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02.02.2022 | Nephrology - Original Paper

Leonurine attenuates cisplatin nephrotoxicity by suppressing the NLRP3 inflammasome, mitochondrial dysfunction, and endoplasmic reticulum stress

verfasst von: Qi Zhang, Qiuhong Sun, Yan Tong, Xiao Bi, Lin Chen, Jianxin Lu, Wei Ding

Erschienen in: International Urology and Nephrology | Ausgabe 9/2022

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Abstract

Purpose

Cisplatin has been widely accepted as an effective chemotherapy drug with various side effects, including nephrotoxicity. The mechanisms of cisplatin-induced acute kidney injury (AKI) are complex, and there are limited renoprotective approaches. Leonurine is the main active compound of a Chinese herb and has recently been reported to have a protective effect on the kidneys. This study aimed to verify the renoprotective effect of leonurine in attenuating cisplatin-induced AKI and explore the potential associated mechanisms.

Methods

C57BL/6 mice were divided into four groups (Sham, Cisplatin, Leonurine, and Cisplatin + Leonurine). Mice in the leonurine-treated groups were pretreated with a daily intraperitoneal injection of 25 mg/kg leonurine. AKI was induced by injecting cisplatin once intraperitoneally at 20 mg/kg body weight. Mice were killed on day 5. Kidney injury was assessed using a serum biochemical and histological assay. Apoptosis was evaluated using a terminal deoxyribonucleotide transferase-mediated dUTP nick-end labeling (TUNEL) staining assay and Western blot. Antioxidant enzymes were detected using commercial kits. The improvement in inflammasome activation, mitochondrial dysfunction, and endoplasmic reticulum stress (ERS) were assessed by polymerase chain reaction (PCR) and Western blot, respectively.

Results

Leonurine treatment improved kidney function by preventing renal tubular injury and apoptosis. Expression of nucleotide-binding leucine-rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome components and inflammatory cytokines, mitochondrial dysfunction, and ERS were all alleviated by leonurine.

