Heart

Atherosclerosis

Atherosclerosis, also known as hardening of the arteries, is a chronic inflammatory process in which lipids and immune cells gradually accumulate in the vessel wall, forming atherosclerotic plaques. This condition arises from a complex interplay of genetic and lifestyle factors, which are well documented both clinically and epidemiologically.

For calculating the atherosclerosis score in Synapse, the standard SCORE-2 formula^[1] (which uses age, sex, systolic blood pressure, total cholesterol, and smoking status) is extended with additional pro-atherogenic factors. These include insulin resistance, excess abdominal fat, chronic inflammation, cholesterol, chronic kidney insufficiency, physical activity, sedentary behaviour, and stress. By incorporating these additional variables, we can build a more holistic risk profile and implement interventions at an earlier stage.

10-year risk

SCORE2^[1] (Systematic COronary Risk Evaluation 2) is a validated risk model that estimates the 10-year risk of fatal and non-fatal cardiovascular events in individuals aged 40 to 69 years. SCORE2-OP does the same for individuals aged 70 to 89 years. This model builds on the original SCORE table and takes into account age, sex, systolic blood pressure, non-HDL cholesterol, and smoking status.

At Synapse, we apply the following cut-offs^[1]:

An important limitation of SCORE2 is that the risk of atherosclerosis is estimated only over a 10-year period, whereas atherosclerosis is a process that develops over multiple decades and can begin in childhood. This means we often intervene too late and miss a significant opportunity for prevention. To compensate for this, Synapse also considers additional parameters that help estimate the risk of atherosclerosis more accurately.

30-year risk

To correct for the underestimation of cardiovascular risk in younger populations, Synapse uses the 30-year cardiovascular risk score^[68], developed on the basis of the Framingham Heart Study. This model is applicable between ages 20 and 59 and provides a longer time horizon for risk stratification.

The clinical value of this approach lies in improved risk communication. For example, a young individual with a 10-year risk of 2% (1 in 50) may still have a 30-year risk of 12–15% (e.g. 1 in 8). This longer time horizon demonstrably increases motivation for lifestyle interventions.

At Synapse, we apply the following age-dependent model selection:

• Under 20 years: no cardiovascular risk score
• 20 to 59 years: 30-year cardiovascular risk
• 60 years and older: SCORE2 / SCORE2-OP

The cut-offs we apply at Synapse are:

Kidney function

Chronic kidney disease (CKD) is widely recognised as an important risk factor for atherosclerosis^[5], although the extent to which this relationship is direct or indirect is not yet fully understood. Indirectly, CKD contributes to two of the most prominent risk factors for atherosclerosis: dyslipidaemia and hypertension.

Through the accumulation of various substances that can irritate the vessel wall, CKD may also contribute directly to the development of atherosclerosis^[5]. These metabolites inhibit nitric oxide synthase (NOS), reducing vasodilation and accelerating vascular wall damage.

Homocysteine

Elevated homocysteine^[70], ^[71] is associated with increased all-cause mortality and with numerous conditions, particularly cardiovascular disease. An independent and partly causal relationship has been described for venous thrombosis, peripheral arterial disease, coronary atherosclerosis, and stroke. The underlying mechanisms include oxidative stress, inflammation, and endothelial dysfunction, with reduced nitric oxide availability.

At Synapse, we apply the following cut-offs^[70], ^[71]:

Inflammation

Chronic inflammation^[5] (CI) refers to a persistent, low-grade activation of the immune system present in the body without a clear infectious cause. This form of inflammation is characterised by increased production of pro-inflammatory cytokines such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and C-reactive protein (CRP).

Research has shown that CI plays a crucial role in the development and progression of atherosclerosis^[7]. Inflammatory mediators promote endothelial dysfunction, stimulate the accumulation of immune cells in the vessel wall, and contribute to the instability of atherosclerotic plaques. This increases the risk of cardiovascular complications such as myocardial infarction and stroke.

Insulin sensitivity

Insulin sensitivity^[8] is a key determinant of glucose homeostasis and metabolic regulation. A decline in insulin sensitivity (insulin resistance) leads to compensatory hyperinsulinaemia by the pancreatic β-cells to maintain euglycaemia. This process lies on a continuum from insulin resistance to prediabetes and ultimately type 2 diabetes, where progressive β-cell dysfunction results in hyperglycaemia and increased cardiovascular risk.

