Mineralocorticoid receptor blockade with spironolactone has no direct effect on plasma IL-17A and injury markers in urine from kidney transplant patients

Thangaraj, Sai Sindhu; Thiesson, Helle C.; Svenningsen, Per; Stubbe, Jane; Palarasah, Yaseelan; Bistrup, Claus; Jensen, Boye L.; Mortensen, Line Aas

doi:10.1152/ajprenal.00104.2021

Cited by 3 publications

(3 citation statements)

References 61 publications

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“…Of note, in this trial, MR antagonism led to a statistically significant increase in serum potassium levels ( p ‐value <.001) 24 . Coherently with these findings, another post hoc analysis study in the same trial failed to impact several inflammatory parameters, including tumour necrosis factor‐alpha, interleukin‐6/17A/10 or urine calbindin‐to‐creatinine, clusterin‐to‐creatinine, kidney injury molecule‐1‐tocreatinine, osteoactivin‐to‐creatinine, trefoil factor 3 (TFF3)‐to‐creatinine and VEGF‐to creatinine ratios 25 . A meta‐analysis by Abdelhakim et al.…”

Section: Renoprotective Effects Of Mra Agents In Kidney Transplant Re...mentioning

confidence: 85%

“…24 Coherently with these findings, another post hoc analysis study in the same trial failed to impact several inflammatory parameters, including tumour necrosis factor-alpha, interleukin-6/17A/10 or urine calbindin-to-creatinine, clusterin-to-creatinine, kidney injury molecule-1-tocreatinine, osteoactivin-to-creatinine, trefoil factor 3 (TFF3)-to-creatinine and VEGF-to creatinine ratios. 25 A meta-analysis by Abdelhakim et al in 2020 26 Clearly, further studies are required for a definitive conclusion regarding MR antagonism on kidney function.…”

Section: Reduction In Oxidative Stressmentioning

confidence: 99%

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Mineralocorticoid receptor antagonists in kidney transplantation

Kanbay,

Copur,

Mizrak

et al. 2024

Eur J Clin Investigation

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BackgroundThe fundamental role of the renin–angiotensin–aldosterone system in the pathophysiology of chronic kidney disease, congestive heart failure, hypertension and proteinuria is well established in pre‐clinical and clinical studies. Mineralocorticoid receptor antagonists are among the primary options for renin–angiotensin–aldosterone system blockage, along with angiotensin‐converting enzyme inhibitors and angiotensin receptor blockers.MethodsIn this narrative review, we aim to evaluate the efficiency and safety of mineralocorticoid receptor antagonists in kidney transplant recipients, including the potential underlying pathophysiology.ResultsThe efficiency and safety of mineralocorticoid receptor antagonists in managing chronic kidney disease and proteinuria, either non‐nephrotic or nephrotic range, have been demonstrated among nontransplanted patients, though studies investigating the role of mineralocorticoid receptor antagonists among kidney transplant recipients are scarce. Nevertheless, promising results have been reported in pre‐clinical and clinical studies among kidney transplant recipients regarding the role of mineralocorticoid receptor antagonists in terms of ischaemia–reperfusion injury, proteinuria, or calcineurin inhibitor‐mediated nephrotoxicity without considerable adverse events such as hypotension, hyperkalaemia or worsening renal functions.ConclusionEven though initial results regarding the role of mineralocorticoid receptor antagonist therapy for kidney transplant recipients are promising, there is clear need for large‐scale randomized clinical trials with long‐term follow‐up data.

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Section: Renoprotective Effects Of Mra Agents In Kidney Transplant Re...mentioning

confidence: 85%

Section: Reduction In Oxidative Stressmentioning

confidence: 99%

Mineralocorticoid receptor antagonists in kidney transplantation

Kanbay,

Copur,

Mizrak

et al. 2024

Eur J Clin Investigation

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“…These biomarkers include Neutrophil Gelatinase-Associated Lipocalin (NGAL), Vascular Endothelial Growth Factor (VEGF), Osteoactivin, Kidney Injury Molecule-1 (KIM-1), Trefoil factor 3 (TFF3), Clusterin, and Calbindin. Each of these biomarkers plays a distinct role in kidney physiology and is expressed in the specific tubular or interstitial component of the kidney [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of low pneumoperitoneum on renal function and acute kidney injury biomarkers during robot-assisted radical prostatectomy (RARP): a randomised clinical trial

Alhusseinawi,

Sander,

Handberg

et al. 2024

J Robotic Surg

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The objective of this study was to evaluate the effect of low pneumoperitoneum pressure (Pnp) on renal function and renal injury biomarkers during robot-assisted radical prostatectomy (RARP). A single-centre, triple-blinded, randomised clinical trial was conducted with 98 patients undergoing RARP, who were assigned to either standard Pnp of 12 mmHg or low Pnp of 7 mmHg. The primary outcome was urinary neutrophil gelatinase-associated lipocalin (u-NGAL), and several other kidney injury biomarkers were assessed as secondary outcomes. Acute kidney injury (AKI) was evaluated using the Kidney Disease Improving Global Outcomes (KDIGO) criteria, the gold standard method for defining AKI. The trial was registered on ClinicalTrials.gov (NCT04755452). Patients in the low Pnp group had significantly lower levels of u-NGAL (mean difference − 39.9, 95% CI − 73.7 to − 6.1, p = 0.02) compared to the standard Pnp group. No significant differences were observed for other urinary biomarkers. Interestingly, there was a significant difference in intraoperative urine production between the groups (low Pnp median: 200 mL, IQR: 100–325 vs. standard Pnp median: 100 mL, IQR: 50–200, p = 0.01). Similarly, total postoperative urine production also varied significantly (low Pnp median: 1325 mL, IQR: 1025–1800 vs. standard Pnp median: 1000 mL, IQR: 850–1287, p = 0.001). The occurrence of AKI, as defined by the KDIGO criteria, did not differ significantly between the groups. Low Pnp during RARP resulted in lower u-NGAL levels, suggesting a potential benefit in terms of reduced renal injury. However, the lack of a notable difference in AKI as defined by the KDIGO criteria indicates that the clinical significance of this finding may be limited. Further research is needed to validate and expand on these results, ultimately defining the optimal Pnp strategy for RARP and improving patient outcomes.

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