Oxalate Nephropathy Research Articles

Crystalline Bone Marrow in Systemic Oxalosis

A 43-year-old woman with a history of two failed orthotopic kidney transplants, ventricular tachycardia, and recurrent nephrolithiasis underwent a bone marrow biopsy during an evaluation for refractory anemia. The aspirate revealed extensive crystal deposition with nearly absent residual hematopoiesis (Fig. 1). The crystals were birefringent under polarized light (Fig. 2) suggestive of calcium oxalate. The plasma oxalate level was elevated at 42.8 umol/l (normal < 1.8 umol/l), consistent with a diagnosis of systemic oxalosis from presumed primary hyperoxaluria. Figure 1 Bone marrow biopsy demonstrating extensive calcium oxalate crystal deposition. Figure 2 Same view under polarized light. Primary hyperoxaluria is a rare, autosomal recessive disorder of hepatic glyoxylate metabolism resulting in overproduction of oxalate.1 Oxalate nephropathy results in renal failure, which leads to a further increase in the plasma concentration of oxalate. Calcium oxalate can then deposit into a wide array of tissues including bone, retina, peripheral nerves, arterial media, and the heart.2 For some patients, treatment with pyridoxine to reduce urine oxalate levels may be beneficial, though liver and kidney transplantation is often required.3 Both kidney transplants had taken place overseas, and the patient’s initial renal failure and first transplant failure were attributed to obstructive nephropathy from renal calculi. The second transplant loss was from rejection related to a reduction of immunosuppression, though biopsy revealed deposition of calcium oxalate crystals as well.

Quiz Page August 2013: Kidney Failure in a Transplant From an Identical Twin

Quiz Page August 2013: Kidney Failure in a Transplant From an Identical Twin

Oxalate Nephropathy and Intravenous Vitamin C

Oxalate nephropathy is a rare condition characterized by extensive calcium oxalate deposition in the renal tubules, resulting in kidney injury. There are primary forms of the disease that arise from genetic mutation causing overproduction of oxalate. More commonly, this condition is seen as a secondary phenomenon. The clinical presentation is nonspecific, with acute kidney injury and normal serologic study results. The characteristic finding on kidney biopsy is the presence of acute tubular injury associated with polarizable crystals in the tubular lumen and epithelial cytoplasm. We present a case of acute oxalate nephropathy in a patient with underlying systemic lupus erythematosus who recently received intravenous vitamin C.

Orlistat Induced Oxalate Nephropathy

Orlistat Induced Oxalate Nephropathy

Renal Failure Due to Acute Oxalate Nephropathy Following Moviprep® Bowel Cleasing

Renal Failure Due to Acute Oxalate Nephropathy Following Moviprep® Bowel Cleasing

Acute Oxalate Nephropathy Secondary to Orlistat‐Induced Enteric Hyperoxaluria

NephrologyVolume 18, Issue 3 p. 241-242 Correspondence Acute Oxalate Nephropathy Secondary to Orlistat-Induced Enteric Hyperoxaluria Tony K Kwan, Tony K Kwan Department of Renal Medicine, Royal Prince Alfred HospitalSearch for more papers by this authorSteve J Chadban, Steve J Chadban Department of Renal Medicine, Royal Prince Alfred Hospital University of Sydney, Sydney, New South Wales, AustraliaSearch for more papers by this authorPaul R McKenzie, Paul R McKenzie Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital University of Sydney, Sydney, New South Wales, AustraliaSearch for more papers by this authorJohn R Saunders, John R Saunders Department of Renal Medicine, Royal Prince Alfred HospitalSearch for more papers by this author Tony K Kwan, Tony K Kwan Department of Renal Medicine, Royal Prince Alfred HospitalSearch for more papers by this authorSteve J Chadban, Steve J Chadban Department of Renal Medicine, Royal Prince Alfred Hospital University of Sydney, Sydney, New South Wales, AustraliaSearch for more papers by this authorPaul R McKenzie, Paul R McKenzie Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital University of Sydney, Sydney, New South Wales, AustraliaSearch for more papers by this authorJohn R Saunders, John R Saunders Department of Renal Medicine, Royal Prince Alfred HospitalSearch for more papers by this author First published: 25 February 2013 https://doi.org/10.1111/j.1440-1797.2012.01649.xCitations: 17Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume18, Issue3March 2013Pages 241-242 RelatedInformation

