Contents

Content Page
Unites Conversion 5
Complete blood count (CBC) 7
Fasting Plasma glucose , Random plasma
14
glucose and A1C
Glycemic targets in pregnant diabetic
16
woman
Erythrocyte Sedimentation Rate (ESR) 18
C Reactive Protein 02
Hemoglobin electrophoresis
00
interpretation
Renal function evaluation in primary
05
health care
Urine Albumin to creatinine ratio 07
Blood test to evaluate renal functions 08
Estimated glumerular rate (eGFR) 08
potassium (s.K) disorder 31
Sodium (s. Na) disorder 35
Evaluation of Abnormal Liver Chemistries 39
Causes of elevated ALT/AST 44
Viral hepatitis 46
 ELEVATION OF TOTAL BILIRUBIN LEVEL 49
Causes of high level alkhaline phosphatase 52
Lipid profiles 53
Bone profiles 57
Brucella test 61
Urinalysis: A Comprehensive Review 63
Stool analysis 74
Sources 81
 Unites Conversion
Conventional SI to
Conventional
Test to SI (multiply SI Units Conventional
Unite
by) (multiply by)
Alanine
units/L NA units/L NA
aminotransferase (ALT)
Albumin, serum g/dL 10 g/L 0.10

Alkaline phosphatase units/L NA units/L NA

Amylase, serum units/L NA units/L NA

Aspartate
units/L NA units/L NA
aminotransferase (AST)
Total Bilirubin, serum mg/dL 17.1 μmol/L 0.0585

Direct Bilirubin, serum mg/dL 17.1 μmol/L 0.0585

Serum Calcium Mg/dl 0.25 Mmol/l 4

Serum Ionized calcium Mg/dl 0.25 Mmol/l 4

Serum Chloride mEq/L 1 mmol/L 1

Cholesterol mg/dL 0.0259 mmol/L 38.61

HDL or LDL mg/dL 0.0259 mmol/L 38.61

Serum Creatinine Mg/dl 88.4 μmol/L 0.0113

Ferritin, serum ng/mL 1 μg/L 1

Blood Glucose mg/dL 0.0555 mmol/L 18.02

Iron μg/dL 0.179 μmol/L 5.587

Iron-binding capacity,
μg/dL 0.179 μmol/L 5.587
total (TIBC)

Blood Potassium mEq/L 1 mmol/L 1

Blood sodium mEq/L 1 mmol/L 1

Triglycerides mg/dL 0.0113 mmol/L 88.5

Urea nitrogen, blood (BUN) mg/dL 0.357 mmol/L 2.80

Serum Uric acid mg/dL 0.059 mmol/L 16.9

 CME
J R Coll Physicians Edinb 2014; 44:36–41
http://dx.doi.org/10.4997/JRCPE.2014.109
© 2014 Royal College of Physicians of Edinburgh

Interpretation of the full blood count in

systemic disease – a guide for the physician
M Leach
Consultant Haematologist and Honorary Senior Lecturer, Gartnavel Hospital, Glasgow, UK

ABSTRACT The full blood count (FBC) is perhaps the single most common Correspondence to M Leach
investigation performed in medical patients. It has the potential, when interpreted Department of Haematology
Leukaemia Research Lab
carefully and in relation to the clinical history, to provide very useful information Shelley Road
to assist in diagnosis and management. Clinicians are often alerted to the Gartnavel Hospital site
presence of a primary haematological disorder by abnormalities in the FBC. For Glasgow G12 0YN, UK
the purpose of this review these diseases will not be discussed in detail but the
e-mail
reader will be alerted to pointers which might indicate primary blood disorders mike.leach@ggc.scot.nhs.uk
throughout the text. The haematology laboratory in large teaching hospitals will
often provide up to 1,500 automated FBC analyses each day. These are
individually checked for ‘flags’ provided by the analyser which indicate values
outside the normal range. It is clearly essential that clinical information is
provided with the request as this will influence how the result is handled by
scientific and medical staff. Furthermore, significant abnormalities will generate
a blood film request and the report will be most useful when interpreted in light
of the patient’s working diagnosis. In cases where a diagnosis is not yet known,
even brief information on presentation, for example ‘collapse with hypotension’,
EDUCATION

‘fever on return to UK’, ‘weight loss and anorexia’, can all be important and help
the lab provide clinicians with guidance.

This short review aims to provide physicians with a workable guide to the
interpretation of some of the commoner findings in the full blood count. Some
of these will be very familiar to you but some will not. This review is not meant
to be exhaustive as the rare minutiae will obscure the essential core material.
Your haematology colleagues are always happy to help and available for
assistance in difficult or problematic cases. I have not specified normal ranges in
relation to each entity as these will be defined by your local laboratory.

KEYWORDS Full blood count, infection, inflammation, neoplasia, anaemia,

systemic disease

DECLARATIONS OF INTERESTS No conflicts of interest declared.

OVERVIEW
Haemoglobin
Anaemia is a common finding in medical patients. It is
best characterised in relation to the mean cell volume
(MCV). The important causes of microcytic anaemia
(MCV <80 fl) are outlined below in order of frequency.
In the presence of microcytosis with hypochromia (low
mean cell haemoglobin [MCH]) it is essential to check a
serum ferritin assay. A low serum ferritin is diagnostic of
iron deficiency. Ferritin levels, however, can be elevated
in the acute phase response often in parallel to the
erythrocyte sedimentation rate (ESR) so a normal
ferritin does not exclude iron deficiency. A ferritin level
over 100 ng/ml virtually excludes iron deficiency
regardless of circumstances. A mild microcytosis may be
seen in anaemia of chronic disease (discussed below)
but the MCV is rarely less than 70 fl and the serum
ferritin is normal. The thalassaemias and thalassaemia
traits frequently cause microcytosis and hypochromia
but the serum ferritin is normal. If thalassaemia trait is
suspected in the presence of a low ferritin it is important
to correct the iron deficiency before requesting a
haemoglobinopathy screen.
The finding of a macrocytic anaemia/macrocytosis is also
of diagnostic importance. The differential diagnosis is
summarised in Table 2.
A normochromic normocytic anaemia (MCV 80–100 fl)
is frequently present in hospitalised patients. It can result
from blood loss or may be a reflection of the effects of
ongoing systemic infective, inflammatory, and neoplastic
disorders and chronic organ failure, when it is known as
anaemia of chronic disease (ACD) or anaemia of

