Inflammation and kidney stones: cause and effect?

Capolongo, Giovanna; Ferraro, Manuel; Unwin, Robert J.

doi:10.1097/mou.0000000000001066

Cited by 9 publications

(8 citation statements)

References 57 publications

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“…A variety of processes including supersaturation of urinary stone components, reduction of inhibitors of stone formation (Cicerello et al, 2019 ), and renal tubular epithelial cell injury (Aggarwal et al, 2013 ) are involved. Metabolism and inflammation are considered important factors involved in the formation of renal stones (Tian et al, 2022 ; Capolongo et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Causal relationship in gut microbiota and upper urinary urolithiasis using Mendelian randomization

Zhang

Zhao

et al. 2023

Front. Microbiol.

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BackgroundSeveral reports in recent years have found an association between gut microbiota and upper urinary urolithiasis. However, the causal relationship between them remains to be clarified.MethodsGenetic variation is used as a tool in Mendelian randomization for inference of whether exposure factors have a causal effect on disease outcomes. We selected summary statistics from a large genome-wide association study of the gut microbiome published by the MiBioGen consortium with a sample size of 18,340 as an exposure factor and upper urinary urolithiasis data from FinnGen GWAS with 4,969 calculi cases and 213,445 controls as a disease outcome. Then, a two-sample Mendelian randomization analysis was performed by applying inverse variance-weighted, MR-Egger, maximum likelihood, and weighted median. In addition, heterogeneity and horizontal pleiotropy were excluded by sensitivity analysis.ResultsIVW results confirmed that class Deltaproteobacteria (OR = 0.814, 95% CI: 0.666–0.995, P = 0.045), order NB1n (OR = 0.833, 95% CI: 0.737–0.940, P = 3.15 × 10−3), family Clostridiaceae1 (OR = 0.729, 95% CI: 0.581–0.916, P = 6.61 × 10−3), genus Barnesiella (OR = 0.695, 95% CI: 0.551–0.877, P = 2.20 × 10−3), genus Clostridium sensu_stricto_1 (OR = 0.777, 95% CI: 0.612–0.986, P = 0.0380), genus Flavonifractor (OR = 0.711, 95% CI: 0.536–0.944, P = 0.0181), genus Hungatella (OR = 0.829, 95% CI: 0.690–0.995, P = 0.0444), and genus Oscillospira (OR = 0.758, 95% CI: 0.577–0.996, P = 0.0464) had a protective effect on upper urinary urolithiasis, while Eubacterium xylanophilum (OR =1.26, 95% CI: 1.010–1.566, P = 0.0423) had the opposite effect. Sensitivity analysis did not find outlier SNPs.ConclusionIn summary, a causal relationship was found between several genera and upper urinary urolithiasis. However, we still need further randomized controlled trials to validate.

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Section: Introductionmentioning

confidence: 99%

Causal relationship in gut microbiota and upper urinary urolithiasis using Mendelian randomization

Zhang

Zhao

et al. 2023

Front. Microbiol.

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“…Studies have demonstrated that renal stones can cause inflammation, which can in turn lead to stone recurrence. In this way, a toxic cycle of kidney tissue injury and recurrent stone formation ensues [ 12 ]. Kidney stones can cause oxidative stress and trigger an inflammatory response with the release of pro-inflammatory cytokines like IL-1β and IL18 [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Renal Artery Thrombosis Leading to Renal Infarct in a Patient With Recurrent Nephrolithiasis

Vedire¹,

Imburgio²,

Chakrabarti³

et al. 2023

Cureus

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Renal infarction is a rare entity that presents similarly to other common renal conditions such as nephrolithiasis, which can often result in a missed or delayed diagnosis. As a result, a high degree of suspicion for this diagnosis is warranted in patients presenting with flank pain. We present a patient with recurrent nephrolithiasis who presented with flank pain. A subsequent workup revealed a renal infarct due to underlying renal artery thrombosis. We also explore if there was a possible mechanism between this event and his history of recurrent nephrolithiasis.

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“…Renal papilla specimens from patients with RPs exhibit extensive cell damage and interstitial fibrosis surrounding the crystal blockages, with the stone matrix containing inflammation‐related proteins 40,81 . Basic studies examining renal epithelial cell responses to high concentration of oxalate or CaOx crystals and animal models of hyperoxaluria‐induced CaOx crystal deposition have further highlighted the importance of oxidative stress and inflammation 82–84 . Overwhelming oxidative stress and inflammatory responses can lead to the expression of molecules involved in crystal binding, disruption of tight junctions, injury, cell death and shedding in RTECs 77,82 .…”

Section: Oxidative Stress and Inflammationmentioning

confidence: 99%

“… 40 , 81 Basic studies examining renal epithelial cell responses to high concentration of oxalate or CaOx crystals and animal models of hyperoxaluria‐induced CaOx crystal deposition have further highlighted the importance of oxidative stress and inflammation. 82 , 83 , 84 Overwhelming oxidative stress and inflammatory responses can lead to the expression of molecules involved in crystal binding, disruption of tight junctions, injury, cell death and shedding in RTECs. 77 , 82 Additionally, oxidative stress and inflammation mediate the polarization of macrophages, collagen mineralization, macrophage‐mediated stone clearance, interstitial fibrosis and the formation of RPs in the kidney interstitium.…”

Section: Oxidative Stress and Inflammationmentioning

confidence: 99%

Understanding formation processes of calcareous nephrolithiasis in renal interstitium and tubule lumen

Dong,

Zhou,

et al. 2024

J Cellular Molecular Medi

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Kidney stone, one of the oldest known diseases, has plagued humans for centuries, consistently imposing a heavy burden on patients and healthcare systems worldwide due to their high incidence and recurrence rates. Advancements in endoscopy, imaging, genetics, molecular biology and bioinformatics have led to a deeper and more comprehensive understanding of the mechanism behind nephrolithiasis. Kidney stone formation is a complex, multi‐step and long‐term process involving the transformation of stone‐forming salts from free ions into asymptomatic or symptomatic stones influenced by physical, chemical and biological factors. Among the various types of kidney stones observed in clinical practice, calcareous nephrolithiasis is currently the most common and exhibits the most intricate formation mechanism. Extensive research suggests that calcareous nephrolithiasis primarily originates from interstitial subepithelial calcified plaques and/or calcified blockages in the openings of collecting ducts. These calcified plaques and blockages eventually come into contact with urine in the renal pelvis, serving as a nidus for crystal formation and subsequent stone growth. Both pathways of stone formation share similar mechanisms, such as the drive of abnormal urine composition, involvement of oxidative stress and inflammation, and an imbalance of stone inhibitors and promoters. However, they also possess unique characteristics. Hence, this review aims to provide detailed description and present recent discoveries regarding the formation processes of calcareous nephrolithiasis from two distinct birthplaces: renal interstitium and tubule lumen.

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Inflammation and kidney stones: cause and effect?

Cited by 9 publications

References 57 publications

Causal relationship in gut microbiota and upper urinary urolithiasis using Mendelian randomization

Causal relationship in gut microbiota and upper urinary urolithiasis using Mendelian randomization

Renal Artery Thrombosis Leading to Renal Infarct in a Patient With Recurrent Nephrolithiasis

Understanding formation processes of calcareous nephrolithiasis in renal interstitium and tubule lumen

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