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The renin-angiotensin system and hypertension in autosomal recessive polycystic kidney disease.
Pediatr Nephrol. 2010 Dec; 25(12):2449-57.PN

Abstract

Hypertension is a well-recognized complication of autosomal recessive polycystic kidney disease (ARPKD). The renin-angiotensin system (RAS) is a key regulator of blood pressure; however, data on the RAS in ARPKD are limited and conflicting, showing both up- and down-regulation. In the current study, we characterized intrarenal and systemic RAS activation in relationship to hypertension and progressive cystic kidney disease in the ARPKD orthologous polycystic kidney (PCK) rat. Clinical and histological measures of kidney disease, kidney RAS gene expression by quantitative real-time PCR, angiotensin II (Ang II) immunohistochemistry, and systemic Ang I and II levels were assessed in 2-, 4-, and 6-month-old cystic PCK and age-matched normal rats. PCK rats developed hypertension and progressive cystic kidney disease without significant worsening of renal function or relative kidney size. Intrarenal renin, ACE and Ang II expression was increased significantly in cystic kidneys; angiotensinogen and Ang II Type I receptor were unchanged. Systemic Ang I and II levels did not differ. This study demonstrates that intrarenal, but not systemic, RAS activation is a prominent feature of ARPKD. These findings help reconcile previous conflicting reports and suggest that intrarenal renin and ACE gene upregulation may represent a novel mechanism for hypertension development or exacerbation in ARPKD.

Authors+Show Affiliations

Department of Research, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20798958

Citation

Goto, Miwa, et al. "The Renin-angiotensin System and Hypertension in Autosomal Recessive Polycystic Kidney Disease." Pediatric Nephrology (Berlin, Germany), vol. 25, no. 12, 2010, pp. 2449-57.
Goto M, Hoxha N, Osman R, et al. The renin-angiotensin system and hypertension in autosomal recessive polycystic kidney disease. Pediatr Nephrol. 2010;25(12):2449-57.
Goto, M., Hoxha, N., Osman, R., & Dell, K. M. (2010). The renin-angiotensin system and hypertension in autosomal recessive polycystic kidney disease. Pediatric Nephrology (Berlin, Germany), 25(12), 2449-57. https://doi.org/10.1007/s00467-010-1621-z
Goto M, et al. The Renin-angiotensin System and Hypertension in Autosomal Recessive Polycystic Kidney Disease. Pediatr Nephrol. 2010;25(12):2449-57. PubMed PMID: 20798958.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The renin-angiotensin system and hypertension in autosomal recessive polycystic kidney disease. AU - Goto,Miwa, AU - Hoxha,Nita, AU - Osman,Rania, AU - Dell,Katherine Macrae, Y1 - 2010/08/27/ PY - 2010/02/25/received PY - 2010/07/14/accepted PY - 2010/06/28/revised PY - 2010/8/28/entrez PY - 2010/8/28/pubmed PY - 2011/2/4/medline SP - 2449 EP - 57 JF - Pediatric nephrology (Berlin, Germany) JO - Pediatr. Nephrol. VL - 25 IS - 12 N2 - Hypertension is a well-recognized complication of autosomal recessive polycystic kidney disease (ARPKD). The renin-angiotensin system (RAS) is a key regulator of blood pressure; however, data on the RAS in ARPKD are limited and conflicting, showing both up- and down-regulation. In the current study, we characterized intrarenal and systemic RAS activation in relationship to hypertension and progressive cystic kidney disease in the ARPKD orthologous polycystic kidney (PCK) rat. Clinical and histological measures of kidney disease, kidney RAS gene expression by quantitative real-time PCR, angiotensin II (Ang II) immunohistochemistry, and systemic Ang I and II levels were assessed in 2-, 4-, and 6-month-old cystic PCK and age-matched normal rats. PCK rats developed hypertension and progressive cystic kidney disease without significant worsening of renal function or relative kidney size. Intrarenal renin, ACE and Ang II expression was increased significantly in cystic kidneys; angiotensinogen and Ang II Type I receptor were unchanged. Systemic Ang I and II levels did not differ. This study demonstrates that intrarenal, but not systemic, RAS activation is a prominent feature of ARPKD. These findings help reconcile previous conflicting reports and suggest that intrarenal renin and ACE gene upregulation may represent a novel mechanism for hypertension development or exacerbation in ARPKD. SN - 1432-198X UR - https://www.unboundmedicine.com/medline/citation/20798958/The_renin_angiotensin_system_and_hypertension_in_autosomal_recessive_polycystic_kidney_disease_ L2 - https://dx.doi.org/10.1007/s00467-010-1621-z DB - PRIME DP - Unbound Medicine ER -