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Expression of components of the renin-angiotensin system in autosomal recessive polycystic kidney disease.
J Histochem Cytochem. 2005 Aug; 53(8):979-88.JH

Abstract

Hypertension is a common complication in children with autosomal recessive polycystic kidney disease (ARPKD) who have survived the neonatal period. No information is available regarding the mechanism of hypertension in this condition. The renin-angiotensin system (RAS) is thought to play a role in hypertension associated with the more common autosomal dominant polycystic kidney disease (ADPKD). Occasional reports have documented increased activity of the intrarenal RAS in ADPKD, with ectopic renin expression within cysts and dilated tubules. Because of similarities between ARPKD and ADPKD, we hypothesized that increased intrarenal RAS activity might also be found in ARPKD. We performed immunohistochemical studies on kidney tissues from two infants with ARPKD and two control kidneys. The cystic dilated tubules showed staining with the peanut lectin arachis hypogaea, a marker of distal tubules and collecting ducts, but not with lotus tetragonolobus, a marker of proximal tubules. Strong renin staining was seen in many cysts and tubules of ARPKD kidneys, but only in the afferent arterioles of the normal control kidneys. Angiotensinogen staining was also observed in some cysts and in proximal tubules. Staining for angiotensin-converting enzyme, angiotensin II type 1 receptor, and angiotensin II peptide was present in many cystic dilated tubules. These immunohistochemical studies document for the first time ectopic expression of components of the RAS in cystic-dilated tubules of ARPKD and suggest that overactivity of RAS could result in increased intrarenal angiotensin II production, which may contribute to the development of hypertension in ARPKD.

Authors+Show Affiliations

Department of Pediatrics and Pediatric Research Institute, Saint Louis University, St. Louis, Missouri, USA. mloghman@att.netNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15879580

Citation

Loghman-Adham, Mahmoud, et al. "Expression of Components of the Renin-angiotensin System in Autosomal Recessive Polycystic Kidney Disease." The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society, vol. 53, no. 8, 2005, pp. 979-88.
Loghman-Adham M, Soto CE, Inagami T, et al. Expression of components of the renin-angiotensin system in autosomal recessive polycystic kidney disease. J Histochem Cytochem. 2005;53(8):979-88.
Loghman-Adham, M., Soto, C. E., Inagami, T., & Sotelo-Avila, C. (2005). Expression of components of the renin-angiotensin system in autosomal recessive polycystic kidney disease. The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society, 53(8), 979-88.
Loghman-Adham M, et al. Expression of Components of the Renin-angiotensin System in Autosomal Recessive Polycystic Kidney Disease. J Histochem Cytochem. 2005;53(8):979-88. PubMed PMID: 15879580.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of components of the renin-angiotensin system in autosomal recessive polycystic kidney disease. AU - Loghman-Adham,Mahmoud, AU - Soto,Carlos E, AU - Inagami,Tadashi, AU - Sotelo-Avila,Cirilo, Y1 - 2005/05/06/ PY - 2005/5/10/pubmed PY - 2005/9/20/medline PY - 2005/5/10/entrez SP - 979 EP - 88 JF - The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society JO - J. Histochem. Cytochem. VL - 53 IS - 8 N2 - Hypertension is a common complication in children with autosomal recessive polycystic kidney disease (ARPKD) who have survived the neonatal period. No information is available regarding the mechanism of hypertension in this condition. The renin-angiotensin system (RAS) is thought to play a role in hypertension associated with the more common autosomal dominant polycystic kidney disease (ADPKD). Occasional reports have documented increased activity of the intrarenal RAS in ADPKD, with ectopic renin expression within cysts and dilated tubules. Because of similarities between ARPKD and ADPKD, we hypothesized that increased intrarenal RAS activity might also be found in ARPKD. We performed immunohistochemical studies on kidney tissues from two infants with ARPKD and two control kidneys. The cystic dilated tubules showed staining with the peanut lectin arachis hypogaea, a marker of distal tubules and collecting ducts, but not with lotus tetragonolobus, a marker of proximal tubules. Strong renin staining was seen in many cysts and tubules of ARPKD kidneys, but only in the afferent arterioles of the normal control kidneys. Angiotensinogen staining was also observed in some cysts and in proximal tubules. Staining for angiotensin-converting enzyme, angiotensin II type 1 receptor, and angiotensin II peptide was present in many cystic dilated tubules. These immunohistochemical studies document for the first time ectopic expression of components of the RAS in cystic-dilated tubules of ARPKD and suggest that overactivity of RAS could result in increased intrarenal angiotensin II production, which may contribute to the development of hypertension in ARPKD. SN - 0022-1554 UR - https://www.unboundmedicine.com/medline/citation/15879580/Expression_of_components_of_the_renin_angiotensin_system_in_autosomal_recessive_polycystic_kidney_disease_ L2 - http://journals.sagepub.com/doi/full/10.1369/jhc.4A6494.2005?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -