Combining Acute Kidney Injury with Gastrointestinal Pathology: A Clue to Acute Oxalate Nephropathy

Fox, Benjamin; Saxena, Nishkarsh; Schuppener, Leah M.; Maursetter, Laura

doi:10.1155/2018/8641893

Cited by 3 publications

(3 citation statements)

References 14 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During the acute supersaturation phase, CaOx complexes are the most common type of kidney stone, which was initially referred to as type 2 crystalline nephropathy ( Mulay et al, 2018 ). Under this condition, tubular injury is associated with crystals and/or Tamm–Horsfall protein (THP) complexes, apoptotic and inflammatory responses consistent with acute kidney injury (AKI), in addition to the risk for recurrence and/or chronic kidney disease (CKD) progression ( Lorenz et al, 2014 ; Pfau and Knauf, 2016 ; Fox et al, 2018 ; Mulay et al, 2018 ; Efe et al, 2019 ). However, clinical evidence and experimental models of ischemia-reperfusion have revealed that frequently, the recovery of renal function after AKI is incomplete and accompanied by proteinuria, tubular injury and glomerular filtration rate (GFR) decline, leading to end-stage renal disease (ESRD) ( Hingorani et al, 2009 ; Basile et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Sodium Oxalate-Induced Acute Kidney Injury Associated With Glomerular and Tubulointerstitial Damage in Rats

et al. 2020

View full text Add to dashboard Cite

Acute crystalline nephropathy is closely related to tubulointerstitial injury, but few studies have investigated glomerular changes in this condition. Thus, in the current study, we investigated the factors involved in glomerular and tubulointerstitial injury in an experimental model of crystalline-induced acute kidney injury (AKI). We treated male Wistar rats with a single injection of sodium oxalate (NaOx, 7 mg•100 g −1 •day −1 , resuspended in 0.9% NaCl solution, i.p.) or vehicle (control). After 24 h of treatment, food and water intake, urine output, body weight gain, and renal function were evaluated. Renal tissue was used for the morphological studies, quantitative PCR and protein expression studies. Our results revealed that NaOx treatment did not change metabolic or electrolyte and water intake parameters or urine output. However, the treated group exhibited tubular calcium oxalate (CaOx) crystals excretion, followed by a decline in kidney function demonstrated along with glomerular injury, which was confirmed by increased plasma creatinine and urea concentrations, increased glomerular desmin immunostaining, nephrin mRNA expression and decreased WT1 immunofluorescence. Furthermore, NaOx treatment resulted in tubulointerstitial injury, which was confirmed by tubular dilation, albuminuria, increased Kim-1 and Ki67 mRNA expression, decreased megalin and Tamm-Horsfall protein (THP) expression. Finally, the treatment induced increases in CD68 protein staining, MCP-1, IL-1β, NFkappaB, and α-SMA mRNA expression, which are consistent with proinflammatory and profibrotic signaling, respectively. In conclusion, our findings provide relevant information regarding crystalline-induced AKI, showing strong tubulointerstitial and glomerular injury with a possible loss of podocyte viability.

show abstract

Section: Introductionmentioning

confidence: 99%

Sodium Oxalate-Induced Acute Kidney Injury Associated With Glomerular and Tubulointerstitial Damage in Rats

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Furthermore, in vitro studies showed that prostaglandins may decrease the adhesion ability of calcium oxalate to renal epithelial cells ( 25 , 26 ). As NSAIDs downregulate prostaglandin production ( 27 ), it is feasible to speculate that NSAID use is predisposed to a greater likelihood of adhesion of oxalate crystals to the tubular epithelium. In this regard, we hypothesize that factors, which either decrease urinary flow in renal tubules or increase the adhesion ability of oxalate crystals to the epithelium, contribute convergently to the development of acute oxalate nephropathy when superimposed on hyperoxaluria in DM.…”

Section: Discussionmentioning

confidence: 99%

Acute oxalate nephropathy: A potential cause of acute kidney injury in diabetes mellitus—A case series from a single center

Bao

Wang

et al. 2022

Front. Med.

