The traditional Metabolic Syndrome framework has evolved into the CKM (Cardio-Kidney-Metabolic) framework, which should further include the liver as CKLM, because liver fat is a primary driver of metabolic dysfunction. Microalbuminuria serves as a critical 'window' to vascular health, as the renal glomerular capillaries reflect systemic arterial changes and run parallel to atherosclerosis. Heart risk begins to spike significantly at UACR levels of 10 mg/g, not just at the traditional 30 mg/g cutoff. The Urine Albumin-Creatinine Ratio (UACR) is superior to serum creatinine for early detection of kidney disease and cardiovascular risk. Aggressive triple therapy combining RAS blockers, SGLT2 inhibitors, and MRAs can reduce albuminuria by over 50%, with the goal being as low as possible for maximum vascular protection.
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Beyond Syndrome X: The Evolutionary Jump to CKM and CKLM | Dr Anil Pareek | TheRightDoctorsAdded:
[music] >> I am Dr. Professor P.C. Manoria, Executive President Fourth World Congress Cardio Kidney Metabolic Medicine at Hotel Lila, Mumbai, 18th-19th April 2026. And with me is Dr. Anil Parikh, President Medical Affairs at Cadila Healthcare.
Dr. Parikh, what was the necessity of coining this term CKM? What is the interrelation, interconnection, and what is the bidirectional connection?
Sir, I think we are all familiar with the term earlier with metabolic syndrome. When you have a, you know, constellation of abnormalities along with visceral adiposity, which was first noticed, it was noticed coined as syndrome X and metabolic syndrome where along with, you know, abnormalities of glucose metabolism, impaired glucose homeostasis with elevated fasting glucose along with insulin resistance, elevated systolic blood pressure was found, and also we had, you know, high triglyceride, low HDL cholesterol.
So, two out of five criteria was labeled as metabolic syndrome. And later on we found that, you know, this is associated with increased proneness to atherosclerosis.
So, and the involvement of kidney also takes place. So, multi-organ involvement is there.
So, that's how it was found that, you know, it's a risk factor which then involves the multi-system organs, particularly liver, where there is fat accumulation, hepatic steatosis, subsequently, you know, there is a also fibrosis develops as a more complications.
And then we have chronic kidney disease, and also we have coronary artery disease. So, I think the outset I would like to first be express my gratitude to you for always allowing me to participation in this very important conferences, and there is always learning.
So, in the first, I think last year conference when I I spoke on seek evolution of cardio kidney metabolic syndrome, there I think I included CKLM. The term should be CKLM because these guidelines by American Heart Association in November '23 when the presidential advisory of AHA came, uh it was coined as CKM syndrome, but actually liver involvement is also equally there, and so it should be coined more CKLM syndrome so that, you know, we indicate primary role played by liver in visceral adiposity. That is also very important to to know.
So, this is how it is. But when I went little more in the literature, I found that the WHO in 1998 itself had along with the various criterias which were there like five for two out of five criterias which we had impaired glucose homeostasis in the background of insulin resistance, then you have, you know, abdominal obesity with waist circumference enlargement, high triglyceride, low HDL, elevated blood pressure.
The WHO had included microalbuminuria 1998 itself. So, that shows that, you know, and then but the NCATP3 criteria and subsequent, you know, lipid guidelines, they did not include microalbuminuria. That emphasis was not received. So, probably that's why we find that microalbuminuria is a window to the vascular health.
Because the kidney, the renal glomerular capillaries, they unlike the capillaries at other sites, they have arteriolar end at both the both sides, not arteriolar and venular end. Instead of that, we have arteriolar end at both the sides of the glomerular capillary. So, they reflect the arterial changes in in systemic vasculature where it is reflected. So, we have, you know, like we have atherosclerosis, we have glomerulosclerosis. So, they run very very parallel to each other. And that's how we have both cardiac complication and the kidney complication. CKD and ASCVD, they run sort of parallel in many patients.