Conclusion

The results indicate that leonurine plays a protective role in cisplatin-induced AKI and may represent an effective multi-targeted intervention strategy.
Literatur
2.
Zurück zum Zitat Wang D, Lippard SJ (2005) Cellular processing of platinum anticancer drugs. Nat Rev Drug Discov 4(4):307–320PubMedCrossRef Wang D, Lippard SJ (2005) Cellular processing of platinum anticancer drugs. Nat Rev Drug Discov 4(4):307–320PubMedCrossRef
3.
Zurück zum Zitat Kociba RJ, Sleight SD (1971) Acute toxicologic and pathologic effects of cis-diamminedichloroplatinum (NSC-119875) in the male rat. Cancer Chemother Rep 55(1):1–8PubMed Kociba RJ, Sleight SD (1971) Acute toxicologic and pathologic effects of cis-diamminedichloroplatinum (NSC-119875) in the male rat. Cancer Chemother Rep 55(1):1–8PubMed
4.
Zurück zum Zitat Goldstein RS, Mayor GH (1983) Minireview. The nephrotoxicity of cisplatin. Life Sci 32(7):685–690PubMedCrossRef Goldstein RS, Mayor GH (1983) Minireview. The nephrotoxicity of cisplatin. Life Sci 32(7):685–690PubMedCrossRef
6.
Zurück zum Zitat Pabla N, Dong Z (2008) Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. Kidney Int 73(9):994–1007PubMedCrossRef Pabla N, Dong Z (2008) Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. Kidney Int 73(9):994–1007PubMedCrossRef
7.
Zurück zum Zitat Bajwa A et al (2015) Sphingosine 1-phosphate receptor-1 enhances mitochondrial function and reduces cisplatin-induced tubule injury. J Am Soc Nephrol 26(4):908–925PubMedCrossRef Bajwa A et al (2015) Sphingosine 1-phosphate receptor-1 enhances mitochondrial function and reduces cisplatin-induced tubule injury. J Am Soc Nephrol 26(4):908–925PubMedCrossRef
8.
Zurück zum Zitat Guo Y et al (2018) MicroRNA-709 mediates acute tubular injury through effects on mitochondrial function. J Am Soc Nephrol 29(2):449–461PubMedCrossRef Guo Y et al (2018) MicroRNA-709 mediates acute tubular injury through effects on mitochondrial function. J Am Soc Nephrol 29(2):449–461PubMedCrossRef
9.
Zurück zum Zitat Un H et al (2020) Phloretin and phloridzin guard against cisplatin-induced nephrotoxicity in mice through inhibiting oxidative stress and inflammation. Life Sci 266:118869PubMedCrossRef Un H et al (2020) Phloretin and phloridzin guard against cisplatin-induced nephrotoxicity in mice through inhibiting oxidative stress and inflammation. Life Sci 266:118869PubMedCrossRef
11.
Zurück zum Zitat Xu Y et al (2019) Prohibitin 2-mediated mitophagy attenuates renal tubular epithelial cells injury by regulating mitochondrial dysfunction and NLRP3 inflammasome activation. Am J Physiol Renal Physiol 316(2):F396–F407PubMedCrossRef Xu Y et al (2019) Prohibitin 2-mediated mitophagy attenuates renal tubular epithelial cells injury by regulating mitochondrial dysfunction and NLRP3 inflammasome activation. Am J Physiol Renal Physiol 316(2):F396–F407PubMedCrossRef
12.
Zurück zum Zitat Bi X et al (2018) MnTBAP treatment ameliorates aldosterone-induced renal injury by regulating mitochondrial dysfunction and NLRP3 inflammasome signalling. Am J Transl Res 10(11):3504–3513PubMedPubMedCentral Bi X et al (2018) MnTBAP treatment ameliorates aldosterone-induced renal injury by regulating mitochondrial dysfunction and NLRP3 inflammasome signalling. Am J Transl Res 10(11):3504–3513PubMedPubMedCentral
13.
Zurück zum Zitat Jiang S et al (2020) Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway. J Steroid Biochem Mol Biol 206:105789PubMedCrossRef Jiang S et al (2020) Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway. J Steroid Biochem Mol Biol 206:105789PubMedCrossRef
14.