View full text Add to dashboard Cite

BackgroundAcute oxalate nephropathy (AON) is an uncommon condition that causes acute kidney injury (AKI), characterized by the massive deposition of calcium oxalate crystals in the renal parenchyma. In previous studies, urinary oxalate excretion has been found to be increased in patients with diabetes mellitus (DM). Here, we report a case series of diabetic patients with AKI with biopsy-proven AON, aiming to alert physicians to the potential of AON as a trigger of AKI in diabetic patients in clinical practice.Materials and methodsCases with pathological diagnosis of AON who presented with AKI clinically and had DM between January 2016 and December 2020 were retrospectively enrolled. Their clinical and pathological manifestations, treatment, and prognosis were collected.ResultsSix male patients with biopsy-proven AON out of a total of 5,883 native kidney biopsies were identified, aged 58.3 ± 9.1 years at the time of kidney biopsy. Only one patient who had received Roux-en-Y gastric bypass surgery took oxalate-rich food before the onset of the disease. None of them had clinical features of enteric malabsorption. Three patients were currently on renin-angiotensin system inhibitor treatment for hypertension, and 5 of them received non-steroidal anti-inflammatory drugs. Three patients presented with oliguria and 4 patients needed dialysis at the beginning with none requiring dialysis at discharge. Four patients received a course of corticosteroid treatment empirically. Among them, two patients had estimated glomerular filtration rate (eGFR) recovered to over 60 ml/min/1.73 m2, while the other two patients remained with kidney dysfunction at the last follow-up. In two patients without corticosteroid treatment, one patient fully recovered with eGFR over 90 ml/min/1.73 m2 and the other patient remained with kidney dysfunction at the last follow-up.ConclusionAON might be a rare but potentially trigger of AKI in patients with DM. A kidney biopsy could help physicians to make the correct diagnosis. The proper treatment to alleviate oxalate-induced injury needs to be further studied.

show abstract

“…Prostaglandins may decrease calcium oxalate adhesion to renal epithelial cells [ 58 , 59 ]. Nonsteroidal anti-inflammatory drugs downregulate prostaglandin production; therefore, it is feasible that Nonsteroidal anti-inflammatory drugs predispose to a greater likelihood of stone formation [ 60 ]. Furthermore, proteins such as osteopontin are also constantly embedded in the interstitium in the CaOx formation progress, which binds to CD44, a membrane-bound glycoprotein on proximal renal tubular epithelial cells.…”

Section: Oxalate Nephropathy and Kidney Injurymentioning

confidence: 99%

Oxalate Nephropathy and the Mechanism of Oxalate-Induced Kidney Injury

Bao¹,

Wang²,

Zhao³

2023

Kidney Dis

View full text Add to dashboard Cite

Background Hyperoxaluria is a major cause of oxalate nephropathy, which can lead to impaired renal function presenting as acute kidney injury, acute chronic kidney disease, or chronic kidney disease. The Chronic Renal Insufficiency Cohort study showed that higher urinary oxalate is associated with renal outcome in patients with chronic kidney disease, supporting the nephrotoxicity of oxalate. Therefore, a better understanding of the role of oxalate in kidney injury is needed. This review describes the metabolism of oxalate and the clinical and pathology presentation of oxalate nephropathy. It also summarizes the available evidence for the underlying pathogenic mechanism and the development of treatments for oxalate-induced kidney injury. Summary Disruption to any key step in the oxalate pathway including abnormal endogenous generation, ingestion of abnormally high dose of oxalate, increased absorption or attenuation of oxalate degradation in the gut, and reduced excretion through the kidney, may lead to disrupted oxalate homeostasis. Oxalate nephropathy is mainly caused by hyperoxaluria. Oxalate crystal deposition in the kidney is usually accompanied with tubular toxicity, obstruction, interstitial fibrosis and tubular atrophy. The mechanism of oxalate-induced renal injury has not been fully clarified. Evidence from both in vivo and in vitro studies shows that NLRP3 inflammasome activation and macrophage infiltration are involved in the processes of crystals adhesion, aggregation, and elimination and promote intrarenal inflammation and renal fibrosis. Novel treatment strategies have been developed and targeted therapies tested for oxalate nephropathy. Key Messages Prompt diagnosis and management may help to reduce the deposition of calcium oxalate crystals in the kidney. Further studies are needed to clarify the underlying mechanisms to help develop more targeted therapies for oxalate nephropathy.

show abstract

Combining Acute Kidney Injury with Gastrointestinal Pathology: A Clue to Acute Oxalate Nephropathy

Cited by 3 publications

References 14 publications

Sodium Oxalate-Induced Acute Kidney Injury Associated With Glomerular and Tubulointerstitial Damage in Rats

Sodium Oxalate-Induced Acute Kidney Injury Associated With Glomerular and Tubulointerstitial Damage in Rats

Acute oxalate nephropathy: A potential cause of acute kidney injury in diabetes mellitus—A case series from a single center

Oxalate Nephropathy and the Mechanism of Oxalate-Induced Kidney Injury

Contact Info

Product

Resources

About