Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

Cao, Yimei; Liu, Wanpeng; Hui, Limei; Zhao, Jianjun; Yang, Xuecheng; Wang, Yonghua; Niu, Haitao

doi:10.1007/s00240-016-0876-7

Cited by 10 publications

(7 citation statements)

References 26 publications

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“…It can be speculated that a decrease in GFR was not the only cause of oxalosis in patients with AKD, and that tubular injury itself may play an important role in promoting crystallization. Some researchers reported that ischemia-induced renal tubular epithelial cell injury accelerated the deposition of calcium oxalate crystals and aggravated the injury in an ethylene glycol-induced hyperoxaluria animal model [18]. In the present study, laboratory parameters re ecting the function of proximal tubules did not differ signi cantly among patients with different degrees of oxalate crystal deposition.…”

Section: Discussioncontrasting

confidence: 46%

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Zhou¹,

Yu²,

Tao³

et al. 2020

Preprint

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Backgrounds: This study aimed to summarize and analyze the clinicopathological features of acute kidney disease patients with renal oxalosis, to improve understanding of the disease characteristics. Methods: Data for patients with acute kidney disease (AKD) diagnosed from January 2011 to October 2018 and confirmed by renal biopsy showing oxalate crystal deposition were collected. The underlying diseases, dietary habits before disease onset, pathological characteristics of newly emerging kidney disease, renal oxalosis, and causes of AKD were analyzed. Urine volume, serum creatinine, uric acid, and electrolyte clearance were recorded. The long-term renal prognosis was observed. Results: A total of 23 patients with AKD and renal oxalosis were included. The patients comprised 18 men (78.3%) and 5 women (21.7%) with a mean age of 51.6 ± 15.9 years. The peak serum creatinine was 669.9 ± 299.8 μmol/L, and 95.7% of patients had stage 3 acute kidney injury. Drug-induced AKD was the most common cause (65.2%), followed by severe nephrotic syndrome (17.4%). Other causes included severe glomerulonephritis, and infection. All patients had pathological changes indicating tubulointerstitial disease (TIN), and 11 patients were complicated with newly emerging glomerular disease (GD). Oxalate deposits caused by increased enterogenous oxalate absorption accounted for 26.1%, and most of the causes came from new kidney diseases. Oxalate crystals were located in the renal tubule. The majority (75%) of moderate to severe oxalate crystal deposition occurred in patients without GD. There were no significant differences in the total score for acute tubulointerstitial injury, score for tubular injury (T-IS), and score for interstitial inflammation in patients with different severities of renal oxalosis. Rate of serum creatinine decrease (ΔScr%) was negatively correlated with severity of oxalosis (R = −0.542, P = 0.037), score for acute tubular injury (R = −0.553, P = 0.033), and age (R = −0.736, P = 0.002). ΔScr% at week 4 was correlated with T-IS (R = −0.433, P = 0.050), but was not correlated with severity of oxalosis. Conclusions: The present findings revealed that 95.7% of AKD cases with renal oxalosis occurred in critically ill patients, secondary to kidney injury with tubular injury, and that drug-induced AKD was the most common cause. Severe oxalosis contributed to delayed early recovery of renal function.

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Section: Discussioncontrasting

confidence: 46%

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Zhou¹,

Yu²,

Tao³

et al. 2020

Preprint

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“…Severe acute tubular necrosis can also promote formation of calcium oxalate crystals in renal tissue [14]. Progressive ATN may therefore have played a role in the severity of oxalate deposition in this case.…”

Section: Discussionmentioning

confidence: 99%

Accelerated Oxalosis Contributing to Delayed Graft Function after Renal Transplantation

