HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.
Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.
Thanks
Lipid abnormalities in nephrotic syndrome
Author :Jai Radhakrishnan, MD, MS
Abnormal lipid metabolism is common in patients with renal disease [1-6]. This effect is most prominent in the nephrotic syndrome, where marked elevations in the plasma levels of cholesterol, LDL, triglycerides and lipoprotein(a) often occur [1-5,7,8]. Total HDL cholesterol levels are usually normal or reduced in the nephrotic syndrome and there is often a pronounced decline in the cardioprotective HDL2 fraction. The mechanism by which this occurs is unclear, but elevations in the plasma concentration of cholesteryl ester transfer protein in nephrotic patients may contribute by shuttling cholesteryl esters from HDL2 to very low-density lipoproteins (VLDL) [9,10].
The concentration of plasma apolipoproteins in the nephrotic syndrome generally reflects the alterations in lipoprotein metabolism. Thus, there are elevated levels of apo B, C-II, and E, which are associated with VLDL and LDL; on the other hand, the levels of the major apolipoproteins associated with HDL, apo A-I and A-II, are usually normal [11]. A review of the functions of the different apolipoproteins is discussed separately. (See "Lipoprotein classification, metabolism, and role in atherosclerosis".)
This topic will review the pathogenesis and treatment of lipid abnormalities in patients with the nephrotic syndrome. The pathogenesis and significance of lipid abnormalities in patients with chronic kidney disease and following kidney transplantation are discussed separately. (See "Lipid abnormalities in patients with chronic kidney disease not requiring dialysis" and "Lipid abnormalities after renal transplantation".). For more plz read at following link and paper
Best Regards
http://www.uptodate.com/contents/lipid-abnormalities-in-nephrotic-syndrome
Thanks for the information, but some of the hypothesis i exposed didnt found them. Such as the combination of pioglitazone plus ezetimibe and simvastatin for the management of dyslipidemias and better outcome. Also i havent found consensus regarding on preventive use of anti-aggregating or anti-coagulant factors on N-S, the only data i have found is on the use of aspirin or heparin when albumin is below 2 gr/dl but not all data supports this approach but havent found information to use it or any other therapies when dyslipidemia is present.
No studies of lipid-lowering agents (statins or fibrates) in patients with NS have reported patient-centred outcomes including all-cause mortality, cardiovascular mortality, or non-fatal myocardial infarction; only single studies reported cholesterol (HDL, LDL and total cholesterol), There is no data on second-line agents (incl. ezetimibe) and outcomes in NS.
There is also little evidence that secondary hyperlipidemia in NS has the same effect on cardiovascular outcomes. Bring the NS into remission and hyperlipidemia will resolve without the need of treating dylipidemia.
Thanks Pablo, but what happens when the patient has a poor response to the NS treatment, no response to steroids and poor response to inmune suppressors? do we believe that events such as stroke cannot be prevented with management of dyslipidemia and use of profilactic aspirin; so complications cannot be prevented on patients with poor response to NS treatment?
Effective control of proteinuria in NS is mandatory.I had a Ns infant whose S.cholesterol was 1100mg/ dl and after controlling her proteinuria with steroids ,her s.cholesterol dropped to 200mg/dl. Her renal biopsy was MCN
But if its steroid non responser and poor responser to other drugs with some relapses.
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