GANGGUAN GINJAL AKUT AKIBAT RHABDOMIOLISIS

Majalah Biomorfologi

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Title GANGGUAN GINJAL AKUT AKIBAT RHABDOMIOLISIS
 
Creator Hasanatuludhhiyah, Nurina
Basori, Achmad
Suhartati, Suhartati
 
Subject Acute kidney injury; rhabdomyolysis; myoglobin; renal vasoconstriction; oxidative injury; Gangguan ginjal akut; rhabdomiolisis; mioglobin; vasokonstriksi ginjal; perlukaan oksidatif
 
Description Acute kidney injury (AKI) is the most serious complication of rhabdomyolysis, a syndrome characterized by skeletal muscle destruction causing leakage of myoglobin and other intracellular protein as well as electrolytes into circulation. Due to its light molecular weight, myoglobin is readily filtered by the glomerus, and enters renal tubules, which may cause acute kidney injury with myoglobinuria. It is also characterized by significant increase of serum creatine kinase (CK) as well as electrolyte abnormalities. This review is intended to elucidate the mechanisms involved in pathogenesis of rhabdomyolysis induced AKI, which is related with its clinical as well as laboratory manifestations. This is used as a basis to determine correct diagnosis and management.The basic mechanisms in the pathogenesis of rhabdomyolysis induced AKI include: 1) renal vasoconstriction and ischemia induced by the release of several mediators which promote vasoconstriction including endothelin-1 and vasopressin which is triggered by activation of sympathetic system and rennin angiotensin aldosteron (RAA) system to compensate hypovolemia. Additionally TNF-α, thromboxane A2, and F2 Isoprostane are also generated in inflammatory response to muscle injury, endothelial dysfunction as well as oxidative injury, 2) formation of myoglobin cast, which is precipitation of myoglobin-Tamm Horsfal protein complex producing obstruction of distal tubules, 3) direct cytotoxic effect of myoglobin on proximal tubules through oxidative injury generated by Fenton Reaction and myoglobin redox cycling. It is concluded that rhabdomyolysis induced AKI is produced by renal ischemia, tubular obstruction and oxidative injury on tubular cells.
 
Publisher Department of Anatomy and Histology, Faculty of Medicine, Universitas Airlangga
 
Contributor
 
Date 2019-11-15
 
Type info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion

 
Format application/pdf
 
Identifier https://e-journal.unair.ac.id/MBIO/article/view/16102
10.20473/mbiom.v28i2.2015.20-25
 
Source Majalah Biomorfologi; Vol 28, No 2 (2015): Majalah Biomorfologi; 26-31
2716-0920
0215-8833
 
Language eng
 
Relation https://e-journal.unair.ac.id/MBIO/article/view/16102/8645
 
Rights Copyright (c) 2019 Majalah Biomorfologi
http://creativecommons.org/licenses/by-nc-sa/4.0
 

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