Oxalate nephropathy: An important cause of renal failure after bariatric surgery

Obesity is a major public health issue all over the world. Bariatric surgery is increasingly becoming popular as a surgical treatment for morbid obesity. Nephrologists need to be aware of possible renal complications after bariatric surgery. We report a 54-year-old male patient who presented with progressive worsening of renal function following a duodenal switch procedure for morbid obesity, and he was found to have oxalate nephropathy on renal biopsy.

Acute oxalate nephropathy due to ′Averrhoa bilimbi′ fruit juice ingestion

Irumban puli (Averrhoa bilimbi) is commonly used as a traditional remedy in the state of Kerala. Freshly made concentrated juice has a very high oxalic acid content and consumption carries a high risk of developing acute renal failure (ARF) by deposition of calcium oxalate crystals in renal tubules. Acute oxalate nephropathy (AON) due to secondary oxalosis after consumption of Irumban puli juice is uncommon. AON due to A. bilimbi has not been reported before. We present a series of ten patients from five hospitals in the State of Kerala who developed ARF after intake of I. puli fruit juice. Seven patients needed hemodialysis whereas the other three improved with conservative management.

Acute Oxalate Nephropathy Associated with Orlistat: A Case Report with a Review of the Literature

Orlistat is a gastrointestinal lipase inhibitor used for weight reduction in obese individuals. Enteric hyperoxaluria caused by orlistat leads to oxalate absorption. Acute oxalate nephropathy is a rare complication of treatment with orlistat. Herein we report a patient presenting with acute renal failure which improved minimal with intravenous hydration. She was found to have oxalate crystals on renal biopsy. Patient admitted orlistat use over the counter for weight reduction on further questioning. The purpose of this case review is to increase awareness among patients since they are more focused on losing weight. This case also calls for the provider attention to educate patients regarding side effects of orlistat because of easy availability of orlistat over the counter.

Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion

Nephrocalcinosis, acute calcium oxalate (CaOx) nephropathy, and renal stone disease can lead to inflammation and subsequent renal failure, but the underlying pathological mechanisms remain elusive. Other crystallopathies, such as gout, atherosclerosis, and asbestosis, trigger inflammation and tissue remodeling by inducing IL-1β secretion, leading us to hypothesize that CaOx crystals may induce inflammation in a similar manner. In mice, intrarenal CaOx deposition induced tubular damage, cytokine expression, neutrophil recruitment, and renal failure. We found that CaOx crystals activated murine renal DCs to secrete IL-1β through a pathway that included NLRP3, ASC, and caspase-1. Despite a similar amount of crystal deposits, intrarenal inflammation, tubular damage, and renal dysfunction were abrogated in mice deficient in MyD88; NLRP3, ASC, and caspase-1; IL-1R; or IL-18. Nephropathy was attenuated by DC depletion, ATP depletion, or therapeutic IL-1 antagonism. These data demonstrated that CaOx crystals trigger IL-1β-dependent innate immunity via the NLRP3/ASC/caspase-1 axis in intrarenal mononuclear phagocytes and directly damage tubular cells, leading to the release of the NLRP3 agonist ATP. Furthermore, these results suggest that IL-1β blockade may prevent renal damage in nephrocalcinosis.

Acute kidney injury after ingestion of rhubarb: secondary oxalate nephropathy in a patient with type 1 diabetes

BackgroundOxalosis is a metabolic disorder characterized by deposition of oxalate crystals in various organs including the kidney. Whereas primary forms result from genetic defects in oxalate metabolism, secondary forms of oxalosis can result from excessive intestinal oxalate absorption or increased endogenous production, e.g. after intoxication with ethylene glycol.Case presentationHere, we describe a case of acute crystal-induced renal failure associated with excessive ingestion of rhubarb in a type 1 diabetic with previously normal excretory renal function. Renal biopsy revealed mild mesangial sclerosis, but prominent tubular deposition of oxalate crystals in the kidney. Oxalate serum levels were increased.ConclusionAcute secondary oxalate nephropathy due to excessive dietary intake of oxalate may lead to acute renal failure in patients with preexisting renal disease like mild diabetic nephropathy. Attention should be payed to special food behaviors when reasons for acute renal failure are explored.