Insulin resistance is a strongly associated risk factor for atherosclerosis and cardiovascular disease^[9], ^[10], ^[11], through the combination of metabolic dysregulation and secondary dyslipidaemia with endothelial dysfunction, pro-inflammatory activation, and accelerated arterial calcification.

Waist circumference

Excess abdominal fat is closely linked to an increased risk of atherosclerosis. Excessive fat accumulation affects multiple risk factors such as blood pressure, glucose levels, and lipid metabolism, and contributes to systemic inflammation. Adipocytes also secrete adipokines that can directly disrupt the functioning of endothelial cells, arterial smooth muscle cells, and macrophages in the vessel wall, further contributing to the development of atherosclerosis^[18], ^[19].

Exercise

Regular physical activity has a protective effect on the vasculature by reducing systemic inflammation, improving endothelial function, and thereby slowing atherosclerotic progression^[12], ^[13]. Epidemiological studies demonstrate an inverse dose-response relationship between the amount of physical activity and cardiovascular risk^[14].

Sedentary behaviour

Prolonged sitting is increasingly recognised as an independent risk factor for atherosclerosis. Physical inactivity leads to increased expression of vascular NADPH oxidase, resulting in greater production of reactive oxygen species (ROS)^[15]. This additional oxidative stress worsens endothelial dysfunction and promotes atherosclerotic processes^[13].

Stress

Chronic stress is an important lifestyle factor that contributes to both the onset and progression of atherosclerosis^[13]. One plausible explanation is that stress damages the endothelium, leading to macrophage activation and foam cell formation, thereby initiating and advancing atherosclerotic plaques. Inflammation, cell signalling, lipid metabolism, and endothelial function all play a crucial role in this process^[16], ^[17].

History

A prior myocardial infarction, coronary stent or bypass, ischaemic stroke or TIA and peripheral arterial disease together count as established atherosclerotic cardiovascular disease (ASCVD). They share one mechanism, atherosclerosis with thrombosis, and under the ESC guideline place a person straight into the very high risk category, without the need for a risk score^[74]. Residual risk stays real under treatment: after a first event-free year, roughly one in five still has a new event within three years, highest after a recent coronary syndrome, with polyvascular disease, diabetes and kidney failure^[75].

The LDL goals come from the ESC/EAS dyslipidaemia guideline and were left unchanged in the 2025 update^[55], ^[73]. In Synapse a stent, bypass, infarction or stroke changes the starting point of the atherosclerosis score; a TIA or peripheral arterial disease is shown as history.

Other heart and vascular problems

What a member enters here (for example atrial fibrillation, heart failure, valve disease or an aneurysm) is shown verbatim and is not part of any calculation. These conditions are not atherosclerosis and do not automatically count as established ASCVD^[74]. In atrial fibrillation stroke risk is central and the CHA₂DS₂-VA score decides on anticoagulation^[76]; an aortic aneurysm, by contrast, is often an expression of systemic atherosclerosis and receives the same strict risk factor control^[77]. Heart failure together with a prior vascular event makes the risk very high^[74].

Risk of heart and vascular disease

This factor sums up cardiovascular risk in four steps (low, average, high, very high). Up to age 45 it rests on the Framingham 30-year risk, because the 10-year chance in young adults is almost always low, even with clear risk factors^[78]. From age 46 it rests on SCORE2, or SCORE2-OP from age 70, with the age-dependent ESC thresholds^[1], ^[79], ^[74]. Anyone with established cardiovascular disease sits on the highest step straight away.

Chronic inflammation

Inflammation is the body's natural defence response to injury or infection. In acute inflammation, we see a temporary increase in pro-inflammatory activity, briefly activating the immune system to neutralise the harmful stimulus. Once recovery occurs, the immune system returns to a resting state.

In chronic low-grade inflammation, however, the immune system remains persistently active below the surface. This can not only cause ongoing tissue damage but also lead to disruptions in metabolism and hormonal balance. Over time, this smouldering inflammatory response increases the risk of a broad range of conditions, including cardiovascular disease, diabetes, hepatic steatosis, neurodegenerative disease, and even certain forms of cancer.

How to measure chronic low-grade inflammation?

The best-known and most sensitive parameter for detecting an inflammatory response is C-reactive protein (CRP). Although this acute-phase protein provides a useful initial indication, the test alone is insufficiently specific to accurately determine the risk of chronic low-grade inflammation.