Zurück zum Zitat Yang SK et al (2020) Mitochondria targeted peptide SS-31 prevent on cisplatin-induced acute kidney injury via regulating mitochondrial ROS-NLRP3 pathway. Biomed Pharmacother 130:110521PubMedCrossRef Yang SK et al (2020) Mitochondria targeted peptide SS-31 prevent on cisplatin-induced acute kidney injury via regulating mitochondrial ROS-NLRP3 pathway. Biomed Pharmacother 130:110521PubMedCrossRef
15.
Zurück zum Zitat Li S et al (2019) NLRP3 inflammasome inhibition attenuates cisplatin-induced renal fibrosis by decreasing oxidative stress and inflammation. Exp Cell Res 383(1):111488PubMedCrossRef Li S et al (2019) NLRP3 inflammasome inhibition attenuates cisplatin-induced renal fibrosis by decreasing oxidative stress and inflammation. Exp Cell Res 383(1):111488PubMedCrossRef
16.
Zurück zum Zitat Gao H et al (2020) Omeprazole attenuates cisplatin-induced kidney injury through suppression of the TLR4/NF-kappaB/NLRP3 signaling pathway. Toxicology 440:152487PubMedCrossRef Gao H et al (2020) Omeprazole attenuates cisplatin-induced kidney injury through suppression of the TLR4/NF-kappaB/NLRP3 signaling pathway. Toxicology 440:152487PubMedCrossRef
17.
Zurück zum Zitat Cybulsky AV (2017) Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases. Nat Rev Nephrol 13(11):681–696PubMedCrossRef Cybulsky AV (2017) Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases. Nat Rev Nephrol 13(11):681–696PubMedCrossRef
19.
Zurück zum Zitat Liu H, Baliga R (2005) Endoplasmic reticulum stress-associated caspase 12 mediates cisplatin-induced LLC-PK1 cell apoptosis. J Am Soc Nephrol 16(7):1985–1992PubMedCrossRef Liu H, Baliga R (2005) Endoplasmic reticulum stress-associated caspase 12 mediates cisplatin-induced LLC-PK1 cell apoptosis. J Am Soc Nephrol 16(7):1985–1992PubMedCrossRef
20.
Zurück zum Zitat Peyrou M et al (2007) Cisplatin, gentamicin, and p-aminophenol induce markers of endoplasmic reticulum stress in the rat kidneys. Toxicol Sci 99(1):346–353PubMedCrossRef Peyrou M et al (2007) Cisplatin, gentamicin, and p-aminophenol induce markers of endoplasmic reticulum stress in the rat kidneys. Toxicol Sci 99(1):346–353PubMedCrossRef
21.
Zurück zum Zitat Zhang Y et al (2012) SCM-198 attenuates early atherosclerotic lesions in hypercholesterolemic rabbits via modulation of the inflammatory and oxidative stress pathways. Atherosclerosis 224(1):43–50PubMedCrossRef Zhang Y et al (2012) SCM-198 attenuates early atherosclerotic lesions in hypercholesterolemic rabbits via modulation of the inflammatory and oxidative stress pathways. Atherosclerosis 224(1):43–50PubMedCrossRef
22.
Zurück zum Zitat Xu D et al (2014) Leonurine ameliorates LPS-induced acute kidney injury via suppressing ROS-mediated NF-kappaB signaling pathway. Fitoterapia 97:148–155PubMedCrossRef Xu D et al (2014) Leonurine ameliorates LPS-induced acute kidney injury via suppressing ROS-mediated NF-kappaB signaling pathway. Fitoterapia 97:148–155PubMedCrossRef
23.
Zurück zum Zitat Cheng H et al (2015) Leonurine ameliorates kidney fibrosis via suppressing TGF-beta and NF-kappaB signaling pathway in UUO mice. Int Immunopharmacol 25(2):406–415PubMedCrossRef Cheng H et al (2015) Leonurine ameliorates kidney fibrosis via suppressing TGF-beta and NF-kappaB signaling pathway in UUO mice. Int Immunopharmacol 25(2):406–415PubMedCrossRef
24.
Zurück zum Zitat Liu X et al (2018) Leonurine ameliorates adriamycin-induced podocyte injury via suppression of oxidative stress. Free Radic Res 52(9):952–960PubMedCrossRef Liu X et al (2018) Leonurine ameliorates adriamycin-induced podocyte injury via suppression of oxidative stress. Free Radic Res 52(9):952–960PubMedCrossRef
25.
Zurück zum Zitat Liu Y et al (2018) Inhibition of COX-2/mPGES-1 and 5-LOX in macrophages by leonurine ameliorates monosodium urate crystal-induced inflammation. Toxicol Appl Pharmacol 351:1–11PubMedCrossRef Liu Y et al (2018) Inhibition of COX-2/mPGES-1 and 5-LOX in macrophages by leonurine ameliorates monosodium urate crystal-induced inflammation. Toxicol Appl Pharmacol 351:1–11PubMedCrossRef
