BloodWorker — Comprehensive Medical Data and Lab Analysis Report

What is this test?

The CMP is a panel of 14 blood tests that gives a broad snapshot of your body's chemical balance and metabolism. It evaluates kidney function, liver function, blood sugar, electrolyte and fluid balance, and protein levels. It's one of the most commonly ordered screening panels.

Interpretation

Glucose (95 mg/dL): Your fasting glucose sits at the upper end of the normal range (70–99) but remains below the pre-diabetes cutoff of 100 mg/dL per ADA criteria. Combined with your HbA1c of 4.9% (see Section 5), this confirms excellent long-term glycemic control. The fact that you have glucose spilling into your urine (2+ on UA) while your blood glucose is clearly normal is a critical paradox that we will examine in the Cross-Correlations section — it is almost certainly explained by your dapagliflozin.

CO2 / Bicarbonate (19 mmol/L — LOW): This is 1 point below the reference floor. CO2 on a CMP actually measures serum bicarbonate (HCO3⁻), which is a key buffer in your blood's acid-base system. A low bicarbonate can mean your blood is running slightly acidic (a mild metabolic acidosis). This is a recognized, dose-dependent effect of SGLT2 inhibitors like dapagliflozin, which promote ketone body production and mild urinary bicarbonate losses. The finding of trace urinary ketones on your UA further supports this mechanism. Your anion gap calculates to 18, which is elevated above the typical cutoff of 12. This is consistent with a mild anion-gap metabolic acidosis — again, fitting the SGLT2-inhibitor ketoacidosis-spectrum pattern. At this level (CO2 of 19, trace ketones, no symptoms of DKA), this is at the mild end and is a known pharmacologic effect, not an emergency. However, it is important for your provider to be aware of this pattern, especially since you are non-diabetic — the risk-benefit calculus for monitoring is slightly different.

Kidney markers (Creatinine 1.0, eGFR 85, BUN 22): Your creatinine and eGFR place you in KDIGO category G2 — mildly decreased kidney function. For a 63-year-old male, an eGFR of 85 is quite common and not necessarily pathologic, but it is worth knowing where you stand. The KDIGO classification is: G1 ≥ 90 (normal), G2 = 60–89 (mildly decreased), G3a = 45–59 (mild-to-moderate decrease). Your BUN/creatinine ratio of 22 is within range but on the higher side, which can be seen with mild dehydration, high protein intake, or dapagliflozin's diuretic effect (SGLT2 inhibitors promote osmotic diuresis). Your urine microalbumin/creatinine ratio of 4 mg/g (see Section 8) is reassuringly normal, placing you in KDIGO albuminuria category A1 (normal). So overall: G2/A1 = low risk for CKD progression.

BUN/Creatinine Ratio (22 — high-normal): This is worth mentioning because dapagliflozin causes your kidneys to excrete more water (osmotic diuresis from glucosuria). A ratio near the upper end of normal can be a subtle marker of relative volume depletion. Make sure you are staying well hydrated.

Electrolytes (Sodium 139, Potassium 4.2, Chloride 102): All beautifully mid-range. Your potassium of 4.2 is reassuring because dapagliflozin can occasionally shift potassium. No concern here.

Calcium (9.1 mg/dL): Normal. Adjusting for albumin: corrected calcium ≈ 9.1 + 0.8 × (4.0 − 4.5) = 8.7 mg/dL — still normal. No hypercalcemia despite your high vitamin D level (see Section 10). This is an important safety check.

Liver panel (AST 25, ALT 12, Alk Phos 96, Total Bilirubin 0.7, Albumin 4.5): All completely normal. AST and ALT are well within range with a normal AST/ALT ratio. No evidence of hepatocellular injury, cholestatic disease, or synthetic dysfunction. This is relevant context for the urine bilirubin finding (see Urinalysis) — since all serum liver markers are normal, a positive urine bilirubin is most likely a false positive.

Total Protein (6.9) and Albumin (4.5): Both normal. Your albumin at 4.5 reflects good nutritional status and liver synthetic function. The albumin/globulin ratio of 1.88 is normal and unremarkable.

What is this test?

The CBC measures the cellular components of your blood: red cells (oxygen carriers), white cells (immune system), and platelets (clotting). The differential breaks down white cell types to look for infection patterns, allergic activity, or blood cell disorders.

Interpretation

Red Cell Line: Hemoglobin of 14.6 and hematocrit of 41.3% are solidly normal for a 63-year-old male. No anemia. Your MCV of 92 is perfectly normocytic (normal-sized red cells), MCH and MCHC are both normal, and your RDW of 12.3% (low-normal) indicates uniform red cell size — there is no evidence of iron deficiency, B12/folate deficiency, chronic disease anemia, or any hemolytic process. SGLT2 inhibitors can occasionally increase hematocrit slightly through hemoconcentration (due to their diuretic effect); your hematocrit at 41.3% does not appear significantly affected.

White Cell Line: Total WBC of 5.1 is mid-range normal. Your differential shows a normal neutrophil predominance (66%) with lymphocytes at 20%. The absolute lymphocyte count of 1.0 is within range but sits at the low-normal boundary (range 0.7–3.1). This is not flagged abnormal and can be a normal finding, but it is worth noting because it contributes to your NLR of 3.3 (mildly above the "optimal" range of 1–3). A modestly elevated NLR can be seen with physiologic stress, recent physical activity before blood draw, mild subclinical inflammation, or as a normal variant. In the context of your completely normal ESR (11) and no other inflammatory markers, this is likely not clinically significant. However, if your lymphocyte count trends lower on future labs, that would warrant further evaluation.

Platelets (177): Normal. On the lower-normal side of the range (150–450), but perfectly adequate for normal clotting function. No concern.

Eosinophils (0.2, 4%): Normal. No signal for allergic or parasitic processes.

Regarding your fatigue symptoms: Your CBC does not support anemia as a cause of your morning fatigue or afternoon sleepiness. Hemoglobin, red cell indices, and RDW are all reassuringly normal.

What is this test?

The lipid panel measures cholesterol and triglyceride levels in your blood to assess cardiovascular risk. It includes total cholesterol, HDL ("good" cholesterol — higher is better), LDL ("bad" cholesterol — lower is better for people with risk factors), triglycerides, and VLDL. You are currently taking rosuvastatin 10 mg and just started ezetimibe 10 mg two days before this draw, so the ezetimibe has not yet had time to affect these numbers (it takes 2–4 weeks).

Interpretation

Context — your cardiovascular history: You have a coronary artery calcium (CAC) score that went from 72 → 207 over 2 years but has been stable at 207 for 6 years. This is a genuinely impressive result. CAC scores almost always increase over time; stabilization over 6 years is consistent with effective plaque-modification through statin therapy and lifestyle changes. Your CAC score of 207 places you above the 75th percentile for your age and sex per MESA data, which classifies you as having established subclinical atherosclerosis. This means you are in a secondary-prevention category: the goal is to prevent progression and events, not just screen for risk.

LDL at 102 mg/dL: The lab flags this as "high" against a general-population reference range of < 100. However, the clinically meaningful question is: what LDL target is appropriate for your risk category? Given your CAC of 207 and established coronary atherosclerosis, current AHA/ACC guidelines generally recommend an LDL target of < 70 mg/dL, with some guidelines arguing for < 55 mg/dL in patients with confirmed atherosclerotic cardiovascular disease (ASCVD). At 102 mg/dL on rosuvastatin 10 mg alone, your LDL remains above these guideline targets. The recent addition of ezetimibe (started 2 days before this draw) is a standard next step that typically reduces LDL by an additional 15–25%, which would project your LDL toward approximately 77–87 mg/dL. Repeat lipid testing in 6–8 weeks after ezetimibe has reached steady state would be informative.

HDL at 79 mg/dL: This is excellent. An HDL this high in a 63-year-old male is protective and well above the > 40 mg/dL floor. It drives your total cholesterol/HDL ratio down to 2.49, which is in the low-risk category.

Triglycerides at 99 mg/dL: Optimal. Well below the 150 threshold. Combined with your high HDL, the TG/HDL ratio of 1.25 strongly suggests large, buoyant (Pattern A) LDL particles rather than small, dense (Pattern B) particles. Pattern A particles are less prone to penetrating arterial walls and oxidizing, which is favorable for your atherogenic risk profile even though LDL number is above target.

Non-HDL Cholesterol at 118: Non-HDL is increasingly viewed as a more comprehensive measure of atherogenic lipoproteins than LDL alone because it includes VLDL, IDL, and Lp(a). For your risk profile, a non-HDL target < 100 mg/dL would be ideal. Ezetimibe should help close this gap as well.

Rosuvastatin side-effect cross-check: Statins can occasionally raise liver enzymes (AST/ALT) or blood glucose. Your AST (25) and ALT (12) are both low-normal, and your fasting glucose (95) and HbA1c (4.9%) are normal. No signal of adverse statin effects in this panel.

What is this test?

HbA1c measures the percentage of your hemoglobin (the oxygen-carrying protein in red blood cells) that has glucose permanently attached to it. Because red blood cells live about 90–120 days, HbA1c gives a weighted average of your blood sugar over the past 2–3 months. It is the gold-standard screening test for diabetes and pre-diabetes per ADA criteria.

Interpretation

Your HbA1c of 4.9% is at the very low end of the normal range. Your estimated average glucose of 94 mg/dL aligns nearly perfectly with your measured fasting glucose of 95 mg/dL — the two cross-validate each other beautifully. There is no evidence of diabetes, pre-diabetes, or insulin resistance by glycemic markers.

This is important context because you are taking dapagliflozin (an SGLT2 inhibitor) in a non-diabetic indication — presumably for cardioprotective or other benefits. SGLT2 inhibitors work by blocking glucose reabsorption in the kidney's proximal tubule, forcing glucose into the urine regardless of blood sugar level. In a non-diabetic patient with already-normal glucose, the drug will still produce glucosuria (urine glucose), which is exactly what your urinalysis shows. The HbA1c of 4.9% confirms that this drug-induced glycosuria is not a sign of diabetes.

What is this test?

TSH is produced by your pituitary gland and tells your thyroid how much thyroid hormone to make. It is the best single screening test for thyroid dysfunction. High TSH suggests hypothyroidism (underactive thyroid); low TSH suggests hyperthyroidism (overactive thyroid). Thyroid disorders are a common cause of fatigue, heart rate changes, and exercise intolerance.

Interpretation

Your TSH of 2.58 sits squarely in the middle of the reference range, suggesting normal thyroid function. This is clinically relevant because both hypothyroidism and hyperthyroidism can cause fatigue, exercise intolerance, and palpitations — all symptoms you have reported. A normal TSH argues against thyroid dysfunction as a cause of your symptoms.

Some clinicians consider a TSH in the upper-normal range (3.0–4.5) as a potential contributor to fatigue symptoms in certain patients, but at 2.58, you are not in that zone. If there were strong clinical suspicion, free T4 and free T3 levels could be checked to complete the picture, but there is no lab-based reason to suspect thyroid disease from this result alone.

What is this test?

A urinalysis (UA) is a group of physical, chemical, and microscopic tests on your urine. It screens for urinary tract infections, kidney disease, diabetes, liver disease, and other metabolic conditions. A dipstick is used for the chemical portion, and microscopy is performed only if the dipstick triggers a reflex (it was not triggered here, meaning no microscopic abnormalities were expected).

Interpretation

Urine Glucose (2+ — ABNORMAL): This is the most notable finding on the UA. Glucose does not normally appear in urine until blood glucose exceeds approximately 180 mg/dL (the "renal threshold"). Your blood glucose is 95 mg/dL — far below that threshold. This means your kidneys are being forced to spill glucose into the urine by a mechanism other than hyperglycemia. The explanation is dapagliflozin. This drug is an SGLT2 (sodium-glucose cotransporter 2) inhibitor that blocks glucose reabsorption in the proximal tubule of the kidney, deliberately causing glycosuria to lower blood sugar — or, in non-diabetic patients like you, to provide cardioprotective and renal-protective benefits via glucose excretion and associated hemodynamic effects. 2+ glucosuria with a blood glucose of 95 and an HbA1c of 4.9% is the textbook pharmacologic signature of an SGLT2 inhibitor. This is expected, not alarming.

Urine Ketones (Trace — ABNORMAL): When glucose is being dumped into the urine, the body slightly shifts toward using fatty acids for fuel, producing ketone bodies. In a non-diabetic patient on an SGLT2 inhibitor, trace ketones are a common and expected finding. Your serum CO2 (bicarbonate) of 19 — just below normal — is consistent with this mild ketotic shift. This constellation is well-described in the SGLT2 literature. It becomes a concern only if ketones are moderate-to-large, you develop symptoms (nausea, vomiting, abdominal pain, fruity breath, rapid breathing), or bicarbonate drops substantially. At trace levels with CO2 of 19, this is the mild end of the spectrum.

Urine Bilirubin (Positive — ABNORMAL): The dipstick detected bilirubin in your urine, with a comment suggesting evaluation for liver dysfunction. However, all of your serum liver markers are normal: total bilirubin 0.7 (well within range), AST 25, ALT 12, alkaline phosphatase 96, and albumin 4.5. There is no evidence of hepatocellular injury, cholestasis, or synthetic dysfunction. Urine bilirubin dipstick tests are prone to false positives. Common causes include: (1) medications that color the urine or interfere with the dipstick chemistry, (2) high specific gravity specimens (yours is 1.025 — on the concentrated side), and (3) prolonged specimen standing. Given the entirely normal serum liver panel, this is most likely a false-positive dipstick result. No further workup is likely needed unless this recurs on future testing.