As a complement to CRP, Synapse also evaluates:

• Aggregate scores that take into account the distribution of white blood cells, platelets, and other inflammatory markers
• Individual biomarkers, such as ferritin and uric acid, to build a more complete picture of inflammatory status
• Lifestyle factors such as poor diet, sedentary behaviour, and other environmental factors that underlie the onset and perpetuation of chronic inflammation

Aggregate scores

Because the literature lacks consensus on which aggregate biomarker has the highest validity for estimating chronic inflammation, Synapse uses the three most extensively described scores in its score calculation.

INFLA score

Chronic low-grade inflammation is an important risk factor for cardiometabolic disease and can be detected at an early stage using the Low-Grade Inflammation Score (INFLA score)^[20], ^[21], ^[22]. In simple terms, a higher INFLA score means more inflammation in the body.

The INFLA score is a composite measure that integrates four components:

• hs-CRP
• leukocytes
• platelets
• granulocyte-to-lymphocyte ratio (sum of neutrophils, eosinophils, and basophils)

Each biomarker is categorised based on deciles:

• Values in the highest deciles (7th–10th) receive a score of +1 to +4.
• Values in the middle deciles (5th–6th) receive a score of 0.
• Values in the lowest deciles (1st–4th) receive a score of -4 to -1.

By summing the scores of all four components, a total INFLA score is obtained that can range from -16 to +16. A higher score indicates greater low-grade inflammation and an elevated risk of future cardiometabolic problems. Routinely measuring the INFLA score in adults without existing cardiometabolic disease can contribute to timely intervention and prevention of cardiometabolic pathology^[22].

The cut-offs we apply at Synapse are:

SII

The Systemic Inflammation Index (SII)^[23], ^[24], ^[25] is another biomarker for chronic inflammation that is widely studied in the literature and also correlates with both total and cardiovascular mortality. This index is calculated using the following formula:

SII = (P × N) / L

Here P represents the peripheral platelet count (10³/μL), N the absolute neutrophil count (10³/μL), and L the absolute lymphocyte count (10³/μL). The resulting unit of the SII is therefore 10³/μL. A lower SII score indicates a lower level of chronic inflammation, making the SII a useful biomarker for estimating subclinical cardiovascular risk.

There is no consensus on exact cut-off values for the SII. At Synapse, the following cut-offs have been adopted:

SIRI

The Systemic Inflammation Response Index (SIRI)^[24], ^[26] is a third aggregate score that can be used as a biomarker in screening for chronic inflammation. Like the INFLA score and the SII, it correlates with both total and cardiovascular mortality. The SIRI is calculated using the following formula:

SIRI = (N × M) / L

Here N represents the neutrophil concentration, M the monocyte concentration, and L the lymphocyte concentration. To obtain the correct units, Synapse calculates:

SIRI = ( N (%) × M (%) × leukocytes (/μL) ) / ( L (%) × 10⁵ )

A higher SIRI score indicates higher levels of smouldering inflammatory activity and elevated cardiovascular risk. There is no consensus on exact cut-off values for the SIRI. Synapse has adopted the following cut-offs:

Individual biomarkers

Given the crucial importance of chronic low-grade inflammation (CLI) in the development of various chronic diseases and the lack of consensus on the most valid aggregate inflammation scores, Synapse has chosen to evaluate individual inflammatory biomarkers alongside the indices described above.

hsCRP

C-reactive protein (CRP)^[27], ^[28], ^[29], ^[30], ^[31] is an acute-phase reactant produced in the liver in response to inflammation. The high-sensitivity variant (hs-CRP) is a well-characterised biomarker with high sensitivity for detecting chronic low-grade inflammation. "High sensitivity" refers to the much lower detection limit (<0.6 mg/L) compared to most standard CRP assays (<6 mg/L). Elevated hs-CRP values are associated in numerous studies with an increased risk of cardiovascular disease^[32], ^[33], ^[34]. The following risk categories for chronic inflammation and cardiovascular disease are generally used:

Ferritin

Ferritin^[35], ^[36], ^[37], ^[38] is a protein responsible for iron storage and also functions as an acute-phase reactant, as its concentration rises with inflammation. Several studies suggest that ferritin may play a role in detecting chronic low-grade inflammation and argue that it can serve as a prognostic biomarker.