36
 Interpretation of the full blood count in systemic disease – a guide for the physician

TABLE 1 Causes of microcytic anaemia

Mean cell Mean cell Ferritin (ng/ Red blood Blood film History
volume (fl) haemoglobin ml) cell count
(pg/ml) (x1012/L)
Iron deficiency <80, Low Low (normal Low Target cells Bleeding
occasionally if acute phase Pencil cells
normal response)
Anaemia 70–80, often Normal Normal or high Low No specific Medical disease
chronic disease normal features
Thalassaemia/ Low, often Low Normal High Target cells Ethnic origin
trait 50–60 Poikilocytes
Tear drop cells
Nucleated red
blood cells
Lead poisoning Low or normal Normal Normal Normal Basophilic History of
stippling exposure
Rare red cell Low Normal Normal Low/Normal According to Congenital
disorders, e.g. condition
sideroblastic
anaemia,
pyro-
poikilocytosis

EDUCATION
TABLE 2 Causes of macrocytic anaemia

Full blood count Blood film History Investigation

Vitamin B12 May cause Oval macrocytes Pernicious anaemia B12 assay
deficiency pancytopenia Ileal surgery Intrinsic factor Ab
Folate deficiency May cause Oval macrocytes Diet Serum folate
pancytopenia Coeliac disease TTG Ab
Duodenal Bx
Liver disease Thrombocytopenia Regular macrocytes Alcohol According to history
Target cells Hep B, C,
etc.
Hypothyroidism Normal WBC and Unhelpful Thyroiditis According to history
platelets Radiotherapy
Hereditary Normal Hb Unhelpful Family history HFE gene studies
haemochromatosis Mild macrocytosis Ferritin
Transferrin saturation

Drug therapy Variable Unhelpful Azathioprine According to history

Mercaptopurine
Folate antagonists
Hydroxycarbamide
Haemolysis with Anaemia Spherocytes Drugs Retic count
reticulocytosis Bite cells Systemic lupus Direct Coombs test
polychromasia erythematosus (SLE) Bilirubin
Lymphoma Haptoglobin
Myelodysplastic May cause Dysplastic neutrophils Exclude other causes Bone marrow (BM)
syndrome pancytopenia biopsy
Marrow cytogenetics

Plasma cell Anaemia Rouleaux Bone pain Immunoglobulins

dyscrasias Fractures Serum electrophoresis
Renal failure Serum free light chains
BM biopsy

J R Coll Physicians Edinb 2014; 44:36–41

© 2014 RCPE
37
 M Leach

TABLE 3 Causes of polycythaemia

Type Red cell mass Plasma volume Erythropoietin level* Causes

Myeloproliferative Raised Normal Low Janus kinase 2 gene
disease (MPD) (JAK2) mutation
(primary
polycythaemia)
Secondary Raised Normal Normal Chronic hypoxia due
polycythaemia to cardiopulmonary
with hypoxia diseases, smoking, high
altitude
Secondary Raised Normal High Ectopic erythropoietin
polycythaemia (Renal tumours/cysts,
without hypoxia hepatic tumours,
fibroids, cerebellar
tumours)
Spurious or Normal Reduced Normal Dehydration
apparent Diuretics
polycythaemia Alcohol
Stress
*
Erythropoietin levels are mainly of use in secondary polycythaemia due to ectopic production. In routine practice, levels in
the other groups are often normal.

inflammation (AI). These patients have a normal or this mutation will often mean that investigations such as
EDUCATION

raised serum ferritin and normal reticulocyte count and
do not respond to iron replacement therapy. In parallel,
it is common to find elevated polyclonal gammaglobulins
and raised ESR or C-reactive protein (CRP) in
inflammatory and infective disorders, respectively. In any
patient with such an anaemia and raised ESR it is clearly
important to perform serum electrophoresis to exclude
a paraprotein and possible plasma cell dyscrasia. The
anaemia in ACD will only respond to effective
management of the underlying disorder though in renal
anaemia with erythropoietin deficiency it will often
respond to erythropoietin replacement. Anaemia of
chronic disease is a secondary anaemia that results from
cytokine-mediated suppression of bone marrow
erythroid activity and shortened red cell lifespan. When
present, it should always lead the physician to consider
its cause. It is an important anaemia to recognise as in
some patients it can be the first manifestation of an
occult tumour. The anaemia resolves when the tumour
is excised.
Polycythaemia (abnormal high haemoglobin and
haematocrit) may be the result of a primary
myeloproliferative disorder (MPD), particularly if
associated with neutrophilia, thrombocytosis, and
splenomegaly. Over 90% of patients with primary
polycythaemia and approximately 50% of those with
myelofibrosis and essential thrombocythaemia harbour a
mutation (V617F) in the Janus kinase 2 gene (JAK2)
which renders haemopoietic cells more sensitive to
growth factors. This mutation can be detected by
polymerase chain reaction (PCR) studies on peripheral
blood and shows high specificity for myeloproliferative
diseases so is very helpful in diagnosis. The presence of
blood volume studies and erythropoietin levels are not
necessary. Polycythaemia is relatively frequently seen as
a sole abnormality of the full blood count in medical
patients in the circumstances outlined in Table 3
(compared with primary polycythaemia). In many
patients the cause will be obvious but in others the
finding may be unexpected.
Leucocytes
Changes in peripheral leucocyte count can be highly
informative in medical practice and the cell line involved
can be specific to certain scenarios.
Neutrophilia is commonly seen in patients with bacterial
infection. The most severe infections are associated with
more marked neutrophilia and often a degree of myeloid
left shift (the presence of immature myeloid cells in
peripheral blood) with ‘toxic’ neutrophil granulation.
Neutrophilia may also be seen in non-infective disorders.
It is a common response to steroid therapy, severe
exercise, and following surgery or splenectomy, but can
also occur in systemic vasculitis, in the presence of tissue
necrosis/burns, and as a response to certain tumours
(summarised below).
• Bacterial infection
• Steroid therapy
• Post-surgery
• Extreme exercise
• Tissue necrosis
• Burns
• Systemic vasculitis
• Carcinoma