So, for, you know, to detect kidney disease early, as we all know that CKD a patient of CKD has the highest incidence of acute coronary syndrome.
They die of acute coronary syndrome rather than anything else. So, can we, you know, do some prevention here? So, but when we by the time renal insufficiency develops, uh the serum creatinine or eGFR, it's too late. And often we find that majority of the patients have microalbuminuria.
Substantial number of patients, they have albuminuria in the urine. And now the UACR is quite standardized. It's a very useful tool to to not only detect the kidney disease progression, but earlier to kidney disease progression, even window to the vascular health, we can say.
And now the recent guidelines are emphasizing that more and more. Uh the recent ACC/AHA guideline for, you know, hypertension, for lipids, they are saying that if you have microalbuminuria more than 30, then you are that patient is at higher atherosclerotic ASCVD risk. So, we need to be more aggressive in other risk factor control as well like more stringent control of blood pressure, more control of glycemic targets.
>> conception, the misconception is still prevails. That for diagnosing CKD, people only look at serum creatinine or eGFR, which is totally wrong.
Microalbuminuria is in the early phase of CKD, and it has a direct correlation with the cardiovascular system. Rather, it is a red flag for the cardiologist to utilize all his treatment to minimize cardiovascular disease. But in real practice, we see UACR is not often done, less often done by the cardiologist. And we they just do serum creatinine and not even eGFR, which is totally, you know, this is you cannot have diagnosis of CKD. CKD has to be diagnosed both. I think you have very very rightly you pointed out, and this is very very important to create awareness about urine albumin creatinine ratio. And now it is standardized. So, early morning UACR if it is elevated, rather now the recent recently there is emphasis that not only 30 as the cutoff, 30 mg/g as the cutoff. The cutoff people have gone back that just about 10 mg/g also there is a between 10 to 30 also there is a window.
So, so if it is elevated above 10, then, you know, to a lot of patients when you say it non-albuminuric CKD, if we consider 10 mg/g, then many patients, I think majority of the patients will land into albuminuria, which is which is considered now within the normal range, but actually it is slightly elevated like uh more emphasis on prevention. So, we have more tighter control. LDL cholesterol goal is getting down and down. And for high risk, it is now less than 70 to less than 55. Recent guidelines emphasize. So, similarly for UACR also, I think the levels may fall below 30 over time. But at present, even 30 is awareness is not there. So, we need to create more awareness. UACR is like But pressure is a continuum. Even when it is in the normal range, the hazard ratio for cardiovascular mortality, for all cause mortality is 1.77. So, you are right. Even within the normal range, the risk is more. Risk is more. So, just like a continuum, blood pressure lower is better. So, lower is better. So, 115 onwards the systolic blood pressure, the risk is there. So, what is the target? Suppose somebody has microalbuminuria or a macroalbuminuria, what should be the target?
Target should be actually depending on initial initial levels of albuminuria, we should we have now agents which can decrease it remarkably like we have now RAS blockers are there for a long time, and they have been emphasized when in a type 2 diabetes patients particularly if there is microalbuminuria. So, blood pressure control, we need to use RAS blockers. So, those are there already.
And then we have SGLT2 inhibitors now which can, you know, further control the microalbuminuria. And then the newer non-steroidal anti-non-steroidal drugs, the the mineralocorticoid receptor antagonists are there. And even the recent GLP-1 agonists also, they also reduce albuminuria. So, we have the tools available to, you know, decrease the albuminuria, but the goal should be at least 50% reduction than whatever is the initial levels are there.
But as low as we can go. So, if the patient has hypertension, type 2 diabetes, then I would like to use maybe all three if required. So, and, you know, so goal is as low you can get. I think and it is possible with the modern tools which are available. Yes, yes. LDL, we have lower is better. Correct. So, thank you very much, Dr. Parikh, for the wonderful takeaways. Thank you very much.
>> Thank you, sir.
>> [music]
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