The ferritin cut-off values applied at Synapse are:

These cut-offs apply to the inflammation score, which only penalises a high ferritin. The colour of the ferritin value itself also has a lower bound, because a low ferritin points to depleted iron stores: up to 15 μg/L red, up to 30 μg/L orange, up to 45 μg/L yellow. The value's optimal range is therefore 45–400 μg/L in men and 45–150 μg/L in women.

Uric acid

Uric acid is an end product of purine metabolism and a well-known risk factor for atherosclerosis and cardiometabolic disease^[39]. Hyperuricaemia is also associated with chronic inflammation^[40].

Elevated uric acid levels can promote oxidative stress and endothelial dysfunction, contributing to persistent inflammation and atherogenesis. Measuring uric acid can therefore help in estimating both cardiovascular risk and chronic low-grade inflammation.

Lifestyle factors

Synapse not only maps the current inflammatory status but also takes into account how lifestyle factors influence the future risk of chronic inflammation. Based on the literature, several well-documented determinants have been selected: smoking, poor diet, and alcohol use. These factors contribute significantly to both the onset and the perpetuation of low-grade inflammatory processes. <!-- chronic stress, disrupted sleep, sedentary behaviour -->

Smoking

Smoking^[41], ^[42] is one of the most pronounced risk factors for chronic inflammation and cardiovascular disease. During smoking, toxic compounds including free radicals enter the bloodstream, leading to oxidative stress and activation of immune cells.

These processes stimulate the production of pro-inflammatory cytokines and cause a persistent inflammatory response that damages the vessel wall and accelerates atherosclerotic processes.

Inflammatory food

Diet^[43], ^[44] plays a major role in chronic inflammation, particularly when too many refined carbohydrates and processed foods are consumed and fibre intake is insufficient. These patterns disrupt the gut microbiome, promote insulin resistance, and elevate pro-inflammatory cytokines.

Within Synapse, "inflammatory diet" refers to a dietary pattern high in unhealthy fats, refined sugars, and processed foods, and low in fibre.

Alcohol

Chronic or excessive alcohol use^[45], ^[46] can cause liver damage and increase intestinal permeability, allowing bacterial endotoxins to enter the bloodstream more easily. This leads to sustained production of pro-inflammatory mediators and promotes oxidative stress in various organs, contributing to the onset and perpetuation of chronic inflammation.

Sleep

Disrupted sleep can lead to an increase in systemic inflammatory markers^[47], ^[48]. During poor sleep, the normal resolution of inflammatory processes becomes imbalanced, as key molecules that promote recovery (including resolvins) remain suppressed for extended periods. This can give rise to smouldering inflammation that increases the risk of various immune-mediated conditions.

Blood pressure

Elevated blood pressure^[49], ^[50] is one of the most important risk factors for cardiovascular disease. Even mildly elevated values can cause damage to the vessel wall, which over time leads to structural changes, endothelial dysfunction, and progressive atherosclerosis.

Kidney function

Reduced kidney function^[52] is an important, often underestimated risk factor for cardiovascular disease. Kidney insufficiency is accompanied by accumulation of waste products, dysregulated fluid and electrolyte balance, and hormonal changes that can contribute to hypertension, chronic inflammation, and atherosclerosis. Synapse assesses kidney function using the race-free CKD-EPI 2021 formula^[53].

ACR

The albumin-to-creatinine ratio (ACR)^[69] is a biomarker that corrects the amount of albumin for urine concentration via creatinine. The ACR detects early glomerular damage, often before a decline in eGFR becomes apparent. Albuminuria is also an independent predictor of cardiovascular morbidity and mortality, meaning the ACR refines not only kidney function assessment but also the overall vascular risk profile.

At Synapse, we apply the following ACR categories^[69]:

By combining eGFR and ACR, the KDIGO risk matrix^[69] is obtained, providing more accurate risk stratification than eGFR alone. The table below shows the corresponding risk level for each combination of eGFR stage and ACR category.

Cholesterol

Hypercholesterolaemia is a well-known and well-documented risk factor for cardiovascular disease, as it directly contributes to the development of atherosclerosis.

To make interpretation easier for patients, Synapse uses a single composite cholesterol score that integrates several relevant parameters, including non-HDL cholesterol, HDL cholesterol, apoB, and Lp(a).

Non-HDL cholesterol

Cholesterol is a fatty substance produced in the liver and transported in the blood via various lipoproteins. Because the atherogenic lipoproteins include not only LDL but also IDL and VLDL, non-HDL cholesterol provides a more accurate estimate of the atherogenic lipid profile than LDL alone^[54].

Non-HDL = total cholesterol - HDL

In line with the 2025 focused update of the ESC/EAS guidelines^[73], Synapse applies risk-dependent cut-offs for non-HDL cholesterol. A cardiovascular risk category is determined for each individual. One criterion is sufficient to place a person in a category; the highest category takes precedence:

Very high risk

• SCORE2/SCORE2-OP >20%
• Severe kidney insufficiency based on eGFR and ACR
• Documented atherosclerotic vascular disease (coronary, cerebrovascular, or peripheral)
• Diabetes mellitus with organ damage (based on eGFR and ACR)
• Diabetes mellitus with ≥3 cardiovascular risk factors (smoking, hypertension, dyslipidaemia, obesity)
• Type 1 diabetes with duration >20 years
• Familial hypercholesterolaemia with an extremely elevated risk factor
• One extremely elevated risk factor: total cholesterol >310 mg/dL, LDL >190 mg/dL, or blood pressure >180/110 mmHg

High risk

• SCORE2/SCORE2-OP 10-20%
• Moderate kidney insufficiency based on eGFR and ACR
• Diabetes mellitus without organ damage, with duration ≥10 years or an additional risk factor
• Familial hypercholesterolaemia without extremely elevated risk factors

Moderate risk

• SCORE2/SCORE2-OP above the age-dependent threshold but <10%
• Other diabetes mellitus (short duration, no additional risk factors, no organ damage)

Low risk

None of the above criteria apply, or a SCORE2/SCORE2-OP^[1] below the age-dependent threshold (<2.5% at <50 years, <5% at 50-69 years, <7.5% at ≥70 years).

The highest risk category across all criteria determines the final classification. Based on this, the following non-HDL cut-offs are applied^[55], ^[73]:

ApoB

ApoB is the structural protein on all atherogenic lipoproteins (LDL, VLDL, IDL, and Lp(a)); each particle carries exactly one ApoB molecule. The ApoB concentration therefore directly reflects the number of atherogenic particles in circulation, whereas (non-)HDL cholesterol primarily reflects the cholesterol mass within those particles. Recent research shows that ApoB is consequently a better predictor of atherosclerotic risk than non-HDL cholesterol^[55].

Cholesterol levels say nothing about particle size or number: many small, cholesterol-poor LDL particles can yield a normal non-HDL-C value but a high ApoB and thus a greater atherogenic risk. ApoB captures this discordance and therefore correlates more strongly with clinical outcomes than non-HDL-C.

At Synapse, the following cut-offs^[56] have been adopted:

HDL cholesterol

High-density lipoprotein (HDL) is described in the literature as a protective factor against cardiovascular disease^[55], as it plays a crucial role in the transport of cholesterol from peripheral tissues back to the liver. In general, higher HDL levels are associated with lower cardiovascular risk. Although exact cut-off values may vary between guidelines, the following generally apply^[57]:

Very high HDL (above 90 mg/dL) is also associated with increased risk and is therefore scored as high-risk.

Lp(a)

Lipoprotein(a) [Lp(a)] is a lipoprotein particle containing both apoB100 and apolipoprotein(a) and is 70–90% genetically determined. Elevated Lp(a) levels are an independent and causal risk factor for atherosclerotic cardiovascular disease, primarily because they can promote atherogenesis, inflammation, and thrombosis. Unlike LDL cholesterol and apoB, a high Lp(a) concentration continues to increase the risk of cardiovascular disease even when LDL and apoB are lowered^[60].

Although research from sources such as the UK Biobank^[61] shows that an Lp(a) value above 30 nmol/L is already associated with increased cardiovascular risk, universally standardised measurement methods and guidelines for both diagnosis and treatment are currently lacking^[62]. Synapse therefore incorporates Lp(a) separately in the cholesterol score, so that individuals with elevated Lp(a) can be identified and monitored at an early stage.

At Synapse, we apply the following cut-offs^[61]:

Risk category

The risk category decides which targets apply to LDL, non-HDL and ApoB. It follows the ESC/EAS guideline: established ASCVD, diabetes with organ damage or long-standing type 1 diabetes, severe kidney failure and familial hypercholesterolaemia with an additional risk factor place a person at high or very high risk; in apparently healthy people SCORE2 decides^[55], ^[1]. A single markedly raised risk factor (total cholesterol >8 mmol/L, LDL >4.9 mmol/L or blood pressure ≥180/110 mmHg) is also enough for at least a high category^[55]; Synapse places that situation at very high risk, because the abnormal value needs attention straight away. Low risk is not shown as a factor.

The 2025 focused update left these goals unchanged^[73].

Anaemia

Anaemia is scored on the haemoglobin, with a threshold per sex: below 13.0 g/dL in men and below 12.0 g/dL in women. At or above the threshold there is no score.

The haemoglobin itself is coloured red below 8.0 g/dL, orange below 11.0, yellow up to 13.5 g/dL in men up to 65 years (13.0 above 65) and up to 12.0 in women up to 65 years (above 65 up to 13.0, as in men), and green up to 16.5 g/dL in men and 16.0 in women; above that it is yellow again, and orange from 18.5 g/dL (men) or 16.5 g/dL (women). In women over 65 the threshold for the score stays at 12.0 g/dL: 12.0 to 12.9 g/dL is yellow without a score. The MCV is green from 80 to 100 fL and yellow outside that range. The brain score keeps its own haemoglobin thresholds (13.4 and 12.2 g/dL).

Haematocrit (the share of red blood cells) is shown to the patient only above 49% in men and 48% in women, in orange; there is no yellow zone, a low haematocrit has no colour, and it does not count in the digital twin. For the doctor, Synapse flags a high haemoglobin or haematocrit (the WHO criteria for polycythaemia vera, 5th edition: haemoglobin above 16.5 g/dL in men or 16.0 in women, or haematocrit above 49% or 48%): a first value asks for a repeat in a well-hydrated patient and a check for a secondary cause (smoking, sleep apnoea, testosterone, SGLT2 inhibitors, diuretics); a confirmed value without explanation asks for erythropoietin and JAK2 V617F, or referral to haematology. A second, separate flag for the doctor signals a possible haemoglobinopathy when the MCV is below 80 fL with ferritin of at least 30 μg/L and CRP of at most 5 mg/L, whatever the haemoglobin; the Mentzer index (MCV divided by the red cell count) only chooses the wording: below 13 suggests haemoglobin electrophoresis, from 13 haemoglobin analysis is considered alongside other causes. A normal HbA2 does not exclude alpha-thalassaemia carriage.

Cause of anaemia

With a haemoglobin from 8.0 g/dL up to the threshold for the sex, Synapse searches the blood values for the most likely cause. The MCV guides the first step (microcytic is an MCV below 80 fL, macrocytic above 100 fL): microcytic usually points to iron deficiency, macrocytic to a lack of vitamin B12 or folate^[80]. A ferritin below 30 μg/L confirms iron deficiency; with inflammation or kidney disease that threshold shifts to about 100 μg/L, and a low transferrin saturation and a raised CRP help to separate iron deficiency from anaemia of inflammation^[80], ^[81]. An eGFR below 45 points to renal anaemia.

Iron deficiency without a clear explanation calls for investigation of the gastrointestinal tract: the BSG advises gastroscopy and colonoscopy in men and postmenopausal women, and coeliac serology in everyone^[82]. The AGA guideline uses a ferritin threshold of 45 μg/L for this^[83]. With a haemoglobin below 8.0 g/dL Synapse shows no cause, only the haemoglobin, because prompt clinical evaluation then comes first.

Developed and reviewed with the Synapse medical advisory board.

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Put it into practice

Heart

• Biological age calculators
• Blood fats and dietary fats
• High ApoB
• Nutrition and blood pressure
• Nutrition and the heart

Biomarkers in this domain

• Cholesterol
• LDL cholesterol
• HDL cholesterol
• Triglycerides
• ApoB
• Lp(a)
• hsCRP
• Ferritin
• Creatinine
• Uric acid
• Albumin/creatinine ratio (ACR)
• Hemoglobin
• Hematocrit
• White blood cells
• RDW (red-cell distribution width)
• Platelets (thrombocytes)
• Vitamin B12
• Folic acid
• Iron
• Transferrin saturation
• MCV
• eGFR (CKD-EPI)