title: Extracorporeal shock wave therapy does not improve hypertensive nephropathy.
abstract: Low-energy extracorporeal shock wave therapy (SWT) has been shown to improve myocardial dysfunction, hind limb ischemia, erectile function, and to facilitate cell therapy and healing process. These therapeutic effects were mainly due to promoting angiogenesis. Since chronic kidney diseases are characterized by renal fibrosis and capillaries rarefaction, they may benefit from a proangiogenic treatment. The objective of our study was to determine whether SWT could ameliorate renal repair and favor angiogenesis in L-NAME-induced hypertensive nephropathy in rats. SWT was started when proteinuria exceeded 1 g/mmol of creatinine and 1 week after L-NAME removal. SWT consisted of implying 0.09 mJ/mm(2) (400 shots), 3 times per week. After 4 weeks of SWT, blood pressure, renal function and urinary protein excretion did not differ between treated (LN + SWT) and untreated rats (LN). Histological lesions including glomerulosclerosis and arteriolosclerosis scores, tubular dilatation and interstitial fibrosis were similar in both groups. In addition, peritubular capillaries and eNOS, VEGF, VEGF-R, SDF-1 gene expressions did not increase in SWT-treated compared to untreated animals. No procedural complications or adverse effects were observed in control (C + SWT) and hypertensive rats (LN + SWT). These results suggest that extracorporeal kidney shock wave therapy does not induce angiogenesis and does not improve renal function and structure, at least in the model of hypertensive nephropathy although the treatment is well tolerated.
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Caron
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France Université Pierre et Marie Curie-Paris 6 UMR S 1155, Paris, France Department of Nephrology, AP-HP Hôpital Tenon, Paris, F-75020, France.
authors.forename: Pierre-Antoine
authors.initials: PA
authors.lastname: Michel
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France Université Pierre et Marie Curie-Paris 6 UMR S 1155, Paris, France Department of physiology, AP-HP Hôpital Saint-Antoine, Paris, F-75012, France.
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Dussaule
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France Université Pierre et Marie Curie-Paris 6 UMR S 1155, Paris, France.
authors.forename: Christos
authors.initials: C
authors.lastname: Chatziantoniou
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France Université Pierre et Marie Curie-Paris 6 UMR S 1155, Paris, France Department of Nephrology, AP-HP Hôpital Tenon, Paris, F-75020, France.
authors.forename: Pierre
authors.initials: P
authors.lastname: Ronco
authors.affiliation: INSERM UNIT 1155, Paris, F-75020, France Université Pierre et Marie Curie-Paris 6 UMR S 1155, Paris, France Department of Nephrology, AP-HP Hôpital Tenon, Paris, F-75020, France jean-jacques.boffa@aphp.fr.
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Boffa
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006977:Hypertension, Renal / Q000139:chemically induced / Q000473:pathology / Q000628:therapy*; D007668:Kidney / Q000473:pathology*; D008096:Lithotripsy; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009393:Nephritis / Q000139:chemically induced / Q000473:pathology / Q000628:therapy*; D051381:Rats; D016896:Treatment Outcome
chemical_list: D019331:NG-Nitroarginine Methyl Ester
keywords: Renal fibrosis; angiogenesis; chronic kidney disease; renal repair