38 J R Coll Physicians Edinb 2014; 44:36–41

© 2014 RCPE
 Interpretation of the full blood count in systemic disease – a guide for the physician
Isolated neutropenia can be seen in connective tissue
disorders, particularly rheumatoid arthritis and Sjogren’s
disease. It can be a result of drug therapy, e.g. clozapine,
azathioprine, carbimazole, such that patients need
careful regular monitoring when treated with these
agents. It is of course seen following cytotoxic
chemotherapy. It is commonly seen following viral
infection e.g. Epstein-Barr virus infection, when it tends
to be mild and self-limiting. A sudden onset neutropenia
can be seen in patients with overwhelming bacterial
infection and appears to be a poor prognostic sign. A
significant persisting neutropenia requires the opinion of
a haematologist particularly in patients with cytopenias
in other lineages. Mild chronic neutropenias not
associated with infection are reasonably common and
are sometimes referred to as benign idiopathic
neutropenia. Finally, Afro-Caribbean patients commonly
show mild neutropenia below the normal range seen in
Caucasians: this racial neutropenia should be recognised
as such and not generate unnecessary investigations.
Eosinophilia is a much less common finding in clinical
practice but the search for a likely cause is often
rewarding. Mild eosinophilia is common in patients with
asthma, hayfever, and eczema but rarely exceeds 1.0 x
109/L. Some of the more common causes are listed in
Table 4.
TABLE 4 Causes of eosinophilia
Cause Condition
Connective tissue Churg-Strauss syndrome
diseases Idiopathic eosinophilic
pneumonia
Parasitic infections
Neoplastic Carcinoma
T cell lymphoma
Hodgkin lymphoma
Myeloproliferative disorders
Myeloid and eosinophilic
leukaemias
Allergy Asthma, hayfever, eczema
Drug hypersensitivity
Food allergy
A few cases remain unexplained and were previously
known as hypereosinophilic syndrome but these
patients are increasingly rare now that molecular
diagnostics are able to characterise many of these as
clonal eosinophilic leukaemias.
Lymphocytosis is commonly seen as a result of viral
infection often with a mild self-limiting neutropenia as
noted above. Stress lymphocytosis is a relatively common
phenomenon in hospital patients and is precipitated by
acute onset illnesses such as myocardial infarction, major
trauma, and status epilepticus.The lymphocytosis appears
J R Coll Physicians Edinb 2014; 44:36–41
© 2014 RCPE
abruptly and resolves within a few days of the insult. Mild
lymphocytosis is also seen post-splenectomy and can
also be a result of smoking. A persistent significant
lymphocytosis (lymphocyte count >6 x 109/L) requires a
haematology opinion and exclusion of a chronic
lymphoproliferative disorder.
Lymphopenia is a common result of therapy with
steroids and other immunosuppressive agents, e.g.
azathioprine. It is seen in advanced HIV infection, can be
a presenting feature in patients with Hodgkin lymphoma,
and is associated with rheumatoid arthritis, systemic
lupus, and sarcoidosis. Mild lymphopenia is a relatively
common finding in a routine FBC and in the absence of
any other specific symptoms should not trigger extensive
investigations. In my experience, the investigation of mild
isolated lymphopenia is rarely rewarding.
Monocytosis can be a feature in chronic infection with
tuberculosis and syphilis, as part of the inflammatory
reaction in Crohn’s disease and ulcerative colitis and as
a response to certain carcinomas. A persistent
monocytosis that is unexplained, particularly if associated
with anaemia or thrombocytopenia, may be a feature of
EDUCATION
myelodysplastic and myeloproliferative disorders, so a
haematology assessment is advised in these cases.
Platelets
Thrombocytosis is commonly seen as a reactive
phenomenon in patients with active chronic infection,
inflammation, and malignancy. The longer the duration
of these disease processes, the more likely is
thrombocytosis to become evident. These patients will
often show an elevation in other inflammatory markers
in parallel and the blood film tends to show small
relatively uniform platelets with little variation in size.
Chronic bleeding and iron deficiency anaemia is
frequently associated with thrombocytosis and it will
resolve when the bleeding source and iron deficiency is
corrected. Reactive thrombocytosis, and the
thrombocytosis seen after splenectomy, accounts for the
majority of cases seen in general medical practice.
Thrombocytosis is also a feature of a number of
myeloproliferative disorders, often in association with
abnormalities in the haemoglobin or platelet count.These
cases will not show elevation of inflammatory markers
and the blood film typically shows large platelets with
wide variation in individual size. As noted above, testing
for the JAK2 mutation can be very helpful in diagnosis.
These patients are at increased risk of vascular occlusive
events so it is important they are identified.
Thrombocytopenia is seen in a myriad of medical
scenarios but it is important to establish that the
thrombocytopenia is real and confirmed on a blood film.
Spurious thrombocytopenia can result from in vitro
platelet clumping in ethylenediaminetetraacetic acid
39
 M Leach

(EDTA)-anticoagulated specimens.This is an idiosyncratic SUMMARY

phenomenon seen in some patients and is not
associated with disease. The two main groups of The FBC can provide a wealth of important information
conditions causing true thrombocytopenia are firstly which can assist the physician in patient diagnosis and
those associated with increased platelet consumption management. It is essential to assess not only the
and secondly those causing bone marrow failure, as a current lab values but also to establish potential trends
result of primary haematological diseases, bone marrow over time and in relation to known diagnoses, surgical
infiltration, or fibrosis. The causes of consumptive interventions and drug treatment. The cause of many
thrombocytopenia are summarised in Table 5 and more abnormalities will be obvious but any unexpected
than one mechanism can be active in any individual findings need explanation. Not only will this assist in
patient so careful sequential investigation, in light of the achieving a prompt diagnosis in many patients but
clinical history, is essential. awareness of the common causes for each abnormality
might prevent unnecessary investigations in others.
TABLE 5 Causes of consumptive thrombocytopenia
Highlights
Immune Idiopathic
Connective tissue disorders • Abnormalities in the full blood count may be
Drugs informative in all fields of medicine.
HIV infection
• Anaemia is a common finding in medical patients:
Systemic sepsis assessment of the cause of anaemia is essential
Viral infection in patient management.
Heparin • It is important to recognise common reactive full
Alcohol Acute intoxication blood count changes in patients presenting with
active systemic disease.
EDUCATION

Hypersplenism Portal hypertension

Massive transfusion
Cardiac bypass procedures
Post transfusion purpura
Multiorgan failure
Microangiopathy
Splenomegaly
Haemolytic uraemic
syndrome
Thrombotic
thrombocytopenic purpura
Haemolysis, elevated liver
enzymes and low platelet
(HELLP) syndrome
Disseminated intravascular
coagulation
• Certain reactive phenomena, e.g. eosinophilia
may help direct investigations to achieve a
specific diagnosis
• Persisting abnormalities in the full blood count
that remain unexplained should prompt an
opinion from a haematologist.
Further reading
1 Hoffbrand AV, Pettit J, Moss P. Essential haematology. London: John
Wiley and sons; 2011.
2 Hoffbrand AV, Tuddenham EGD, Catovsky D et al. editors.
Postgraduate haematology. London: John Wiley and Sons; 2011.

40 J R Coll Physicians Edinb 2014; 44:36–41

© 2014 RCPE
 Interpretation of the full blood count in systemic disease – a guide for the physician

SELF-ASSESSMENT QUESTIONS
1. Which ONE of the following is not associated 4. A 45-year-old fireman presents with progressive
with thrombocytopenia? numbness in his feet and some unsteadiness of
gait. He was noted to be mildly icteric. The full
A. Massive transfusion. blood count showed Hb 110 g/L, MCV 131 fl, WBC
B. Haemolytic uraemic syndrome. 4 x 109/L, platelets 120 x 109/L. Serum LDH was
C. Secondary antiphospholipid syndrome. 800 U/ml.
D. Essential thrombocythaemia.
E. Portal hypertension. Which ONE of the following would be an appropriate first
line of management?
2. Which ONE of the following is not characteristic
in a patient presenting with a collapse due to an A. Arrange imaging of the liver and biliary tree.
overwhelming bacterial infection? B. Arrange outpatient EMG studies and a neurology
opinion.
A. Lymphocytosis. C. Check a serum B12 assay and commence intramuscular
B. Neutrophilia. B12 therapy.
C. Neutropenia. D. Request an outpatient haematology opinion.
D. Thrombocytopenia. E. Arrange MRI imaging of the brain and spinal cord.
E. Eosinophilia.
5. A 25-year-old man with a history of childhood
3. A 65-year-old male patient presents with a six- asthma presented with a six-week history of fever
week history of anorexia, weight loss, and and night sweats. Physical examination was
lethargy. He is noted to have a low grade fever. unremarkable. The full blood count showed Hb

The physical examination showed no specific
findings. The full blood count showed Hb 90 g/L,
MCV 72 fl, WBC 9 x 109/L, platelets 600 x 109/L.
Serum ferritin was 120 ng/ml, ESR was 50 mm/hr.
Gammaglobulins were diffusely increased. The
chest X-ray was normal.
Which ONE of the following would be an appropriate
management plan?
A. Perform endoscopy and colonoscopy then give iron
replacement. E. Spirometry with reversibility.
B. Request a myeloma screen and skeletal survey.
C. Obtain urine, blood, and sputum for culture then
commence empirical antibiotic therapy.
D. Request a bone marrow biopsy for morphology
and culture.
E. Consider investigations for a systemic inflammatory/
connective tissue disorder or occult neoplasm.
EDUCATION
120 g/L, MCV 91 fl, WBC 11 x 109/L, neutrophils 5
x 109/L, lymphocytes 0.6 x 109/L, eosinophils 4 x
109/L, platelets 450 x 109/L.
Which ONE of the following is a priority investigation?
A. Chest X-ray.
B. Blood, urine and sputum cultures including investigations
for TB.
C. Serology and blood films for helminths.
D. HIV serology.
This paper was originally published as part of the Haematology
module on the RCPE Online Education Portal. Specialty Modules
for continuing medical education, including the answers to these
questions, are available to Fellows and Members at http:/learning.
rcpe.ac.uk

J R Coll Physicians Edinb 2014; 44:36–41

© 2014 RCPE
41
 Fasting Plasma glucose , Random plasma glucose and A1C
Fasting Plasma glucose (FPG) , random plasma glucose (RPG) and A1C
are used to diagnosis and follow up of diabetes mellitus
CRITERIA of diagnosis of diabetes mellitus and prediabetes:

Test Diabetes mellitus Predibetes

Fasting plasma ≥ 126mg/dl 100-125 mg/dl
glucose(FPG) ( 7mmol/l) * (5.6–6.9 mmol/L)
Oral glucose ≥200mg/dl 140-199 mg/dl
tolerance (OGTT) (11.1mmol/l)* (7.8–11.0 mmol/L)
A1C ≥6.5%* 5.7-6.4 %
Random plasma ≥200mg/dl 140-199mg/dl
glucose(RPG) (11.1mmol/l) (7.8–11.0 mmol/L)
*In the absence of unequivocal hyperglycemia, results should be
confirmed by repeat testing. ‡Only diagnostic in a patient with classic
symptoms of hyperglycemia or hyperglycemic crisis. RPG, random
plasma glucose

Summary of Glycemic Recommendations for Many Nonpregnant

Adults With Diabetes

AIC <7%
Preprandial capillary plasma
80-130 mg/dl (4.4–7.2 mmol/L)
glucose
Post prandial plasma glucose <180 mg/dl (10.0 mmol/L)

Postprandial glucose measurements should be made 1–2 h after the beginning

of the meal, generally peak levels in patients with diabetes.
A1c target :
Glycated hemoglobin (A1C) goals in patients with diabetes should be
tailored to the individual, balancing the demonstrated benefits with
regard to prevention and delay in microvascular complications with
the risk of hypoglycemia.

A1C Indicated

≤7.0 percent for most medication-treated

Glycemic targets are generally
set somewhat higher (eg, <8
percent)
More stringent control (A1C <6
percent)
for older adult patients and
those with comorbidities or a
limited life expectancy and little
likelihood of benefit from
intensive therapy.
may be indicated for individual
patients with type 1 diabetes
and during pregnancy

Diabetes in pregnancy

diagnostic criteria for gestational diabetes

The diagnosis of gestational diabetes is made at 24 to 28 weeks of

gestation when one or more plasma glucose values meets or exceeds
the below values.

Test Fasting mg/dl One hour mg/dl 2 hour mg/dl

One step ≥92 (5.1 ≥180 (10.0 ≥153 (8.5
(75-gram load) mmol/L) mmol/L) mmol/L)
 Glycemic targets in pregnant diabetic woman:
the ADA-recommended targets for women with type 1 or type 2 diabetes
(the same as for GDM; described below) are as follows:

Fasting One-hour postprandial Two-hour postprandial

 <95 mg/dL (5.3 mmol/L) <140 mg/dL (7.8 mmol/L) <120 mg/dL (6.7 mmol/L)
and either or

A1C target in pregnancy

A1C is slightly lower in normal pregnancy than in normal nonpregnant women.
The A1C target in pregnancy is 6–6.5% (42–48 mmol/mol);

<6% (42 mmol/mol) may be optimal if this can be achieved without significant
hypoglycemia, but the target may be relaxed to <7% (53 mmol/mol) if necessary
to prevent hypoglycemia
 Erythrocyte Sedimentation Rate (ESR)

It is the rate of downward descent of RBCs in a vertical column of blood.

a relatively nonspecific test that is frequently ordered during the diagnosis and
monitoring of disease

NORMAL VALUES:

1ST HOUR 3-5 mm

MALE
2ND HOUR 6-10 mm
1ST HOUR 8-10 mm
FEMALE
2ND HOUR 16- 20 mm

Calculating Normal Erythrocyte Sedimentation Rate

ESR ♀ (female)= (age +10)/2

ESR ♂ (male )= age /2

Factors affecting ESR testing

Increased ESR Decreased ESR
Old age Newborn
Female male
Pregnancy High atitude
Menstruation Increased RBC count
plasma fibrinogen or globulins is
Increased plasma albumin
increased
Infectious diseases
Neoplasmatic, invasive tumours,
 Anaemias, ,
Chronic and acute diseases of liver
Diseases of connective tissues.

the ESR may provide useful information when:

 used as a diagnostic criterion for temporal arteritis and
polymyalgia rheumatica
 monitoring response to therapy in temporal arteritis and
polymyalgia rheumatica used as a component of some clinical
indices of rheumatoid arthritis
 following the course of patients with rheumatoid arthritis or other
connective tissue disorders
 screening for tissue infection in specific situations, e.g., after
orthopaedic surgery or suspected pelvic inflammatory disease
 assessing response of Hodgkin’s Disease to therapy • monitoring
certain infections such as tuberculosis or osteomyelitis
 assessing elderly persons with vague complaints in whom there is a
moderate to strong possibility of one of the above underlying
diseases, but no definite findings following history and physical
examination

C Reactive Protein
belongs to the pentraxin family of proteins, which has five identical
subunits.
CRP shows a rapid response to infection and inflammation: increasing
within hours of stimulus, and returning rapidly to normal following
resolution.
Normal CRP VALUE
Corrected CRP

♂ (male )= age in years / 5 mg/l

♀ (female ) = (age +6) / 5 mg/l

C REACTIVE PROTEIN IS INDICATION OF severity:

Mild Inflammation, viral or bacterial

10-40 mg/l
infection
Moderate Inflammation, viral or bacterial
40-100 mg/l
infection
100-200 mg/l Marked inflammation, bacterial infection
Severe bacterial infection or extensive
More than 200 mg/ l
trauma
 Hemoglobin electrophoresis
Electrophoresis is the classical method used to separate Hb
proteins based on their net charge.
An electric field is applied to a gel medium at a specific pH. The
gel can be run at alkaline pH (cellulose acetate) or acidic pH
(citrate agar).
At alkaline pH, Hbs with a greater net negative charge will
migrate more rapidly towards the positively charged anode of an
electrical field. Scanning densitometry of the gel can be used to
obtain a semiquantitative measurement of the size of the bands.
 Hemoglobin electrophoresis interpretation

Hemoglobin (Hb) subtype

condition genotype A (%) A2(%) F(%) S(%) C(%)

Normal AA 95-98 2-3 <2 0 0

Sickle Trait AS 50-60 <3.5 <2 35-45 0

Sickle cell disease SS 0 <3.5 5-15 85-95 0

BETA A/(β0 OR 1-3 OR
90-95 >3.5 0 0
Thalasemia trait β+) MORE
Beta thalasemia Β0β0
0 >5% 0-95 0 0
major orβ0β+
Sickle –β
Sβ 0 >3.5 2-15 80-92 0
thalasemia
Sickle-β+
Sβ+ 5-30 >3.5 2-10 65-90 0
thalasemia
HbSC disease SC 0 <3.5 1-5 45-50 45-50
Alph thalasemia
-- 0 0 0 0 0
(hydrops fetalis)
HbH
HbH 4
Upto 30%
Alph thalasemia Hb barts
minor 3-8%
Alpha thalasemia
Same normal Hb 0 0
trait
 Renal function evaluation in primary health care
Healthy kidneys remove wastes and excess fluid from the blood. Blood
and urine tests show how well the kidneys are doing their job and how
quickly body wastes are being removed
To evaluate renal functions, there are urine test for protein and blood for
creatinine

Urine test:
1. Urine albumenuria( see urine analysis section)
2. Albumin to creatinine ratio (discussed below)
3. 24 hours urine collection

Blood tests:
1. Blood Urea Nitrogen (BUN)
2. Serum creatinine
3. Estimated glomerurial filtration test (Egft)
4. Serum potassium
5. Serum sodium

Urine tests:
1. Urine Albuminuria:
Albuminuria = the presence of albumin in urine

Discussed in details in urine analysis section

2. Urine Albumin to creatinine ratio:

Albuminuria is increased excretion of urinary albumin and a

marker of kidney damage. Normal individuals excrete very small
amounts of protein in the urine. Albumin is the most common type
of protein in the urine
Persistent increased protein in the urine (two positive tests over 3
or more months) is the principal marker of kidney damage, acting
as an early and sensitive marker in many types of kidney disease.

Albumin-to-creatinine ratio (ACR) is the first method of

preference to detect elevated protein. The recommended method to
evaluate Albuminuria is to measure urinary ACR in a spot urine
sample.

ACR is calculated by dividing albumin concentration in milligrams by

creatinine concentration in grams.

Albuminuria in chronic kidney disease

Category ACR (mg/g) Interpretation comment
Normal to mildy
A1 <30
increased
If more than 3
Moderate increased
A2 30-300 months in young
(microalbuminuria)
adult indicate CKD
Severely increased Include nephrotic
A3 >300
(macroalbuminuria) syndrome
Blood test to evaluate renal fuctions:

1. Blood urea nitrogen (BUN):

Urea nitrogen comes from the breakdown of protein in the foods
you eat.
A normal BUN level is between 7 and 20.
As kidney function decreases, the BUN level rises.

2. Serum creatinine :
Creatinine is a waste product that comes from the normal wear
and tear on muscles of the body.
Creatinine levels in the blood can vary depending on age, race
and body size.
A creatinine level of greater than 1.2 for women and greater
than 1.4 for men may be an early sign that the kidneys are not
working properly.
As kidney disease progresses, the level of creatinine in the blood
rises.

3. Estimated glumerular rate (eGFR) :

mathematical formula using the MDRD or CKD-EPI equation
this test is a measure of how well the kidneys are removing
wastes and excess fluid from the blood.
It is calculated from the serum creatinine level using age and
gender with adjustment for those of African American descent.
Estimated GFR (eGFR) is commonly reported by laboratories
or can be estimated using formulae such as the Modification of
 Diet in Renal Disease (MDRD) study equation or the Chronic
Kidney Disease Epidemiology Collaboration(CKD-EPI)
equation
Normal GFR can vary according to age (as you get older it can
decrease)

CKD-EPI equation expressed as a single equation:

GFR = 141 × min (Scr /κ, 1)α × max(Scr /κ, 1)-1.209 × 0.993Age × 1.018 [if
female] × 1.159 [if black]

where:
Scr is serum creatinine in mg/dL,
κ is 0.7 for females and 0.9 for males,
α is -0.329 for females and -0.411 for males,
min indicates the minimum of Scr /κ or 1, and
max indicates the maximum of Scr /κ or 1.
https://qxmd.com/calculate/calculator_251/egfr-using-ckd-epi

The MDRD Equation:

GFR (mL/min/1.73 m2) = 175 × (Scr)-1.154 × (Age)-0.203 × (0.742 if female) ×

(1.212 if African American)
https://qxmd.com/calculate/calculator_140/mdrd-egfr

The Cockcroft and Gault formula

CCr={((l 40–age) x weight)/(72xSCr)}x 0.85 (if female)

Abbreviations/ Units
CCr (creatinine clearance) = mL/minute Age = years

Weight = kg SCr (serum creatinine) = mg/dL

stages of of kidney functions by using eGFR

Stage GFR(mL/min/1.73 m2) Interpretation

Stage 1 >90 Normal or high
Stage 2 60-89 Mildly decreased
Mildly to moderately
Stage 3a 45-59
decreased
Moderately to severely
Stage 3b 30-44
decreased
Stage 4 15-29 Severely decreased
Stage 5 <15 Renal failure
potassium (s.K) disorder:
Hypokalemia :
Hypokalemia (serum potassium level less than 3.6 mEq per
L [3.6 mmol per L])

Causes of hypokalemia:
Evaluation of Hypokalemia
Hyperkalemia :
Hyperkalemia (serum potassium level more than 5 mEq per L [5
mmol per L] in adults, more than 5.5 mEq per L [5.5 mmol per
L] in children, and more than 6 mEq per L [6 mmol per L] in
neonates)

Causes of hyperkalemia :
Evaluation of hyperkalemia
Hypernatremia :
Hypernatremia is defined as a serum sodium level greater than
145 mEq per L

Causes of hypernatremia
Evaluation of hypernatremia
Hyponatermia:
Hyponatremia is commonly defined as a serum sodium concentration
below 135 meq/L but can vary to a small degree in different clinical
laboratories

Causes of hyponatremia
Evaluation of hyponatremia
 Evaluation of Abnormal Liver Chemistries

The most common liver chemistries ordered are serum

alanine aminotransferase (ALT), aspartate
aminotransferase (AST), alkaline phosphatase and
bilirubin
A true healthy normal ALT level ranges from 29 to 33
IU/l for males, 19 to 25 IU/l for females and levels
above this should be assessed
Hepatocellular injury
is defined as disproportionate elevation of AST and
ALT levels compared with alkaline phosphatase levels
Cholestatic injury
is defined as disproportionate elevation of alkaline
phosphatase level as compared with AST and ALT
levels
 Liver chemistries including ALT, aspartate
aminotransferase (AST), alkaline phosphatase and
bilirubin are markers of liver injury, not liver
function, and should be referred to as liver
chemistries,or liver tests.
 Albumin, bilirubin, and prothrombin time are
markers of hepatocellular function that can be
influenced by extrahepatic factors.
 The laboratory measurements of ALT, AST, and
alkaline phosphatase are highly reproducible.
 Elevations of AST and/or ALT, alkaline
phosphatase, and bilirubin suggest
hepatocellular injury and are the abnormal liver
chemistries that require assessment and potential
evaluation.
 ALT is a more specific marker of hepatic
injury than AST.
 An elevated alkaline phosphatase level of hepatic
origin may be confirmed by elevation of gamma-
glutamyl transferase (GGT) or fractionation of
alkaline phosphatase.
 AST is present in the liver and other organs
including cardiac muscle, skeletal muscle, kidney,
and brain.
 ALT is present primarily in the liver, and thus is a
more specific marker of hepatocellular cell injury
 AST increase without elevation in ALT is
suggestive of cardiac or muscle disease.
 Alkaline phosphatase is found in hepatocytes on
the canalicular membrane, not the bile duct cell.
In addition to being present on the canalicular
membrane of the hepatocyte, alkaline phosphatase
is also found in bone, placenta, intestine, and
kidney with the most common extrahepatic
location originating from bone
 To confirm hepatic origin of alkaline phosphatase,
the canalicular enzyme GGT may be measured.
An elevated GGT suggests that the alkaline
phosphatase elevation is of hepatic origin
 In children and the elderly, alkaline phosphatase
levels increase, especially females over 50 years of
age, in part due to bone turnover
 The total serum bilirubin is usually <1.1 mg/dl
and
 an elevated direct bilirubin (conjugated
bilirubin)indicates hepatocellular dysfunction or
cholestasis
 Two markers of hepatocellular function are
albumin and prothrombin time.
 Albumin is a plasma protein exclusively
synthesized by the liver with a circulating half-life
of 3 weeks. A reduction in albumin (normal ≥3.5
 g/dl) usually indicates liver disease of more than 3
weeks duration
 Prothrombin time is a far more sensitive measure
of liver function than albumin because
prothrombin time may be prolonged in patients
with severe liver disease of <24 h duration

Sex ALT normal range

males 29 to 33 IU/l
Females 19 to 25 IU/l
Sex AST normal range
Males 10 to 40 international unit/L

Females 9 to 32 international unit/l

Sex Alkhaline phosphotase

Male 45 to 115 international unit/L

Female 30 to 100 international unit/L

Albumin 3.3 to 5.0 g/dL (33 to 50 g/L)

TOTAL BILIRUBIN < 1 mg/dL (17 micromol/liter)

DIRECT BILRUBIN 0.0-0.4mg/dl

Causes of elevated ALT/AST

Hepatic (generally AST>ALT)

Alcoholic liver disease
Cirrhosis (of any etiology)
Ischemic hepatitis
Congestive hepatopathy
Acute Budd-Chiari syndrome
Hepatic artery damage/thrombosis/occlusion
TPN (total parenteral nutrition.)
Hepatic (generally ALT>AST)
NAFLD (non-alcoholic fatty liver disease)
Steatosis
NASH (non-alcoholic steatohepatitis)
Chronic viral hepatitis
 Acute viral hepatitis
Medications and drug-induced liver injury
Prescription medications Herbal products and
supplements Over-the-counter agents
Toxic hepatitis (amanita exposure)
Hemochromatosis
Autoimmune hepatitis
Wilson’s disease
Alpha-1-antitrypsin defi ciency
C
Celiac disease
Acute bile duct obstruction
Liver trauma Post-liver surgery
Veno-occlusive disease/sinusoidal obstruction
syndrome
Diffuse infi ltration of the liver with cancer
H
HELLP syndrome
Acute fatty liver of pregnancy
Sepsis
 Hemophagocytic lymphohistiocytosis
Non-hepatic
Skeletal muscle damage/rhabdomyolysis
Cardiac muscle damage
Thyroid disease
Macro-AST
Strenous exercise
Heat stroke
Hemolysis
Adrenal insuffi ciency

Viral hepatitis
HEPATITIS B
Hepatitis b serology interpretation

Serology marker
Interpretation
HbsAG HbcAB HbsAB
Susceptible to HBV infection
Negative Negative Negative
(should be vaccinated)
negative Negative Positive Immune because of vaccination

Positive Positive Negative Acute or chronic HBV infection

negative Positive Negative Interpretation unclear; four

 possibilities:
1. Resolved HBV infection (most
common)
2. False-positive HBcAb, thus
susceptible
3. “Low-level” chronic HBV infection
4. Resolving acute HBV infection

HBcAb = hepatitis B core antibody; HBsAb = hepatitis B surface antibody; HBsAg = hepatitis B
surface antigen; HBV = hepatitis B virus

 The presence of HBsAg indicates that the person is infectious.

 HBcAb appears at the onset of acute HBV infection. Presence may
also indicate chronic HBV infection or a false-positive test.
 The presence of HBsAb indicates recovery and immunity from
HBV infection or successful immunization against HBV.
Hepatitis C
Hepatitis C serology interpretation
SOURCE
https://www.aafp.org/afp/2015/0615/p835.html
ELEVATION OF TOTAL BILIRUBIN LEVEL

TEST LEVEL
TOTAL BILIRUBIN < 1.1 mg/dL (17 micromol/liter)

DIRECT BILRUBIN
0.0-0.4mg/dl
(conjugated)

Causes of hyperbilirubinemia
Causes of high level alkhaline phosphatase:
 Alkaline phosphatase is found in hepatocytes on
the canalicular membrane, not the bile duct cell.
In addition to being present on the canalicular
membrane of the hepatocyte, alkaline phosphatase
is also found in bone, placenta, intestine, and
kidney with the most common extrahepatic
location originating from bone
 To confirm hepatic origin of alkaline phosphatase,
the canalicular enzyme GGT may be measured.
An elevated GGT suggests that the alkaline
phosphatase elevation is of hepatic origin
 In children and the elderly, alkaline phosphatase
levels increase, especially females over 50 years of
age, in part due to bone turnover

Non hepatic causes:

Pregnancy
Adolescence
Physiological Following a fatty meal in
subjects with blood group O or
B
 Healing Fracture
Paget’s Disease
Osteomalacia
Bone disease Vitamin D insufficiency
Rickets
Malignancy: osteogenic
sarcoma, metastatic

Renal Renal Failure

Heart Heart Failure

Hyperthyroid
Endocrine
Hyperparathyroid
Lymphoma
Leukemia
Malignancy Renal cell carcinoma
Multiple endocrine neoplasia
(MEN) II
Approach to high level alkhaline phosphatase

AMA: antimitochondrial antibodies; ERCP: endoscopic retrograde

cholangiopancreatography; MRCP: magnetic resonance
cholangiopancreatography; ULN: upper limit of normal.
 Lipid profiles

 The lipid profile typical includes total cholesterol, low-density

lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL)
cholesterol, and triglycerides
 Lipids, such as cholesterol and triglyceride, are insoluble in
plasma.
 They are made soluble by attachment to circulating
lipoproteins that transport lipids to various tissues for energy
utilization, lipid deposition, steroid hormone production, and
bile acid formation.
 The lipoprotein consists of esterified and unesterified
cholesterol, triglycerides, and phospholipids, and protein.
 There are five major lipoproteins in blood: chylomicrons;
 very low-density lipoprotein (VLDL);
 intermediate-density lipoprotein (IDL);
 low-density lipoprotein (LDL);
 and high-density lipoprotein (HDL).
 Each of these classes of lipoproteins carries cholesterol and
triglyceride to a varying degree, with LDL carrying the
majority of cholesterol and VLDL carrying the majority of
triglyceride.