26.
Zurück zum Zitat Lieberthal W et al (1996) Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis. Am J Physiol 270(4 Pt 2):F700–F708PubMed Lieberthal W et al (1996) Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis. Am J Physiol 270(4 Pt 2):F700–F708PubMed
27.
Zurück zum Zitat Ramesh G, Reeves WB (2003) TNFR2-mediated apoptosis and necrosis in cisplatin-induced acute renal failure. Am J Physiol Renal Physiol 285(4):F610–F618PubMedCrossRef Ramesh G, Reeves WB (2003) TNFR2-mediated apoptosis and necrosis in cisplatin-induced acute renal failure. Am J Physiol Renal Physiol 285(4):F610–F618PubMedCrossRef
28.
Zurück zum Zitat Cilenti L et al (2005) Omi/HtrA2 protease mediates cisplatin-induced cell death in renal cells. Am J Physiol Renal Physiol 288(2):F371–F379PubMedCrossRef Cilenti L et al (2005) Omi/HtrA2 protease mediates cisplatin-induced cell death in renal cells. Am J Physiol Renal Physiol 288(2):F371–F379PubMedCrossRef
29.
Zurück zum Zitat Park MS et al (2002) Cisplatin induces apoptosis in LLC-PK1 cells via activation of mitochondrial pathways. J Am Soc Nephrol 13(4):858–865PubMedCrossRef Park MS et al (2002) Cisplatin induces apoptosis in LLC-PK1 cells via activation of mitochondrial pathways. J Am Soc Nephrol 13(4):858–865PubMedCrossRef
30.
Zurück zum Zitat Jiang M et al (2006) Regulation of PUMA-alpha by p53 in cisplatin-induced renal cell apoptosis. Oncogene 25(29):4056–4066PubMedCrossRef Jiang M et al (2006) Regulation of PUMA-alpha by p53 in cisplatin-induced renal cell apoptosis. Oncogene 25(29):4056–4066PubMedCrossRef
31.
Zurück zum Zitat Wei Q et al (2007) The pathological role of Bax in cisplatin nephrotoxicity. Kidney Int 72(1):53–62PubMedCrossRef Wei Q et al (2007) The pathological role of Bax in cisplatin nephrotoxicity. Kidney Int 72(1):53–62PubMedCrossRef
32.
Zurück zum Zitat Yin X et al (2007) Induction of renal endonuclease G by cisplatin is reduced in DNase I-deficient mice. J Am Soc Nephrol 18(9):2544–2553PubMedCrossRef Yin X et al (2007) Induction of renal endonuclease G by cisplatin is reduced in DNase I-deficient mice. J Am Soc Nephrol 18(9):2544–2553PubMedCrossRef
33.
Zurück zum Zitat Jiang M et al (2004) Role of p53 in cisplatin-induced tubular cell apoptosis: dependence on p53 transcriptional activity. Am J Physiol Renal Physiol 287(6):F1140–F1147PubMedCrossRef Jiang M et al (2004) Role of p53 in cisplatin-induced tubular cell apoptosis: dependence on p53 transcriptional activity. Am J Physiol Renal Physiol 287(6):F1140–F1147PubMedCrossRef
34.
Zurück zum Zitat Kaushal GP et al (2001) Role and regulation of activation of caspases in cisplatin-induced injury to renal tubular epithelial cells. Kidney Int 60(5):1726–1736PubMedCrossRef Kaushal GP et al (2001) Role and regulation of activation of caspases in cisplatin-induced injury to renal tubular epithelial cells. Kidney Int 60(5):1726–1736PubMedCrossRef
35.
Zurück zum Zitat Nagothu KK et al (2005) Fibrate prevents cisplatin-induced proximal tubule cell death. Kidney Int 68(6):2680–2693PubMedCrossRef Nagothu KK et al (2005) Fibrate prevents cisplatin-induced proximal tubule cell death. Kidney Int 68(6):2680–2693PubMedCrossRef
36.
Zurück zum Zitat Wang J et al (2004) Minocycline up-regulates Bcl-2 and protects against cell death in mitochondria. J Biol Chem 279(19):19948–19954PubMedCrossRef Wang J et al (2004) Minocycline up-regulates Bcl-2 and protects against cell death in mitochondria. J Biol Chem 279(19):19948–19954PubMedCrossRef
37.