Urine pH (5.0 — at the acidic limit): A urine pH of 5.0 is the most acidic the kidneys typically produce. This is consistent with the mild metabolic acidosis picture suggested by your low serum CO2 (19) — your kidneys are compensating by excreting acid, which drives urine pH down. This is a physiologic response and another piece of the SGLT2-inhibitor metabolic fingerprint.

Specific Gravity (1.025): This is concentrated urine. Normal range tops at 1.030. Concentrated urine can reflect mild dehydration or the osmotic diuresis caused by dapagliflozin. In SGLT2-inhibitor patients, the kidneys are excreting extra glucose and water; if fluid intake doesn't fully compensate, urine can actually become more concentrated during certain parts of the day. Make sure you are drinking adequate fluids, especially given the diuretic effect of this medication.

Infection screening: Leukocyte esterase negative, nitrites negative, no blood — no evidence of urinary tract infection. This is worth monitoring periodically because SGLT2 inhibitors increase the glucose content in urine, which can promote urinary tract and genital yeast infections.

What is this test?

This test detects very small amounts of albumin (a protein) leaking into your urine. Healthy kidneys filter very little albumin. Elevated urine albumin ("microalbuminuria" or "moderately increased albuminuria") is one of the earliest signs of kidney damage, often seen in diabetes and hypertension. The ratio normalizes the albumin measurement to urine concentration (via creatinine) so that hydration status doesn't skew the result.

Interpretation

Your urine albumin/creatinine ratio (UACR) of 4 mg/g is well within the normal range (0–29). Per KDIGO classification: < 30 = category A1 (normal to mildly increased), 30–300 = A2 (moderately increased), > 300 = A3 (severely increased). You are firmly in A1 — no albuminuria.

Combined with your serum creatinine of 1.0 and eGFR of 85, this places your overall kidney risk at KDIGO G2/A1 — low risk. This is reassuring both in the context of your occasional hypertension and as a baseline while on dapagliflozin (which is, interestingly, renoprotective — one of its approved indications is reducing albuminuria and slowing CKD progression).

What is this test?

Uric acid is a waste product formed when the body breaks down purines (found in certain foods and in your own cells). High uric acid is associated with gout, kidney stones, and cardiovascular risk. Low uric acid is less commonly discussed but has its own differential.

Interpretation

Your uric acid at 2.6 mg/dL is significantly below the reference floor of 3.8. While high uric acid gets most of the attention (gout, kidney stones), your low uric acid is clinically notable — and has a likely pharmacologic explanation.

Dapagliflozin lowers uric acid. SGLT2 inhibitors are well-documented to reduce serum uric acid by 1.0–1.5 mg/dL on average, though some patients experience larger reductions. The mechanism involves increased uric acid excretion by the kidneys: SGLT2 inhibitors cause glycosuria, which leads to increased urate transport into the urine via the GLUT9 transporter in the proximal tubule. In short, when glucose floods the tubular lumen, uric acid goes with it.

A uric acid of 2.6 in a patient on dapagliflozin is therefore consistent with a known drug effect. Very low uric acid (< 2.0) can occasionally be associated with conditions like Fanconi syndrome or Wilson disease, but at 2.6 with a clear pharmacologic explanation and normal electrolytes/liver function, those are not supported. The practical benefit: you are at essentially zero risk for gout or uric acid kidney stones at this level.

What is this test?

25-hydroxyvitamin D is the main circulating form of vitamin D and the best indicator of your body's vitamin D status. Vitamin D is essential for calcium absorption, bone health, immune function, and is increasingly studied for cardiovascular and mood effects. It is obtained from sun exposure, diet, and supplements.

Interpretation

Your vitamin D level of 112 ng/mL is above the upper reference limit of 100 ng/mL. The Endocrine Society defines deficiency as < 20, insufficiency as 21–29, and sufficiency as 30–100. You are 12% above the ceiling of "sufficient."

Is this dangerous? Vitamin D toxicity is generally not seen until levels exceed 150 ng/mL, and most case reports of clinical toxicity involve levels > 200 ng/mL. At 112, you are in a "supratherapeutic but below toxic" zone. The most important safety check is serum calcium — vitamin D toxicity manifests primarily through hypercalcemia (high blood calcium) because excess vitamin D drives increased intestinal calcium absorption. Your serum calcium is 9.1 mg/dL — normal (and corrected calcium ~8.7, also normal). This is reassuring and argues against acute vitamin D toxicity.

