oxalate nephropathy
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2021 ◽  
Vol 14 (12) ◽  
pp. e246745
Author(s):  
Albert Bui ◽  
Cherise Cortese ◽  
Ivan E Porter

2021 ◽  
Author(s):  
Oliver Lee ◽  
Katherine Park ◽  
Kelly Sun ◽  
John-Paul O’Shea ◽  
Sarah Gordon

ABSTRACT We present a rare case of cashew-induced oxalate nephropathy in a 69 year old veteran male with history of type 2 diabetes mellitus, nephrolithiasis, and undiagnosed chronic kidney disease (CKD). Oxalate nephropathy is a rare cause of acute renal failure with poor prognosis. The various causes of oxalate nephropathy are categorized as primary or secondary hyperoxaluria. Primary hyperoxaluria is caused by genetic mutation in genes involved in the metabolism of glyoxylate. Secondary hyperoxaluria is caused by mal-absorptive state, excessive intake of oxalate-rich diet, inflammatory diseases, and medications such as orlistat and antibiotics. Diet-induced oxalate nephropathy is often identified after unexplained acute kidney injury in patients with underlying CKD. Definitive diagnosis requires renal biopsy as laboratory tests are non-specific. A simple dietary history in CKD patients during routine primary care visit may lead to early diagnosis and lead to prevention of acute renal failure and progression of renal disease.


Author(s):  
Nathalie Demoulin ◽  
Selda Aydin ◽  
Valentine Gillion ◽  
Johann Morelle ◽  
Michel Jadoul
Keyword(s):  

Pathogens ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1087
Author(s):  
Jasmine Hattab ◽  
Antonella Vulcano ◽  
Silvia D’Arezzo ◽  
Fabiana Verni ◽  
Pietro Giorgio Tiscar ◽  
...  

Equine pulmonary aspergillosis is a rare deep mycosis often due to the hematogenous spread of hyphae after gastrointestinal tract disease. We describe herein the main clinic-pathological findings observed in a foal, which spontaneously died after showing diarrhea and respiratory distress. Necropsy and histopathological investigations allowed to diagnose pulmonary aspergillosis, which likely developed after necrotic typhlitis-colitis. Biomolecular studies identified Aspergillus section Fumigati strain as the causative agent. Notably, severe oxalate nephrosis was concurrently observed. Occasionally, oxalate nephropathy can be a sequela of pulmonary aspergillosis in humans. The present case report suggests that the renal precipitation of oxalates can occur also in horses affected by pulmonary aspergillosis and could likely contribute to the fatal outcome of the disease.


Nephron ◽  
2021 ◽  
pp. 1-8
Author(s):  
Shaoshan Liang ◽  
Lijuan Li ◽  
Dacheng Chen ◽  
Dandan Liang ◽  
Feng Xu ◽  
...  

<b><i>Introduction:</i></b> Secondary oxalate nephropathy (OxN) is associated with a variety of causes and has not been well characterized in Chinese population. To investigate the etiology, clinicopathological features, and outcomes of secondary OxN, we report a case series from a single center in China. <b><i>Methods:</i></b> A retrospective analysis of 68 patients diagnosed with secondary OxN by renal biopsy from January 2013 to February 2019 in Jinling Hospital was performed. <b><i>Results:</i></b> Secondary OxN accounted for 0.23% of the renal biopsies and 2.31% of patients who received renal biopsies due to acute kidney injury (AKI). A total of 49 men and 19 women with an average age of 51.6 ± 11.8 years were enrolled. The most common cause was iatrogenic medication, followed by oxalate-rich diet and industry exposure. Stage 1, 2, and 3 AKI and AKI on chronic kidney disease (ACKD) were found in 4.4, 8.8, 69.1, and 17.6% of the patients, respectively. The peak serum creatinine during hospitalization was 8.62 ± 4.67 mg/dL. The median urinary oxalate excretion was 51.5 (23.2–147.1) mg/24 h. Kidney biopsy showed extensive calcium oxalate crystal deposits with acute tubulointerstitial nephritis. Thirty-four patients (50.0%) required renal replacement therapy. At the end of a follow-up that lasted 8.7 (0.1–72.1) months, 81.0% of patients achieved renal function recovery in 50 (14–432) days. Patients with renal function recovery had a lower rate of ACKD, a higher level of hemoglobin, a lower level of urine lysozyme, and a lower degree of interstitial fibrosis/tubular atrophy, interstitial inflammation, and global glomerulosclerosis than those in the nonrecovery group. <b><i>Conclusions:</i></b> In this case series of secondary OxN, the most common cause was iatrogenic medication, and it presented with AKI or ACKD. Half of the patients required renal replacement therapy, and in most of them, the renal function was reversible. Renal biopsy played an important role in diagnosis and prognosis evaluation.


2021 ◽  
Vol 30 (2) ◽  
pp. 183-185
Author(s):  
Tuba Elif Ozler ◽  
◽  
Egemen Cebeci ◽  
Yasemin Ozluk ◽  
Oktay Ozkan ◽  
...  

2021 ◽  
Vol 22 (12) ◽  
pp. 6204
Author(s):  
Chien-Lin Lu ◽  
Te-Yi Teng ◽  
Min-Tser Liao ◽  
Ming-Chieh Ma

Inflammation worsens oxalate nephropathy by exacerbating tubular damage. The transient receptor potential vanilloid 1 (TRPV1) channel is present in kidney and has a polymodal sensing ability. Here, we tested whether TRPV1 plays a role in hyperoxaluria-induced renal inflammation. In TRPV1-expressed proximal tubular cells LLC-PK1, oxalate could induce cell damage in a time- and dose-dependent manner; this was associated with increased arachidonate 12-lipoxygenase (ALOX12) expression and synthesis of endovanilloid 12(S)-hydroxyeicosatetraenoic acid for TRPV1 activation. Inhibition of ALOX12 or TRPV1 attenuated oxalate-mediated cell damage. We further showed that increases in intracellular Ca2+ and protein kinase C α activation are downstream of TRPV1 for NADPH oxidase 4 upregulation and reactive oxygen species formation. These trigger tubular cell inflammation via increased NLR family pyrin domain-containing 3 expression, caspase-1 activation, and interleukin (IL)-1β release, and were alleviated by TRPV1 inhibition. Male hyperoxaluric rats demonstrated urinary supersaturation, tubular damage, and oxidative stress in a time-dependent manner. Chronic TRPV1 inhibition did not affect hyperoxaluria and urinary supersaturation, but markedly reduced tubular damage and calcium oxalate crystal deposition by lowering oxidative stress and inflammatory signaling. Taking all these results together, we conclude that TRPV1 hyperfunction contributes to oxalate-induced renal inflammation. Blunting TRPV1 function attenuates hyperoxaluric nephropathy.


Author(s):  
Jordan Evans ◽  
Abhishek Pandya ◽  
Yanli Ding ◽  
Wajeh Y. Qunibi

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