EFFECT OF SIMVASTATIN ON HISTOPATHOLOGY OF THE HEART AFTER 5/6 SUBTOTAL NEPHRECTOMY
DOI:
https://doi.org/10.22159/ijap.2019.v11s5.T0105Keywords:
Cardiac histopathology, Subtotal 56 nephrectomy, Simvastatin, MyofibrilsAbstract
Objective: This study aims to assess the condition of cardiac histopathology through hematoxylin-eosin staining in 5/6 subtotal nephrectomy
conditions.
Methods: Fifteen male Swiss mice aged 3–5 months will be grouped into 3 treatment groups, namely the nephrectomy group (JSN, n=5), sham
operation (JSO, n=5), and simvastatin 20 mg/kg body weight (JSIM, n=5). The histopathology of the heart will be assessed blindly. Severity is assessed
based on scoring using a scale (−) no damage, (+) mild, (++) medium, and (+++) heavy. Assessment of severity refers to the irregularity of the heart
muscle, increased amount of connective tissue, myofibril hypertrophy, myofibril swelling, sarcoplasmic fragmentation, sarcoplasmic vacuolization,
bleeding in a myofibril, myofibril degeneration, cardiomyocyte damage, and the presence of acidophilic cytoplasm.
Results: The results showed no morphological changes in heart muscle tissue in the JSO group except for fragmentation and vacuolization in minimal
amounts of sarcoplasm (+), whereas in the JSN and JSIM groups, there was moderate damage to sarcoplasm (++) and minimal changes in myofibrils
(hypertrophy and bleeding) (+). The JSN group also found severe damage (+++) to the irregularity of the heart muscle, whereas in JSIM, only moderate
damage was found (++) to the irregularity of the heart muscle.
Conclusion: Simvastatin seems to be able to correct the irregularity of the heart muscle in the condition of 5/6 subtotal nephrectomy.
Downloads
References
et al. Cardiovascular risk factor burden, treatment, and control among
adults with chronic kidney disease in the United States. Am Heart J
2013;166:150-6.
2. Bagshaw SM, Cruz DN, Aspromonte N, Daliento L, Ronco F,
Sheinfeld G, et al. Epidemiology of cardio-renal syndromes: Workgroup
statements from the 7th ADQI consensus conference. Nephrol Dial
Transplant 2010;25:1406-16.
3. Quarles LD. Reducing cardiovascular mortality in chronic kidney
disease: Something borrowed, something new. J Clin Invest
2013;123:542-3.
4. Pecoits-Filho R, Bucharles S, Barberato SH. Diastolic heart failure
in dialysis patients: Mechanisms, diagnostic approach, and treatment.
Semin Dial 2012;25:35-41.
5. U.S. Renal Data System (USRDS). Chronic Kidney Disease in the
Adult NHANES Population. USRDS Annual Report Data; 2009.
Available from: http://www.usrds.org/USRDS/pdf/V1 01 09.PDF. [Last
accessed on 2019 Mar 25].
6. Deedwania PC, Javed U. Statins in heart failure. Cardiol Clin
2008;26:573-87.
7. Miura S, Saku K. Effects of statin and lipoprotein metabolism in heart
failure. J Cardiol 2010;55:287-90.
8. Cahyawati PN, Arfian N, Ngatidjan N. Effect of statin on vascular
wall thickness in kidney disease model. IOP Conf Ser Mater Sci Eng
2018;434:012324.
9. Cahyawati PN, Ngatidjan N, Sari DC, Romi MM, Arfian N. Simvastatin
attenuates renal failure in mice with a 5/6 subtotal nephrectomy. Int J
Pharm Pharm Sci 2017;9:12-7.
10. Cahyawati PN, Aryastuti AA, Ariawan MB, Arfian N, Ngatidjan N.
Statin and Anemia in Chronic Kidney Disease (CKD): An Experimental
Study. MATEC Web of Conferences 197; 2018.
11. Alihemmati A, Yousefi H, Ahmadiasi N, Habibi P. Apoptosis and
histopatology of the heart after renal ischemia-reperfusion in male rat
running title: Ischemia-reperfusion injury. Braz Arch Biol Thechnol
2017;60:e17160244.
12. Lekawanvijit S, Kompa AR, Manabe M, Wang BH, Langham RG,
Nishijima F, et al. Chronic kidney disease-induced cardiac fibrosis is
ameliorated by reducing circulating levels of a non-dialysable uremic
toxin, indoxyl sulfate. PLoS One 2012;7:e41281.
13. López B, González A, Hermida N, Laviades C, Díez J. Myocardial
fibrosis in chronic kidney disease: Potential benefits of torasemide.
Kidney Int Suppl 2008;111:S19-23.
14. Rodrigues Díez R, Rodrigues-Díez R, Lavoz C, Rayego-Mateos S,
Civantos E, Rodríguez-Vita J, et al. Statins inhibit angiotensin II/Smad
pathway and related vascular fibrosis, by a TGF-?-independent process.
PLoS One 2010;5:e14145.
15. Zhou MS, Schuman IH, Jaimes EA, Raij L. Renoprotection by statins is
linked to a decrease in renal oxidative stress, TGF-beta, and fibronectin
with concomitant increase in nitric oxide bioavailability. Am J Physiol
Renal Physiol 2008;295:F53-9.
16. Kavazis AN. Pathological vs. Physiological cardiac hypertrophy.
J Physiol 2015;593:3767.