Oxalate nephropathy in association with gastric bypass.

We present the case of a 46-year-old woman with a history of Roux-en-Y gastric bypass one year prior, who presented to the emergency room with vomiting and oliguria lasting 10 days. Initial evaluation revealed acute kidney injury with serum creatinine 14.9 mg/dL (normal range 0.

A mouse model for the study of diet-induced changes in intestinal microbiome composition on renal calcium oxalate crystal formation.

Currently available animal models for calcium oxalate kidney stones are limited in their translational potential. Particularly with increasing interest in gut microbiota involvement in kidney stone disease, there are limited animal models which can be used. As such, we have developed a novel diet-induced hyperoxaluria murine model which addresses some of the shortcomings of other currently available models.

Stenotrophomonas maltophilia in Hemodialysis: An Opportunistic Pathogen or a Malevolent Foe.

Catheter-related bloodstream infections (CRBSIs) add to the morbidity and mortality of hemodialysis patients. is an extremely resistant, gram-negative, non-lactose-fermenting nosocomial bacterium that contributes significantly to mortality and morbidity. This bacterium is predominantly associated with community-acquired pneumonia, bacteremia, eye afflictions, biliary sepsis, urinary tract infection, skin and soft tissue infection, and very rarely chronic enteritis with colonic ulcers.

Unique Pathological Findings of Polarized Calcium Oxalate Crystals in Spondylodiscitis of an ESRD Hemodialysis Patient: A Case Report.

Patients with end-stage renal disease (ESRD) undergoing chronic hemodialysis are at an increased risk of developing spondylodiscitis, an infectious condition affecting the vertebral column. In this case report, we present a 22-year-old male with ESRD, a history of hyperoxaluria, nephrolithiasis, and anemia, who developed spondylodiscitis. Notably, pathological examination of tissue samples obtained during surgical intervention revealed the presence of polarized calcium oxalate crystals within the lumbar laminae and spinal discs, a rare finding in this clinical context.

Effect of the allelic background on the phenotype of primary hyperoxaluria type I.

Purpose Of Review: Primary hyperoxaluria type 1 (PH1) is an autosomal recessive disorder of hepatic glyoxylate metabolism leading to nephrolithiasis and kidney failure. PH1 is caused by mutations on the AGXT gene encoding alanine:glyoxylate aminotransferase (AGT). The AGXT gene has two haplotypes, the major (Ma) and the minor (mi) alleles.

The lack of trade-off between conformational stability and binding affinity in a nanobody with therapeutic potential for a misfolding disease.

To improve protein pharmaceuticals, we need to balance protein stability and binding affinity with in vivo efficiency. We have recently developed a nanobody (NB-AGT-2) against the alanine:glyoxylate aminotransferase with high stability (T ∼ 86 °C) that may be useful to treat a misfolding disease called primary hyperoxaluria type 1. In this work, we characterize the relationships between protein stability and binding affinity in NB-AGT-2 by generating single and double cavity-creating mutants in its hydrophobic core.

Oxalate nephropathy associated with glyoxylate-containing hair-straightening products: a call for caution.

Recent reports have described acute kidney injury in otherwise healthy individuals after exposure to hair-straightening products. In this issue, Robert et al. help elucidate the underlying mechanisms in a murine model that replicates the human pathology.

[Primary hyperoxaluria: results of a retrospective survey of the diagnostic practices of nephrologists].

Introduction: Primary hyperoxalurias (PH) are rare and serious genetic diseases. Their prognosis is improved with early medical management. However, diagnosis often occurs at the end-stage of renal failure.

Opportunities in Primary and Enteric Hyperoxaluria at the Cross-Roads Between the Clinic and Laboratory.

Hyperoxaluria is a condition in which there is a pathologic abundance of oxalate in the urine through either hepatic overproduction (primary hyperoxaluria [PH]) or excessive enteric absorption of dietary oxalate (enteric hyperoxaluria [EH]). Severity can vary with the most severe forms causing kidney failure and extrarenal manifestations. To address the current challenges and innovations in hyperoxaluria, the 14th International Hyperoxaluria Workshop convened in Perugia, Italy, bringing together international experts for focused presentation and discussion.

Empagliflozin reduces renal calcium oxalate deposition in hyperoxaluria rats induced with ethylene glycol-ammonium chloride.

A retrospective study reported that empagliflozin reduced the risk of urinary stone events in patients with diabetes mellitus. To further investigate empagliflozin's potential, we conducted an animal experiment to determine whether empagliflozin can prevent renal stone formation in hyperoxaluria rats. Hyperoxaluria rat models were constructed by administrating 0.

Primary hyperoxaluria type 3: from infancy to adulthood in a genetically unique cohort.

Background: Primary hyperoxaluria type 3 (PH3) is a rare autosomal recessive disorder caused by bi-allelic genetic variants in the 4 hydroxy-2 oxoglutarate aldolase (HOGA-1) gene. We report the natural history of PH3 in a 16-patient cohort, 15 from a unique genetically isolated population.

Methods: This retrospective single-center study followed PH3 patients between 2003 and 2023 with demographic, clinical, radiographic, genetic, and biochemical parameters.

[Genetics in nephrology - any news?].

While genetic kidney diseases were long regarded as a rare cause of kidney failure, it has been shown in recent years that they account for a relevant proportion of cases. In cohorts of kidney transplant recipients, a monogenic cause is found in up to 30% of cases. Identifying the genetic cause of kidney disease has become much easier thanks to technological advances in DNA sequencing.

A case of alkaptonuria presenting with unexplained dark-stained diapers and spurious hyperoxaluria and proteinuria due to homogentisic acid interference.

Alkaptonuria is characterized by the accumulation of homogentisic acid which causes dark coloration of urine upon standing, ochronosis, and arthritis. A 4-year old child was referred to our pediatric nephrologist with hyperoxaluria and a history of unexplained pink-to-brown discolouration of his diapers associated with a brown-staining of clothes and skin since he was six months old. He had no other symptoms and his past medical history only included minor child illnesses.