Zurück zum Zitat Baliga R et al (1997) Oxidant mechanisms in toxic acute renal failure. Am J Kidney Dis 29(3):465–477PubMedCrossRef Baliga R et al (1997) Oxidant mechanisms in toxic acute renal failure. Am J Kidney Dis 29(3):465–477PubMedCrossRef
38.
Zurück zum Zitat Siddik ZH (2003) Cisplatin: mode of cytotoxic action and molecular basis of resistance. Oncogene 22(47):7265–7279PubMedCrossRef Siddik ZH (2003) Cisplatin: mode of cytotoxic action and molecular basis of resistance. Oncogene 22(47):7265–7279PubMedCrossRef
39.
Zurück zum Zitat Liu H, Baliga R (2003) Cytochrome P450 2E1 null mice provide novel protection against cisplatin-induced nephrotoxicity and apoptosis. Kidney Int 63(5):1687–1696PubMedCrossRef Liu H, Baliga R (2003) Cytochrome P450 2E1 null mice provide novel protection against cisplatin-induced nephrotoxicity and apoptosis. Kidney Int 63(5):1687–1696PubMedCrossRef
40.
Zurück zum Zitat Kruidering M et al (1997) Cisplatin-induced nephrotoxicity in porcine proximal tubular cells: mitochondrial dysfunction by inhibition of complexes I to IV of the respiratory chain. J Pharmacol Exp Ther 280(2):638–649PubMed Kruidering M et al (1997) Cisplatin-induced nephrotoxicity in porcine proximal tubular cells: mitochondrial dysfunction by inhibition of complexes I to IV of the respiratory chain. J Pharmacol Exp Ther 280(2):638–649PubMed
41.
Zurück zum Zitat Li S et al (2004) PPAR alpha ligand protects during cisplatin-induced acute renal failure by preventing inhibition of renal FAO and PDC activity. Am J Physiol Renal Physiol 286(3):F572–F580PubMedCrossRef Li S et al (2004) PPAR alpha ligand protects during cisplatin-induced acute renal failure by preventing inhibition of renal FAO and PDC activity. Am J Physiol Renal Physiol 286(3):F572–F580PubMedCrossRef
42.
Zurück zum Zitat Portilla D et al (2002) Alterations of PPARalpha and its coactivator PGC-1 in cisplatin-induced acute renal failure. Kidney Int 62(4):1208–1218PubMedCrossRef Portilla D et al (2002) Alterations of PPARalpha and its coactivator PGC-1 in cisplatin-induced acute renal failure. Kidney Int 62(4):1208–1218PubMedCrossRef
43.
Zurück zum Zitat Brooks C et al (2009) Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models. J Clin Invest 119(5):1275–1285PubMedPubMedCentralCrossRef Brooks C et al (2009) Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models. J Clin Invest 119(5):1275–1285PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Larsson NG et al (1998) Mitochondrial transcription factor A is necessary for mtDNA maintenance and embryogenesis in mice. Nat Genet 18(3):231–236PubMedCrossRef Larsson NG et al (1998) Mitochondrial transcription factor A is necessary for mtDNA maintenance and embryogenesis in mice. Nat Genet 18(3):231–236PubMedCrossRef
46.
Zurück zum Zitat Zhang Y et al (2014) P2X7 receptor blockade protects against cisplatin-induced nephrotoxicity in mice by decreasing the activities of inflammasome components, oxidative stress and caspase-3. Toxicol Appl Pharmacol 281(1):1–10PubMedCrossRef Zhang Y et al (2014) P2X7 receptor blockade protects against cisplatin-induced nephrotoxicity in mice by decreasing the activities of inflammasome components, oxidative stress and caspase-3. Toxicol Appl Pharmacol 281(1):1–10PubMedCrossRef
47.
Zurück zum Zitat Liu M et al (2006) A pathophysiologic role for T lymphocytes in murine acute cisplatin nephrotoxicity. J Am Soc Nephrol 17(3):765–774PubMedCrossRef Liu M et al (2006) A pathophysiologic role for T lymphocytes in murine acute cisplatin nephrotoxicity. J Am Soc Nephrol 17(3):765–774PubMedCrossRef
48.
Zurück zum Zitat Ramesh G, Reeves WB (2002) TNF-alpha mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity. J Clin Invest 110(6):835–842PubMedPubMedCentralCrossRef Ramesh G, Reeves WB (2002) TNF-alpha mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity. J Clin Invest 110(6):835–842PubMedPubMedCentralCrossRef