Acute oxalate nephropathy caused by ethylene glycol poisoning

Ethylene glycol (EG) is a sweet-tasting, odorless organic solvent found in many agents, such as anti-freeze. EG is composed of four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid in vivo. These metabolites are cellular toxins that can cause cardio-pulmonary failure, life-threatening metabolic acidosis, central nervous system depression, and kidney injury. Oxalic acid is the end product of EG, which can precipitate to crystals of calcium oxalate monohydrate in the tubular lumen and has been linked to acute kidney injury. We report a case of EG-induced oxalate nephropathy, with the diagnosis confirmed by kidney biopsy, which showed acute tubular injury of the kidneys with extensive intracellular and intraluminal calcium oxalate monohydrate crystal depositions.

Oxalate nephropathy induced by octreotide treatment for acromegaly: a case report

IntroductionOxalate nephropathy has various etiologies and remains a rare cause of renal failure. To the best of our knowledge, we report the first case of oxalate nephropathy following octreotide therapy.Case presentationWe report the case of a 78-year-old Caucasian man taking chronic octreotide treatment for acromegaly who presented with acute oxalate nephropathy after antibiotic therapy. The diagnosis was confirmed by urinary analysis and a kidney biopsy. The recovery of renal function was favorable after hydration and withdrawal of octreotide therapy.ConclusionsOxalate nephropathy should be suspected in patients at risk who present with acute kidney injury after prolonged antibiotic treatment. This diagnosis should be distinguished from immuno-allergic interstitial nephritis and requires specific care. The evolution of this condition may be favorable if the pathology is identified correctly. Octreotide therapy should be considered a risk factor for enteric oxaluria.

Acute irreversible oxalate nephropathy in a lung transplant recipient treated successfully with a renal transplant

We report a 29 year old male cystic fibrosis patient with end stage lung disease and normal renal function who underwent a sequential double lung transplant. Medical history included: an ileal resection and pancreatic exocrine dysfunction. The postoperative period was complicated with haemorrhage and repeat surgery, requiring multiple blood transfusions and extensive antibiotic cover. Pancreatic supplements were interrupted. Acute renal failure attributed to haemodynamically-mediated acute tubular necrosis was managed expectantly. He remained dialysis dependent 8 weeks post surgery and was maintained on triple immunosuppression with tacrolimus, mycophenolate and prednisolone. A DTPA study was consistent with ATN. Renal biopsy revealed features consistent with tubular injury due to acute oxalate nephropathy (AON). Further biochemical characterization excluded primary hyperoxaluria but confirmed increased 24 hour urinary oxalate. He was maintained on enhanced frequency HDF and subsequently received an uncomplicated live related renal transplant 10 months post lung transplant with only additional basiliximab. Calcium carbonate was continued to manage post transplant hyperoxaluria and an early renal biopsy excluded recurrent oxalate injury. Enteric hyperoxaluria due to malabsorption in patients with CF especially with ileal resection, in addition to loss of gut Oxalobacter formigenes due to prolonged antimicrobials, increases the risk of AON. Increased awareness of this condition and screening prior to lung transplant is recommended.

An unexpected cause of progressive renal failure in a 66-year-old male after liver transplantation: secondary hyperoxaluria

Hyperoxaluria is a rare metabolic disorder characterized by calcium oxalate deposition in different tissues. It is caused either by an inherited disease of oxalate metabolism [primary hyperoxalurias (PH)] or by an acquired disturbance (secondary hyperoxaluria). We report here an atypical presentation of enteric hyperoxaluria-induced renal failure that occurred after liver transplantation. Despite adapted treatment and intensive haemodialysis, the patient did not recover. This case allows the reviewing of the multiple pathophysiological mechanisms involved in this disease. Oxalate nephropathy should be considered in the differential diagnosis of acute renal failure, especially when previous renal impairment and fat malabsorption are present. We suggest performing renal biopsy early to allow a prompt diagnosis and therapeutic intervention.