Kelly

Weins

Yeung

2019

Case Reports in Transplantation

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Hyperoxaluria is an important and underrecognized cause for allograft dysfunction and loss after transplantation. It is potentially treatable if recognized in a timely fashion. Research is ongoing to expand the array of therapeutic options available to treat this. We present a case of a 59-year-old gentleman who underwent deceased donor renal transplantation that was complicated by delayed graft function necessitating continuation of renal replacement therapy. His initial biopsy showed extensive acute tubular necrosis with associated peritubular capillaritis and interstitial nephritis and oxalate crystals in several tubules. Despite receiving methylprednisolone to treat moderate acute cellular rejection, he remained dialysis dependent with minimal urine output. An interval renal allograft biopsy revealed residual acute tubular necrosis with extensive oxalate crystals now visible in many tubules. His plasma oxalate level was concurrently elevated to 19.3 μmol/L (reference range ≤ 1.9 μmol/L). He commenced calcium citrate to manage his hyperoxaluria and ultimately became dialysis independent at 3 weeks after transplantation. This case provides an important example of accelerated oxalate nephropathy as an underappreciated contributor to delayed graft function after renal transplantation. Our accompanying discussion provides an update on current therapeutic measures for managing this challenging condition.

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“…Consequently, the excess mitochondrial free radicals can damage mitochondrial membranes (MIM and MOM). As a result, mitochondrial ROS, cytochrome c, calcium, and other proinflammatory factors are further released to the cytoplasm (Cao et al, 2016;Fong-Ngern et al, 2017). High level of cytoplasmic ROS can induce lipid peroxidation, which damages cell membranes and further enhances crystal deposition on apical surfaces of renal tubular cells (Cao et al, 2016;Fong-Ngern et al, 2017).…”

Section: Mechanism Imentioning

confidence: 99%

“…As a result, mitochondrial ROS, cytochrome c, calcium, and other proinflammatory factors are further released to the cytoplasm (Cao et al, 2016;Fong-Ngern et al, 2017). High level of cytoplasmic ROS can induce lipid peroxidation, which damages cell membranes and further enhances crystal deposition on apical surfaces of renal tubular cells (Cao et al, 2016;Fong-Ngern et al, 2017). Additionally, apoptotic signaling cascades are activated by cytochrome c that also upsurges renal tubular cell injury, leading to crystal adhesion and intrarenal crystal retention (Cao et al, 2016;Fong-Ngern et al, 2017).…”

Section: Mechanism Imentioning

confidence: 99%

“…High level of cytoplasmic ROS can induce lipid peroxidation, which damages cell membranes and further enhances crystal deposition on apical surfaces of renal tubular cells (Cao et al, 2016;Fong-Ngern et al, 2017). Additionally, apoptotic signaling cascades are activated by cytochrome c that also upsurges renal tubular cell injury, leading to crystal adhesion and intrarenal crystal retention (Cao et al, 2016;Fong-Ngern et al, 2017). The accumulated crystals can be further enlarged and self-aggregated, leading to the stone formation (Figure 1).…”

Section: Mechanism Imentioning

confidence: 99%

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Mitochondrial Dysfunction and Kidney Stone Disease

Chaiyarit

Thongboonkerd

2020

Front. Physiol.

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Mitochondrion is a pivotal intracellular organelle that plays crucial roles in regulation of energy production, oxidative stress, calcium homeostasis, and apoptosis. Kidney stone disease (nephrolithiasis/urolithiasis), particularly calcium oxalate (CaOx; the most common type), has been shown to be associated with oxidative stress and tissue inflammation/ injury. Recent evidence has demonstrated the involvement of mitochondrial dysfunction in CaOx crystal retention and aggregation as well as Randall's plaque formation, all of which are the essential mechanisms for kidney stone formation. This review highlights the important roles of mitochondria in renal cell functions and provides the data obtained from previous investigations of mitochondria related to kidney stone disease. In addition, mechanisms for the involvement of mitochondrial dysfunction in the pathophysiology of kidney stone disease are summarized. Finally, future perspectives on the novel approach to prevent kidney stone formation by mitochondrial preservation are discussed.

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Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

Cited by 10 publications

References 26 publications

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Accelerated Oxalosis Contributing to Delayed Graft Function after Renal Transplantation

Mitochondrial Dysfunction and Kidney Stone Disease

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