49.
Zurück zum Zitat Faubel S et al (2007) Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney. J Pharmacol Exp Ther 322(1):8–15PubMedCrossRef Faubel S et al (2007) Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney. J Pharmacol Exp Ther 322(1):8–15PubMedCrossRef
50.
Zurück zum Zitat Periyasamy-Thandavan S et al (2008) Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells. Kidney Int 74(5):631–640PubMedCrossRef Periyasamy-Thandavan S et al (2008) Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells. Kidney Int 74(5):631–640PubMedCrossRef
51.
Zurück zum Zitat Yang C et al (2008) Autophagy is associated with apoptosis in cisplatin injury to renal tubular epithelial cells. Am J Physiol Renal Physiol 294(4):F777–F787PubMedCrossRef Yang C et al (2008) Autophagy is associated with apoptosis in cisplatin injury to renal tubular epithelial cells. Am J Physiol Renal Physiol 294(4):F777–F787PubMedCrossRef
52.
Zurück zum Zitat Yu X et al (2020) Nuclear receptor PXR targets AKR1B7 to protect mitochondrial metabolism and renal function in AKI. Sci Transl Med 12:543CrossRef Yu X et al (2020) Nuclear receptor PXR targets AKR1B7 to protect mitochondrial metabolism and renal function in AKI. Sci Transl Med 12:543CrossRef
54.
Zurück zum Zitat Han J et al (2016) Autophagy induced by AXL receptor tyrosine kinase alleviates acute liver injury via inhibition of NLRP3 inflammasome activation in mice. Autophagy 12(12):2326–2343PubMedPubMedCentralCrossRef Han J et al (2016) Autophagy induced by AXL receptor tyrosine kinase alleviates acute liver injury via inhibition of NLRP3 inflammasome activation in mice. Autophagy 12(12):2326–2343PubMedPubMedCentralCrossRef
55.
Zurück zum Zitat Qu X et al (2018) Autophagy inhibition-enhanced assembly of the NLRP3 inflammasome is associated with cisplatin-induced acute injury to the liver and kidneys in rats. J Biochem Mol Toxicol 33:e22208 Qu X et al (2018) Autophagy inhibition-enhanced assembly of the NLRP3 inflammasome is associated with cisplatin-induced acute injury to the liver and kidneys in rats. J Biochem Mol Toxicol 33:e22208
56.
Zurück zum Zitat Walter P, Ron D (2011) The unfolded protein response: from stress pathway to homeostatic regulation. Science 334(6059):1081–1086PubMedCrossRef Walter P, Ron D (2011) The unfolded protein response: from stress pathway to homeostatic regulation. Science 334(6059):1081–1086PubMedCrossRef
57.
Zurück zum Zitat Wang M, Kaufman RJ (2016) Protein misfolding in the endoplasmic reticulum as a conduit to human disease. Nature 529(7586):326–335PubMedCrossRef Wang M, Kaufman RJ (2016) Protein misfolding in the endoplasmic reticulum as a conduit to human disease. Nature 529(7586):326–335PubMedCrossRef
58.
Zurück zum Zitat Huang Z et al (2020) Activation of GPR120 by TUG891 ameliorated cisplatin-induced acute kidney injury via repressing ER stress and apoptosis. Biomed Pharmacother 126:110056PubMedCrossRef Huang Z et al (2020) Activation of GPR120 by TUG891 ameliorated cisplatin-induced acute kidney injury via repressing ER stress and apoptosis. Biomed Pharmacother 126:110056PubMedCrossRef
Metadaten
Titel
Leonurine attenuates cisplatin nephrotoxicity by suppressing the NLRP3 inflammasome, mitochondrial dysfunction, and endoplasmic reticulum stress
verfasst von
Qi Zhang
Qiuhong Sun
Yan Tong
Xiao Bi
Lin Chen
Jianxin Lu
Wei Ding
Publikationsdatum
02.02.2022
Verlag
Springer Netherlands
Erschienen in
International Urology and Nephrology / Ausgabe 9/2022
Print ISSN: 0301-1623
Elektronische ISSN: 1573-2584
DOI
https://doi.org/10.1007/s11255-021-03093-1

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