That said, this level suggests you are taking a substantial vitamin D supplement (you did not list one in your medications, but this level would be very unusual without supplementation — most people who don't supplement have levels of 20–50 ng/mL). If you are taking a vitamin D supplement, discuss with your provider whether reducing the dose to target the 40–60 ng/mL range might be appropriate, as there is no demonstrated additional benefit from levels above 60–80 ng/mL, and sustained levels > 100 raise the theoretical risk of soft-tissue calcification over time.

Cross-reference with calcium score: In a patient with a CAC of 207 and supratherapeutic vitamin D, it is worth having a conversation with your provider about whether the high vitamin D level could theoretically promote vascular calcification. The evidence on this is debated — some studies suggest a U-shaped relationship where both very low and very high vitamin D levels are associated with increased cardiovascular calcification. Your CAC has been stable for 6 years, which is reassuring, but maintaining vitamin D in the clearly "sufficient" range (40–60) rather than supratherapeutic may be the most conservative approach.

What is this test?

The Lyme disease immunoblot (Western blot) detects antibodies against specific proteins of Borrelia burgdorferi, the bacteria that causes Lyme disease. The CDC recommends a two-tiered approach: first an EIA (enzyme immunoassay) screen, and then an immunoblot to confirm. The IgG blot requires antibodies to ≥ 5 of the listed B. burgdorferi proteins to be called positive; the IgM blot requires ≥ 2. This test was likely ordered to evaluate your fatigue, palpitations, and exercise intolerance — Lyme disease can cause cardiac involvement (Lyme carditis) and profound fatigue.

Interpretation

Completely negative on all bands for both IgG (indicating past/established infection) and IgM (indicating recent infection). Not a single band was reactive, which is as clean a negative as possible. Per CDC two-tier criteria, this does not support Lyme disease.

An important note from the lab: the immunoblot alone is not recommended for diagnosis without a preceding positive or equivocal EIA screen. If an EIA was performed and was positive/equivocal (triggering reflex to this blot), the negative blot definitively rules out Lyme as the cause of the positive screen. If the blot was ordered directly without an EIA, the result is still informative but the two-tier algorithm was not formally followed. Either way, zero reactive bands out of 13 tested makes Lyme disease extremely unlikely.

With regard to your palpitations and exercise intolerance: Lyme carditis (which can cause heart block, palpitations, and myocarditis) is effectively ruled out by this result.

What is this test?

Rheumatoid factor (RF) is an autoantibody (an antibody directed against your own tissues — specifically against the Fc portion of IgG). It is primarily used to help evaluate rheumatoid arthritis (RA) but can also be elevated in other autoimmune conditions, chronic infections, and even in some healthy older adults. It was likely ordered as part of the evaluation for your intermittent symptoms.

Interpretation

Your RF is < 10 IU/mL, below the positive cutoff of 14. This is a clear negative result that does not support rheumatoid arthritis or other RF-associated autoimmune conditions. Combined with your normal ESR (11) and normal ASO (56.6), there is no serologic signal for systemic autoimmune or rheumatic disease.

What is this test?

The ASO titer measures antibodies against streptolysin O, a toxin produced by group A Streptococcus bacteria. An elevated ASO indicates recent or ongoing streptococcal infection and is used to evaluate post-streptococcal complications such as rheumatic fever (which can cause cardiac valve damage and palpitations) and post-streptococcal glomerulonephritis. This test was likely ordered to explore whether a recent strep infection could explain your palpitations or cardiac symptoms.

Interpretation

Your ASO titer of 56.6 is well within the normal range and does not support recent or active Group A Streptococcus infection. This effectively rules out post-streptococcal rheumatic carditis as an explanation for your palpitations. Combined with the normal echocardiogram and cardiac CT you described, valvular damage from rheumatic fever is not supported.

What is this test?

The erythrocyte sedimentation rate (ESR or "sed rate") measures how quickly your red blood cells settle to the bottom of a test tube in one hour. Faster settling indicates higher levels of inflammatory proteins (especially fibrinogen and immunoglobulins) in the blood. It is a nonspecific marker of inflammation — elevated in infections, autoimmune diseases, cancers, and other inflammatory states. For men, a common age-adjusted upper limit is approximately age ÷ 2 (for you, ~31.5 mm/hr).

Interpretation

Your ESR of 11 is low-normal and well below both the lab reference limit (30) and the age-adjusted limit (~32). This is strong evidence against any significant systemic inflammatory process. Combined with a negative RF, negative ASO, and completely negative Lyme immunoblot, your inflammatory/infectious/autoimmune panel is uniformly clean.