Vitamin C-induced oxalate nephropathy: a case report

Therapeutic benefits of vitamin C is an area of active research and large doses have been suggested by many studies for treatment of various conditions. We are describing a case of oxalate nephropathy leading to end stage kidney disease, which occurred secondary to mega-dose of oral vitamin C. Increasing the awareness between medical personnel as well as patients will clearly decrease the incidence of this debilitating but, at the same time, highly preventable disease.

Acute Oxalate Nephropathy Diagnosed by Renal Biopsy

Acute Oxalate Nephropathy Diagnosed by Renal Biopsy

Impact of Norovirus/Sapovirus-Related Diarrhea in Renal Transplant Recipients Hospitalized for Diarrhea

Diarrhea of unspecified cause frequently occurs after renal transplantation and is usually ascribed to mycophenolic acid toxicity. Norovirus (NoV) and sapovirus (SaV) have been sporadically reported to cause chronic diarrhea in immunocompromised patients. We undertook a retrospective study (2008-2009) to examine the clinical and epidemiologic significance of NoV and SaV infections in adult renal transplant recipients hospitalized for acute or chronic diarrhea. Ninety-six renal transplant recipients were hospitalized for diarrhea at our institution during a 16-month period, 87 of whom were included in the study, including 46 patients with chronic diarrhea. Among 41 patients with unexplained diarrhea, 20 patients were screened for NoV/SaV, 16 of whom were positive. Fifteen of them (94%) had chronic diarrhea. When compared with bacterial and parasitic infections, NoV/SaV infections were associated with a greater weight loss at the time of admission, a 8.7-fold longer duration of symptoms and a more frequent need for mycophenolic acid dosage reduction. Eighty-one percent of patients hospitalized for NoV/SaV-associated diarrhea experienced acute renal failure. Five and one patients subsequently had biopsy-diagnosed active graft rejection and oxalate nephropathy, respectively. Ten of the 14 patients who underwent a longitudinal study of NoV/SaV stool's clearance exhibited a prolonged viral shedding period with a median time of 289 days (107-581 days). Our study indicates that NoV/SaV infection causes posttransplant chronic diarrhea potentially complicated by severe kidney graft impairment.

Oxalate Nephropathy Associated with Chronic Pancreatitis

Enteric overabsorption of oxalate may lead to hyperoxaluria and subsequent acute oxalate nephritis (AON). AON related to chronic pancreatitis is a rare and poorly described condition precluding early recognition and treatment. We collected the clinical characteristics, treatment, and renal outcome of 12 patients with chronic pancreatitis-associated AON followed in four French renal units. Before AON, mild to moderate chronic kidney disease was present in all patients, diabetes mellitus in eight (insulin [n = 6]; oral antidiabetic drugs [n = 2]), and known chronic pancreatitis in only eight. At presentation, pancreas imaging showed gland atrophy/heterogeneity, Wirsung duct dilation, calcification, or pseudocyst. Renal findings consisted of rapidly progressive renal failure with tubulointerstitial profile. Acute modification of glomerular filtration preceded the AON (i.e., diarrhea and diuretics). Increase in urinary oxalate excretion was found in all tested patients and hypocalcemia in nine (<1.5 mmol/L in four patients). Renal biopsy showed diffuse crystal deposits, highly suggestive of oxalate crystals, with tubular necrosis and interstitial inflammatory cell infiltrates. Treatment consisted of pancreatic enzyme supplementation, oral calcium intake, and an oxalate-free diet in all patients and renal replacement therapy in five patients. After a median follow-up of 7 months, three of 12 patients reached end-stage renal disease. AON is an under-recognized severe crystal-induced renal disease with features of tubulointerstitial nephritis that may occur in patients with a long history of chronic pancreatitis or reveal the pancreatic disease. Extrinsic triggering factors should be prevented.

Oxalate nephropathy in a laboratory colony of common marmoset monkeys (Callithrix jacchus) following the ingestion of Eucalyptus viminalis

Seven common marmoset monkeys (Callithrix jacchus) from a laboratory colony of 17 died over a period of eight months. Death of six of these monkeys was attributed to kidney failure...