Measurement of lipids (cholesterol, triglycerides and the component lipids like low density lipoproteins (LDL cholesterol), high density ‘good’ lipoproteins (HDL cholesterol), the ratio of LDL to HDL cholesterol etc … all these are used along with a range of other cardiovascular risk assessments (which include blood pressure, ECG, exercise ECG, echocardiography etc.) to determine the health (or otherwise) of your cardiovascular system and your relative risk of cardiovascular events – like heart attack and stroke.
All sorts of risk assessment tools have been developed to use these ‘markers’ to gauge risk. They are used either singly or in combination – and your primary care doctor (GP) will likely have applied these to your circumstances already.
None of these risk-assessment tools are perfect and most simply refer to ‘additional risk factors’ - like the presence of CKD - as complicating factors … whereas we now know that CKD is an amplifier of all cardiovascular risk, and not just another factor.
What an ‘amplifier’ means is that an amplification factor (like CKD) ramps up the collective risk and shouldn’t be added in as just another risk factor.
As with the previous post, triglycerides are the major form of fat found in the body. The function of triglyceride is to provide energy for the cells. The ideal levels of these substances will vary a little, lab vs lab – as methods for their determination vary, but – broadly – the levels thought to be ideal are:
• Cholesterol <200 mg/dL (5.2 mmol/L)
• HDL-cholesterol > 40 mg/dL (1.05 mmol/L)
• LDL-cholesterol <100 mg/dL* (2.6 mmol/L)
• Triglycerides <150 mg/dL (1.7 mmol/L)
NB: I hope I have those conversions right as we use mmol/l here in Australia. Furthermore, our cardiology colleagues continually pull the upper level of cholesterol down and we shoot, now, for <4.5 mmol/l (not <5.2).
Assessing ‘risk’ is both far more complicated and far more imprecise then you might imagine. Risk assessment is never ‘you’. Risk assessment is, at best, a population risk. Risk assessment can never predict ‘you’ apart from ‘the population. ‘You’ may vary in all sorts of ways from a population … you may have diabetes, be a smoker, be short, overweight and be sedentary. Just as likely, you are an ex-swimmer who has never smoked, has no diabetes (nor family history of it), and be built like a thoroughbred … but … have an horrendous and life-long blood pressure issue. We all vary from societal means in idiosyncratic and individual ways. These variations always pepper risk assessment with ‘ifs and buts’.
That said … there are some risk assessment tools around.
One is put out by the NIH and is contained in the 3rd Report of the National Expert Panel on Cholesterol Education … and was developed from the Framingham (Mass) Heart Study
It can be found at: http://hp2010.nhlbihin.net/atpiii/calculator.asp
Remember, applying such tools does not take into account the ‘you’ in the equation … they are tools developed for ‘them’, the population … but as much as you fit the average of ‘them’, the assessments can be roughly applied to ‘you’.
I am glad you have accepted the ‘we just don’t know’ as a valid answer – because, here it comes again. As regards the benefits of optimum dialysis – and by optimum dialysis, I am meaning more than just 3 x week x variants of 4 hr duration treatments – I think the fairest answer is ‘we just don’t know.
In patients without CKD, there does appear to be a relationship between the blood cholesterol and the risk of coronary artery disease – the greater the degree of CKD, the greater the risk. Several big trials in CKD patients have shown that with statin therapy, the risk of a cardiovascular event – be that cardiovascular death, heart attack (myocardial infarction) or stroke – is reduced as lipid levels improve.
But – and disappointingly - two large studies in dialysis patients … the 4-D trial (atorvastatin in ~1250 dialysis patients) and the AURORA trial (rosuvastatin in nearly 2800 dialysis patients) … found that despite significant lowering of the LDL cholesterol levels in both trials, there appeared to be no reductions in the usual cardiovascular end points of cardiovascular death, myocardial infarction (heart attack) or stroke between the treated and the non-treated groups.
Perhaps a little encouragingly, the SHARP study, which combined two triglyceride and cholesterol-lowering drugs, simvastatin and ezetimibe and was carried out in end-stage CKD and haemodialysis patients, showed a 17% lowering of ‘major atherosclerotic events’. So, while the jury is still out, there is no agreed recommendation to use statins in dialysis patients with only a mild to modest elevation of LDL-cholesterol.
Confusing, isn’t it. And even if you aren’t … I still am – and I am supposed to treat people.
As for optimum dialysis – and here I mean long, slow, frequent dialysis therapies – there are no trials and no group data to say whether optimum dialysis itself has any lipid-lowering effects though I suspect the answer is likely a ‘no’.
But – and it is a very important ‘but’ – long, slow, frequent dialysis regimens do … repeat ‘do’ … control phosphate beautifully – and, via phosphate control, the calcium:phosphate product. Long, slow, frequent dialysis regimens do result in lowered PTH levels, better bone physiology and the reabsorption of extra-osseus (non-bone) calcium deposition.
As the cause of much of the vascular calcification seen in CKD and dialysis patients is circumferential calcification of blood vessels as well as the calcification of existing cholesterol ‘plaques’, one has to be hopeful that reabsorption of calcium deposits from lipid plaques might result from optimal dialysis … and if so, then long, slow, frequent ‘optimal’ dialysis should benefit vascular health.
Andreas Pierratos (Toronto) has reported extra-osseus calcification reabsorption with NHD while Chris Chan (also Toronto) has reported that coronary calcification has been ‘stalled’ by NHD … though there was no control group and these reports are case study reports only and, as such, need to be interpreted with caution.
Intuitively, though, one would have to surmise that better dialysis, with normalized phosphate levels and a normal calcium:phosphate product should be beneficial for vascular health.
Now … shush, till I get back from Beijing!