0.027. No significant adverse events were observed in any of the study arms. Conclusion: Low oxalate diet is more effective than B6/magnesium supplementation at lowering urinary oxalate in idiopathic hyperoxaluric stone formers. Combination therapy did not produce greater reductions in urinary oxalate than either of the monotherapy arms suggesting it is of little clinical utility. Further study with long-term longitudinal follow-up is required to determine if these treatment strategies reduce recurrent stone events in this population.

Effect of a Probiotic Supplement Containing Lactobacillus Acidophilus and Bifidobacterium Animalis Lactis on Urine Oxalate in Calcium Stone Formers with Hyperoxaluria: A Randomized, Placebo-controlled, Double-blind and In-vitro Trial.

PURPOSE: To determine the effect of a probiotic supplement containing native Lactobacillus acidophilus (L. acidophilus) and Bifidobacterium animalis lactis (B. lactis) on 24-hour urine oxalate in recurrent calcium stone formers with hyperoxaluria. Moreover, the in-vitro oxalate degradation capacity and the intestinal colonization of consumed probiotics were evaluated. MATERIALS AND METHODS: The oxalate degrading activity of L. acidophilus and B. lactis were evaluated in-vitro. The presence of oxalyl-CoA decarboxylase (oxc) gene in the probiotic species was assessed. One hundred patients were randomized to receive the probiotic supplement or placebo for four weeks. The 24-hour urine oxalate and the colonization of consumed probiotics were assessed after weeks four and eight. RESULTS: Although the oxc gene was present in both species, only L. acidophilus had a good oxalate degrading activity, in-vitro. Thirty-four patients from the probiotic and thirty patients from the placebo group finished the study. The urine oxalate changes were not significantly different between groups (57.21 ± 11.71 to 49.44 ± 18.14 mg/day for probiotic, and 56.43 ± 9.89 to 50.47 ± 18.04 mg/day for placebo) (P = .776). The probiotic consumption had no significant effect on urine oxalate, both in univariable (P = .771) and multivariable analyses (P = .490). The consumed probiotics were not detected in the stool samples of most participants. CONCLUSION: Our results showed that the consumption of a probiotic supplement containing L. acidophilus and B. lactis did not affect urine oxalate. The results may be due to a lack of bacterial colonization in the intestine.

Kidney transplant dysfunction in a patient with COVID - 19 infection: role of concurrent Sars-Cov 2 nephropathy, chronic rejection and vitamin C-mediated hyperoxalosis: case report.

BACKGROUND: COVID-19 infection in kidney transplant recipients often lead to allograft dysfunction. The allograft injury has various histopathological manifestations. Our case illustrates the unusual combination of allograft rejection, acute kidney injury secondary to oxalate nephropathy and SARS CoV-2 nephropathy as the cause of irreversible allograft failure. CASE PRESENTATION: A 56 year old renal allograft recipient presented with a history of fever and diarrhoea for the preceding 4 weeks, tested positive for Sars-CoV2 on nasal swab and was found to have severe allograft dysfunction, necessitating haemodialysis. He subsequently underwent an allograft biopsy, which demonstrated antibody mediated rejection along with the presence of extensive oxalate deposition in the tubules. Ultrastructural examination demonstrated spherical spiked particles in the glomerular capillary endothelium and the presence of tubulo-reticular inclusions suggestive of an active COVID-19 infection within the kidney. The intra-tubular oxalate deposition was considered to be the result of high dose, supplemental Vitamin C used as an immune booster in many patients with COVID - 19 infection in India. CONCLUSIONS: This case highlights the complex pathology that may be seen in following COVID-19 disease and the need for kidney biopsies in these patients to better understand the aetiology of disease.

Antiurolithic effects of medicinal plants: results of in vivo studies in rat models of calcium oxalate nephrolithiasis-a systematic review.

Urolithiasis is one of the oldest diseases affecting humans, while plants are one of our oldest companions providing food, shelter, and medicine. In spite of substantial progress in understanding the pathophysiological mechanisms, treatment options are still limited, often expensive for common people in most parts of the world. As a result, there is a great interest in herbal remedies for the treatment of urinary stone disease as an alternative or adjunct therapy. Numerous in vivo and in vitro studies have been carried out to understand the efficacy of herbs in reducing stone formation. We adopted PRISMA guidelines and systematically reviewed PubMed/Medline for the literature, reporting results of various herbal products on in vivo models of nephrolithiasis/urolithiasis. The Medical Subject Heading Terms (Mesh term) "Urolithiasis" was used with Boolean operator "AND" and other related Mesh Unique terms to search all the available records (July 2019). A total of 163 original articles on in vivo experiments were retrieved from PubMed indexed with the (MeshTerm) "Urolithiasis" AND "Complementary Therapies/Alternative Medicine, "Urolithiasis" AND "Plant Extracts" and "Urolithiasis" AND "Traditional Medicine". Most of the studies used ethylene glycol (EG) to induce hyperoxaluria and nephrolithiasis in rats. A variety of extraction methods including aqueous, alcoholic, hydro-alcoholic of various plant parts ranging from root bark to fruits and seeds, or a combination thereof, were utilized. All the investigations did not study all aspects of nephrolithiasis making it difficult to compare the efficacy of various treatments. Changes in the lithogenic factors and a reduction in calcium oxalate (CaOx) crystal deposition in the kidneys were, however, considered favorable outcomes of the various treatments. Less than 10% of the studies examined antioxidant and diuretic activities of the herbal treatments and concluded that their antiurolithic activities were a result of antioxidant, anti-inflammatory, and/or diuretic effects of the treatments.

Diet-induced oxalate nephropathy from excessive nut and seed consumption.

Oxalate is a metabolite consumed in nuts, beans and leaves, and excreted in urine. Oxalosis can cause nephropathy. We describe a rare case of a high-oxalate diet intended for irritable bowel syndrome (IBS) treatment causing oxalate nephropathy. A 59-year-old woman with a history of controlled hypertension presented with creatinine 1.8 mg/dL, increased from baseline 1.3 mg/dL. She denied recent illness, urinary stones, medication adjustments, herbal supplements and non-steroidal anti-inflammatory drugs use. Diet included six tablespoons of chia seeds and five handfuls of almonds daily to manage IBS symptoms. Her electrolytes, urinalysis and renal ultrasound were unremarkable. Her 24-hour urine output revealed increased oxalate and low citrate. Renal biopsy showed glomerulosclerosis, fibrosis and calcium oxalate deposition. She switched to a low-oxalate diet, with improvement in laboratory markers. An earlier dietary history could have raised concern for oxalosis prior to renal biopsy. Providers should be trained to identify at-risk patients and provide appropriate dietary counselling.