What does the research show about uric acid (serum urate)?

Uric acid (serum urate)

Uric acid is the end product of purine breakdown. Sex-specific laboratory ranges top out at 5.7 to 6.0 mg/dL for women and 7.0 to 7.2 for men, and gout guidelines set a treatment target below 6. Gout risk climbs steeply with the level. Links to heart and kidney disease were not borne out in genetic studies or allopurinol trials.

Checked 2026-11-13

Status: A blood test ordered by a clinician, included in some chemistry panels and also sold direct to consumers by some US laboratories. FDA classifies uric acid test systems as class I devices [1].
Measures: The concentration of uric acid, the final product of purine metabolism in humans, in serum or plasma [1][2].
Also called: uric acid, serum uric acid, SUA, urate, serum urate, SU, UA, uric acid serum, plasma urate
Tested for: gout, kidney stones, kidney health, metabolic health, heart disease risk, checking urate-lowering medication

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Linked in research5

StrongLinked to gout in a graded way: 15-year incidence ran from 1.1% below 6 mg/dL to 49% at 10 mg/dL or above.
ModerateLinked to more kidney stones in men in one large Korean cohort, 72% more at 10 mg/dL or above, with no such pattern in women.
ModerateLinked to more new high blood pressure, 13% higher risk per 1 mg/dL in a meta-analysis of 18 cohorts.
ModerateLinked to more type 2 diabetes in pooled cohorts, 17% higher risk per 1 mg/dL, while a genetic study found no association.
LimitedOne Korean cohort of 375,163 adults found more deaths at both ends of the uric acid range than in the middle.

Reported risks0

No risks sourced yet.

Reference ranges

Each range is the one its source published, in mg/dL. Also reported in µmol/L. Where sources differ, each is shown.

US national survey laboratory procedure manual, 2017 to 2018, men

Adult men, as the reference range printed for the assay · [2]

Range	What the source calls it
below 3.4 mg/dL	No name given
3.4 to 7 mg/dL	"reference range"
above 7 mg/dL	No name given

The reference range listed in the laboratory manual for the uricase method used in the 2017 to 2018 US National Health and Nutrition Examination Survey (Roche Cobas 6000). It is the range attached to that assay, not one derived from survey participants [2]. A reference range describes the spread of results in people tested and is a different thing from the gout treatment targets below. The conversion factor above is the one printed in the 2024 KDIGO kidney disease guideline [3].

US national survey laboratory procedure manual, 2017 to 2018, women

Adult women, as the reference range printed for the assay · [2]

Range	What the source calls it
below 2.4 mg/dL	No name given
2.4 to 5.7 mg/dL	"reference range"
above 5.7 mg/dL	No name given

From the same manual and method as the range for men [2].

American Board of Internal Medicine laboratory reference ranges, 2026

Adults, both sexes, as the range printed for board examinations · [4]

Range	What the source calls it
below 3 mg/dL	No name given
3 to 7 mg/dL	"reference range"
above 7 mg/dL	No name given

One range for both sexes, published as a reference table for examination candidates. The table does not say how the range was set [4].

Zhu and colleagues, US national survey definition of hyperuricemia, 2011, men

Adult men in the US National Health and Nutrition Examination Survey, 2007 to 2008 · [5]

Range	What the source calls it
7 or below mg/dL	No name given
above 7 mg/dL	"hyperuricemia"

The study's primary definition of hyperuricemia, used to estimate how common it is. By this definition 21.2% of US men had hyperuricemia, at a mean serum urate of 6.14 mg/dL. The study names no category below the cut point [5].

Zhu and colleagues, US national survey definition of hyperuricemia, 2011, women

Adult women in the US National Health and Nutrition Examination Survey, 2007 to 2008 · [5]

Range	What the source calls it
5.7 or below mg/dL	No name given
above 5.7 mg/dL	"hyperuricemia"

By this definition 21.6% of US women had hyperuricemia, at a mean serum urate of 4.87 mg/dL [5].

Reference range in use in many countries, as reported by Desideri and colleagues, 2014, men and postmenopausal women

Adult men and postmenopausal women · [6]

Range	What the source calls it
below 3.5 mg/dL	No name given
3.5 to 7.2 mg/dL	"normal"
above 7.2 mg/dL	No name given

The review reports that these values have been identified as normal in many countries, from the spread of results in people without gout. Its authors argue that this approach is shaped by what is counted as normal, and propose the single threshold in the third block below [6].

Reference range in use in many countries, as reported by Desideri and colleagues, 2014, premenopausal women

Premenopausal women · [6]

Range	What the source calls it
below 2.6 mg/dL	No name given
2.6 to 6 mg/dL	"normal"
above 6 mg/dL	No name given

From the same review as the range for men and postmenopausal women [6].

Desideri and colleagues, proposed threshold, 2014

All adults, as proposed by the review's authors · [6]

Range	What the source calls it
below 6 mg/dL	"healthy subjects"
6 or above mg/dL	No name given

The authors propose that a threshold below 6.0 mg/dL (below 360 µmol/L) better identifies healthy subjects, citing urate crystal deposition without symptoms and observational links to heart, kidney and metabolic disorders. It is a review's proposal, not an adopted guideline [6]. A genetic study and allopurinol trials described under Associations did not support a causal role in heart or kidney disease.

American College of Rheumatology gout guideline, 2020

People with gout taking urate-lowering therapy · [7]

Range	What the source calls it
below 6 mg/dL	"target"
6 or above mg/dL	No name given

A treatment target for people with gout, not a population reference interval. The guideline strongly backs a treat-to-target strategy in which the dose of urate-lowering therapy is adjusted to serial serum urate measurements [7].

European League Against Rheumatism gout recommendations, 2016

People with gout taking urate-lowering therapy · [8]

Range	What the source calls it
below 6 mg/dL	"target"
6 or above mg/dL	No name given

A treatment target for people with gout, not a population reference interval. Printed as below 6 mg/dL (360 µmol/L) [8].

European League Against Rheumatism gout recommendations, 2016, severe gout

People with severe gout taking urate-lowering therapy · [8]

Range	What the source calls it
below 5 mg/dL	"target"
5 or above mg/dL	No name given

A lower treatment target for people the recommendations class as having severe gout. Printed as below 5 mg/dL (300 µmol/L) [8].

What has been shown to move it

Shown to lower it4

AllopurinolModerateVery common

Lowering uric acid in gout

Shown to lower blood uric acid, with 25 of 26 people on 300 mg a day reaching the target within 30 days against none of 25 on placebo.

When the dose was raised step by step, 69% had urate below 6 mg/dL at 12 months against 32% of those left on their starting dose, with mean changes of -1.5 and -0.34 mg/dL.

The numbers and sources

How common: Very common: more than 1 in 10 people.
Effect: In the one placebo-controlled trial in a Cochrane review, 25 of 26 people on allopurinol 300 mg a day reached the target serum urate over 30 days against 0 of 25 on placebo [1]. At a fixed 300 mg a day for 52 weeks, 21% had urate below 6.0 mg/dL at the last three monthly measurements [2]. When the dose was raised step by step, 69% had urate below 6 mg/dL at 12 months against 32% of those left on their starting dose, with mean changes of -1.5 and -0.34 mg/dL [3]. In a 72-week trial that raised doses toward a urate target, 80% reached it on allopurinol or febuxostat with no difference between them [4].
Population: 4,531 participants in 11 trials, 2 of them placebo-controlled [1]; 760 people with gout and urate of at least 8.0 mg/dL [2]; 183 people with gout already on allopurinol, 52% with reduced kidney function [3]; 940 people with gout, at least a third with stage 3 chronic kidney disease [4].
Sources: [1], [2], [3], [4]
Caveats: The placebo comparison rests on one trial of 57 people [1]. The share reaching target depended on whether the dose was fixed or raised [2][3].

AllopurinolModerate

Slowing chronic kidney disease

Not shown to slow loss of kidney function in two placebo-controlled trials, in chronic kidney disease and in type 1 diabetes.

In people with type 1 diabetes and early kidney disease, serum urate fell from 6.1 to 3.9 mg/dL on allopurinol and stayed at 6.1 on placebo.

The numbers and sources

Effect: In adults with stage 3 or 4 chronic kidney disease, eGFR fell 3.33 mL/min/1.73 m² a year on allopurinol and 3.23 on placebo (difference -0.10, 95% CI -1.18 to 0.97) [9]. In people with type 1 diabetes and early kidney disease, serum urate fell from 6.1 to 3.9 mg/dL on allopurinol and stayed at 6.1 on placebo. Measured GFR after 3 years and a washout did not differ (difference 0.001, 95% CI -1.9 to 1.9), and urinary albumin excretion was 40% higher on allopurinol (95% CI 0 to 80) [10].
Population: 363 adults with chronic kidney disease, no gout and a mean eGFR of 31.7, followed 104 weeks [9]; 530 people with type 1 diabetes and a GFR of 40 to 99.9 [10].
Sources: [9], [10]
Caveats: The first trial stopped recruiting early, at 369 of a planned 620 people [9].

AllopurinolLimited

Heart failure

One trial found allopurinol did not improve clinical status, walking distance or quality of life over 24 weeks in heart failure with high uric acid.

Uric acid was lower on allopurinol by 4.2 mg/dL at 12 weeks and 3.5 mg/dL at 24 weeks.

The numbers and sources

Effect: At 24 weeks, clinical status had worsened in 45% on allopurinol and 46% on placebo and improved in 13% and 19%. Quality of life scores, 6-minute walk distance and ejection fraction did not differ. Uric acid was lower on allopurinol by 4.2 mg/dL at 12 weeks and 3.5 mg/dL at 24 weeks [12].
Population: 253 people with symptomatic heart failure, an ejection fraction of 40% or below and uric acid of at least 9.5 mg/dL [12].
Sources: [12]
Caveats: One trial of 24 weeks, at a target dose of 600 mg a day.

Ezetimibe and fenofibrateLimited

Fenofibrate: uric acid and gout

One trial's later analysis found fenofibrate lowered uric acid about 20% and nearly halved first gout attacks over 5 years in type 2 diabetes, 2% against 3%.

Compared with placebo [15]

The numbers and sources

Effect: Uric acid fell 20.2% during the fenofibrate run-in and stayed 20.1% lower than placebo at 1 year. First gout events were 81 (2%) on fenofibrate and 151 (3%) on placebo over 5 years (HR 0.54, 95% CI 0.41 to 0.70), and all gout events halved (HR 0.48) [15].
Population: 9,795 adults aged 50 to 75 with type 2 diabetes [15].
Sources: [15]
Caveats: A post hoc analysis of a heart trial, not a gout trial.
Why limited: This rests on one trial, of 9,795 people. Strength counts independent studies that agree, so one trial is limited at any size.

Shown to raise it2

Thiazide diureticsModerateHow often is not known

Gout and high uric acid

Linked to more than twice the risk of new gout with diuretic use in people with high blood pressure. Trials found thiazides raised uric acid.

Across placebo-controlled trials, thiazides raised uric acid in a dose-related way.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: In a UK case-control study, current diuretic use was associated with incident gout among people with hypertension (RR 2.36, 95% CI 2.21 to 2.52) [19]. Across placebo-controlled trials, thiazides raised uric acid in a dose-related way [1]. Gout was more frequent on hydrochlorothiazide than placebo in the kidney stone trial [13]. The label states that hyperuricemia may occur and acute gout may be precipitated [14].
Population: 24,768 people with new gout and 50,000 matched controls [19]; 11,282 people in 60 trials [1].
Sources: [19], [1], [13], [14]
Caveats: The case-control study grouped all diuretics together and gives no absolute rate [19].

Loop diureticsLimitedVery common

Raised uric acid and gout

Shown to raise uric acid, about 1.2 mg/dL on torsemide 10 mg, with high uric acid in 18.4% of bumetanide patients tested. Studies linked diuretics to gout, inconsistently.

The numbers and sources

How common: Very common: more than 1 in 10 people.
Effect: Torsemide 10 mg a day for 6 weeks raised serum uric acid a mean 1.2 mg/dL, and the change reversed after stopping [1]. High uric acid was reported in 18.4% of patients tested on bumetanide [15]. A systematic review found a trend toward more acute gout attacks with loop and thiazide diuretics, with inconsistent size and independence [16].
Population: Hypertensive patients in torsemide trials [1]; bumetanide-treated patients [15]; 2 trials, 6 cohort and 5 case-control studies [16].
Sources: [1], [15], [16]
Caveats: The two trials in [16] tested thiazide diuretics, not loop diuretics.

Type in your own result

How it compares with the reference method

Matched the reference method1

Limited

Finger-prick meter against a laboratory measurement

One study found a finger-prick uric acid meter agreed closely with laboratory plasma results, and less closely than the laboratory with a reference method.

The numbers and sources

Compared with: Routine laboratory plasma uric acid, and liquid chromatography-mass spectrometry in a subgroup
Effect: In 205 patients with both measurements, capillary results from the HumaSens plus meter and routine plasma results had an intraclass correlation coefficient of 0.90 (95% CI 0.87 to 0.92). Seventeen patients had readings outside the meter's range, and its high out-of-range readings were considered uninterpretable. In 67 patients also measured by mass spectrometry, the coefficient against that reference was 0.84 (0.75 to 0.90) for the meter and 0.96 (0.94 to 0.98) for the laboratory plasma method. The authors describe the meter as reasonably comparable with the laboratory assay [23].
Population: 238 consenting patients with diabetes, 205 with paired results [23].
Sources: [23]
Caveats: One meter model, tested in people with diabetes, not in people with gout. Hematocrit influenced readings slightly [23].

Mixed results1

Limited

Variation from one test to the next

Limited evidence: one study put within-person variation of uric acid at about 6%, with a 16% change needed to exceed expected variation.

The numbers and sources

Compared with: Repeat measurement in the same person
Effect: A study of 730 apparently healthy adults in Bangladesh reported within-person variation of 5.71% for uric acid, variation between people of 23.52% and a reference change value of 16.13%, the size of change between two results that exceeds expected variation [24]. A European study of 91 healthy adults sampled weekly for 10 weeks reported that within-person variation of uric acid was lower than older published estimates and differed between men and women [25].
Population: 730 adults aged 18 to 65 [24]. 91 healthy adults aged 21 to 69 at 6 European laboratories [25].
Sources: [24], [25]
Caveats: The first abstract describes a cross-sectional design and does not say how many samples each person gave [24]. The European abstract gives no figures for uric acid [25]. Neither states a threshold for agreement.

Did not match the reference method1

Limited

During a gout flare

Pooled data from two trials found 14% of people in an acute gout flare had a serum urate of 6 mg/dL or below.

The numbers and sources

Compared with: Acute gout as diagnosed for entry to two treatment trials
Effect: Among 339 patients enrolled during an acute gout attack, 14% had a serum urate of 6 mg/dL or below at baseline and 32% had 8 mg/dL or below. Mean baseline serum urate was 7.1 mg/dL in people taking allopurinol and 8.5 mg/dL in those not taking it. The authors conclude that a normal level at presentation does not exclude an acute attack, and note that attacks occurred below 6.8 mg/dL, which they give as the saturation level for urate [22].
Population: 339 patients in 2 randomized trials of acute gout treatment, 94% men, mean age 50.5 [22].
Sources: [22]
Caveats: A secondary analysis of trials designed to compare two anti-inflammatory drugs. It did not follow the same people between flares [22].

What studies tie it to

Linked in research5

Strong

Gout

Linked to gout in a graded way: 15-year incidence ran from 1.1% below 6 mg/dL to 49% at 10 mg/dL or above.

The numbers and sources

Effect: In pooled individual data from four US cohorts, the 15-year cumulative incidence of gout was 1.1% (95% CI 0.9 to 1.4) at a baseline serum urate below 6 mg/dL and 49% (31 to 67) at 10 mg/dL or above. Against below 6 mg/dL, adjusted hazard ratios were 2.7 at 6.0 to 6.9 mg/dL, 6.6 at 7.0 to 7.9, 15 at 8.0 to 8.9, 30 at 9.0 to 9.9 and 64 at 10 or above [9]. In 2,046 initially healthy men followed for 14.9 years, the annual incidence of gouty arthritis was 4.9% at 9 mg/dL or more, 0.5% at 7.0 to 8.9 mg/dL and 0.1% below 7.0 mg/dL [10]. In a Mendelian randomization study, a genetically higher serum urate of 1 standard deviation went with an odds ratio for gout of 5.84 (95% CI 4.56 to 7.49) [11]. An umbrella review of 136 health outcomes found convincing evidence of a clear role for serum uric acid only for gout and kidney stones [12].
Population: 18,889 gout-free participants followed for a mean of 11.2 years [9]. 2,046 men in the Normative Aging Study [10]. 3,151 gout cases and 68,350 controls [11].
Sources: [9], [10], [11], [12]
Caveats: About half of the people at 10 mg/dL or above did not develop gout within 15 years, which the authors read as a role for other factors and for how long the level stays high [9].

Moderate

Kidney stones

Linked to more kidney stones in men in one large Korean cohort, 72% more at 10 mg/dL or above, with no such pattern in women.

The numbers and sources

Effect: In 239,331 Korean adults having health checkups, men with higher uric acid developed more kidney stones in a dose-response pattern. Against below 6.0 mg/dL, adjusted hazard ratios were 1.06 (95% CI 1.02 to 1.11) at 6.0 to 6.9 mg/dL, 1.11 (1.05 to 1.16) at 7.0 to 7.9, 1.21 (1.13 to 1.29) at 8.0 to 8.9, 1.31 (1.17 to 1.46) at 9.0 to 9.9 and 1.72 (1.44 to 2.06) at 10.0 or above. No dose-response association was seen in women [13]. An umbrella review found that the one trial outcome with robust evidence for urate-lowering treatment was fewer recurrences of kidney stones [12].
Population: 239,331 adults with 18,777 new cases of kidney stones found on ultrasound [13]. 31 meta-analyses of randomized trials within the umbrella review [12].
Sources: [13], [12]
Caveats: The cohort is observational, had no dietary data and did not use CT to confirm stones [13].

Moderate

High blood pressure

Linked to more new high blood pressure, 13% higher risk per 1 mg/dL in a meta-analysis of 18 cohorts.

The numbers and sources

Effect: In a meta-analysis of 18 prospective cohorts, hyperuricemia went with more new hypertension (adjusted risk ratio 1.41, 95% CI 1.23 to 1.58), and each 1 mg/dL higher uric acid with a risk ratio of 1.13 (1.06 to 1.20). The association was larger in younger study populations and tended to be larger in women [14]. An umbrella review found the hypertension association in observational studies and in some trials of intermediate outcomes, and not statistically significant in Mendelian randomization studies [12].
Population: 55,607 participants in 18 cohorts [14].
Sources: [14], [12]
Caveats: Observational. Later and US-based studies reported smaller effects [14]. The absence of a genetic association leaves open whether uric acid causes the rise [12].

Moderate

Type 2 diabetes

Linked to more type 2 diabetes in pooled cohorts, 17% higher risk per 1 mg/dL, while a genetic study found no association.

The numbers and sources

Effect: In a meta-analysis of 11 cohort studies, each 1 mg/dL higher serum uric acid went with a relative risk of type 2 diabetes of 1.17 (95% CI 1.09 to 1.25), or 1.11 (1.03 to 1.20) after adjustment for publication bias [15]. In a Mendelian randomization study, a genetically higher serum urate of 1 standard deviation was not associated with type 2 diabetes [11].
Population: 42,834 participants and 3,305 new cases of type 2 diabetes over 2.0 to 13.5 years [15]. 26,488 cases and 83,964 controls in the genetic study [11].
Sources: [15], [11]
Caveats: The cohort finding is observational and showed signs of publication bias [15]. The genetic study's authors conclude that lowering serum urate may not reduce cardiometabolic risk [11].

Limited

Death from any cause

One Korean cohort of 375,163 adults found more deaths at both ends of the uric acid range than in the middle.

The numbers and sources

Effect: In Korean adults having health checkups, the association with death from any cause was U-shaped. Against the sex-specific reference category, adjusted hazard ratios in the lowest categories (below 3.5 mg/dL for men, below 2.5 mg/dL for women) were 1.58 (95% CI 1.18 to 2.10) and 1.80 (1.10 to 2.93). In the highest categories (9.5 mg/dL or above for men, 8.5 mg/dL or above for women) they were 2.39 (1.57 to 3.66) and 3.77 (1.17 to 12.17). Cardiovascular and cancer deaths followed the same pattern [21].
Population: 375,163 South Korean men and women, with 2,020 deaths over about 2.06 million person-years [21].
Sources: [21]
Caveats: Observational, one cohort, with few deaths in the extreme categories and wide intervals for women. Illness that lowers or raises uric acid before death cannot be ruled out as the explanation [21].

Mixed results2

Moderate

Coronary heart disease, in cohorts and in a trial that lowered urate

Mixed results: cohorts link high uric acid to slightly more coronary heart disease, while a genetic study and an allopurinol trial in 5,721 people found no effect.

The numbers and sources

Effect: In a meta-analysis of 26 prospective studies, hyperuricemia went with an adjusted risk ratio of 1.09 (95% CI 1.03 to 1.16) for coronary heart disease and 1.16 (1.01 to 1.30) for coronary death. Each 1 mg/dL higher went with a risk ratio for coronary death of 1.12 (1.05 to 1.19). The association was not significant in men [16]. In a Mendelian randomization study, genetically higher serum urate was not associated with coronary heart disease, ischemic stroke or heart failure [11]. In a randomized trial in people aged 60 or older with ischemic heart disease and no gout, allopurinol titrated up to 600 mg daily did not change the rate of heart attack, stroke or cardiovascular death against usual care (hazard ratio 1.04, 95% CI 0.89 to 1.21) over a mean of 4.8 years [17].
Population: 402,997 adults in 26 studies [16]. 54,501 coronary heart disease cases and 68,275 controls [11]. 5,721 participants, mean age 72, 75.5% men [17].
Sources: [16], [11], [17]
Caveats: A marker that tracks risk is not always one whose lowering changes it. The trial's abstract does not report how far serum urate fell, and it enrolled older people who already had heart disease [17].

Moderate

Chronic kidney disease, in cohorts and in trials that lowered urate

Mixed results: cohorts link higher uric acid to new kidney disease, while two allopurinol trials found no slowing of kidney function decline.

The numbers and sources

Effect: In a meta-analysis of 13 cohort studies, higher serum uric acid went with more new chronic kidney disease (summary odds ratio 1.15, 95% CI 1.05 to 1.25), and hyperuricemia with an odds ratio of 2.35 (1.59 to 3.46) [18]. In a randomized trial in adults with stage 3 or 4 chronic kidney disease and a mean serum urate of 8.2 mg/dL, eGFR fell by 3.33 mL/min/1.73 m2 a year on allopurinol and 3.23 on placebo (difference -0.10, 95% CI -1.18 to 0.97) [19]. In a randomized trial in people with type 1 diabetes and early kidney disease, allopurinol lowered mean serum urate from 6.1 to 3.9 mg/dL, and measured GFR after 3 years and a 2-month washout did not differ from placebo (difference 0.001 mL/min/1.73 m2, 95% CI -1.9 to 1.9) [20]. KDIGO's 2024 guideline suggests against using urate-lowering drugs to delay kidney disease progression in people with chronic kidney disease whose hyperuricemia causes no symptoms [3].
Population: 190,718 participants in 13 studies [18]. 363 patients analyzed, mean eGFR 31.7 mL/min/1.73 m2 [19]. 530 participants with type 1 diabetes, mean age 51.1 [20].
Sources: [18], [19], [20], [3]
Caveats: The first trial stopped early for slow recruitment after enrolling 369 of 620 intended patients [19]. The cohort finding is observational, and reverse causation, with early kidney decline raising uric acid, cannot be ruled out.

Sources

US Food and Drug Administration. 21 CFR 862.1775, Uric acid test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1775
Centers for Disease Control and Prevention, National Center for Health Statistics. National Health and Nutrition Examination Survey 2017-2018 Laboratory Procedure Manual: Uric Acid, serum, Roche Cobas 6000. Performed by the University of Minnesota Advanced Research and Diagnostic Laboratory. https://wwwn.cdc.gov/nchs/data/nhanes/public/2017/labmethods/BIOPRO-J-MET-Uric-Acid-508.pdf
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. 2024. https://doi.org/10.1016/j.kint.2023.10.018
American Board of Internal Medicine. ABIM Laboratory Test Reference Ranges, January 2026. https://www.abim.org/Media/bfijryql/laboratory-reference-ranges.pdf
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