 LDL cholesterol = Total cholesterol - very low-density

lipoprotein (VLDL) cholesterol - HDL cholesterol
  VLDL cholesterol is approximated by dividing the measured
total triglyceride level by 5

Lipid profiles normal result in adult

Test Normal level

Triglyceride <150 mg/dl
According to Estimate 10-y
Total cholesterol
ASCVD risk
HDL Male : ≥40 mg/dl
HDL Female: ≥50 mg/dl
There are no
recommendations for or
against specific target levels
LDL for LDL-C or non–HDL-C in the
primary or secondary
prevention of ASCVD.
Treatment guidelines
 Bone profiles
Reference Ranges
Calcium
2.15 - 2.60
(corrected for Albumin: 35 - 50 g/L
mmol/L
albumin)

Alkaline
Total protein: 60 - 80 g/L phosphatase 30 - 130 U/L
(adults):

Vitamin d level evaluation in Adult

Vitamin d level
Action
serum 25-hydroxyvitamin D [25(OH)D

The majority of 10 to 20 ng/mL

do not require any additional
healthy adults with [25 to
evaluation.
vitamin D deficiency 50 nmol/L])
we measure serum calcium,
phosphorus, alkaline
phosphatase, parathyroid
hormone (PTH), electrolytes,
blood urea nitrogen (BUN),
at risk for developing
creatinine, and tissue
osteomalacia.,
<10 ng/ml transglutaminase antibodies (to
assess for celiac disease).
Radiographs are necessary in
certain settings, such as the
presence of bone pain
Vitamin d level evaluation in children

PTH: parathyroid hormone; Pi: inorganic phosphorus; Ca: calcium.

* The diagnosis of calcipenic rickets should be confirmed by monitoring
response to therapy.
¶ In phosphopenic rickets, serum inorganic phosphorus (Pi) is often very
low.
Δ Hypophosphatasia is accompanied by low serum alkaline phosphatase
activity.
Biochemical findings in rickets
 Brucella test

Antibodies to Brucella species may not become detectable until 1 to 2

weeks following the onset of symptoms, so serum specimens drawn
during acute disease may be negative by serology in patients with
brucellosis

If serology is performed, the Centers for Disease Control and Prevention

(CDC) currently recommends that specimens testing positive or
equivocal for IgG or IgM by a screening EIA be confirmed by a Brucella-
specific agglutination method.

Serum agglutination testing (SAT)

. The best serological definition of brucellosis is confirmation by a fourfold or

greater rise in Brucella agglutination titer between acute- and convalescent-
phase serum specimens obtained ≥2 weeks apart and studied at the same
laboratory

Serum agglutination
testing (SAT) result
Interpretation

≤ 1:40 or negative normal, healthy population

clinically significant; however, a

4-fold or greater increase in titer
≥1:80 between acute and convalescent
phase sera is required to
diagnose acute infection.

≥1:160 in endemic areas

 Urinalysis: A Comprehensive Review
JEFF A. SIMERVILLE, M.D., WILLIAM C. MAXTED, M.D., and JOHN J. PAHIRA, M.D.
Georgetown University School of Medicine, Washington, D.C.

A complete urinalysis includes physical, chemical, and microscopic examinations. Midstream

clean collection is acceptable in most situations, but the specimen should be examined within
two hours of collection. Cloudy urine often is a result of precipitated phosphate crystals in alka-
line urine, but pyuria also can be the cause. A strong odor may be the result of a concentrated
specimen rather than a urinary tract infection. Dipstick urinalysis is convenient, but false-posi-
tive and false-negative results can occur. Specific gravity provides a reliable assessment of the
patient’s hydration status. Microhematuria has a range of causes, from benign to life threatening.
Glomerular, renal, and urologic causes of microhematuria often can be differentiated by other
elements of the urinalysis. Although transient proteinuria typically is a benign condition, persis-
tent proteinuria requires further work-up. Uncomplicated urinary tract infections diagnosed by
positive leukocyte esterase and nitrite tests can be treated without culture. (Am Fam Physician
2005;71:1153-62. Copyright© 2005 American Academy of Family Physicians.)

U
See page 1046 for rinalysis is invaluable in the
strength-of-recommenda-
tion labels.
diagnosis of urologic conditions
such as calculi, urinary tract
infection (UTI), and malig-
nancy. It also can alert the physician to the
presence of systemic disease affecting the
kidneys. Although urinalysis is not recom-
mended as a routine screening tool except
in women who may be pregnant, physicians
should know how to interpret urinalysis
results correctly. This article reviews the
correct method for performing urinalysis
and the differential diagnosis for several
abnormal results.
Specimen Collection
A midstream clean-catch technique usually
is adequate in men and women. Although
prior cleansing of the external genitalia
often is recommended in women, it has no
proven benefit. In fact, a recent study1 found
that contamination rates were similar in
specimens obtained with and without prior
cleansing (32 versus 29 percent). Urine must
be refrigerated if it cannot be examined
promptly; delays of more than two hours
between collection and examination often
cause unreliable results.2
Physical Properties: Color and Odor
Foods, medications, metabolic products,
and infection can cause abnormal urine col-
ors (Table 1).3 Cloudy urine often is a result
of precipitated phosphate crystals in alkaline
urine, but pyuria also can be the cause.
The normal odor of urine is described as
urinoid; this odor can be strong in concen-
trated specimens but does not imply infec-
tion. Diabetic ketoacidosis can cause urine
to have a fruity or sweet odor, and alkaline
fermentation can cause an ammoniacal odor
after prolonged bladder retention. Persons
with UTIs often have urine with a pungent
odor. Other causes of abnormal odors include
gastrointestinal-bladder fistulas (associated
with a fecal smell), cystine decomposition
(associated with a sulfuric smell), and medi-
cations and diet (e.g., asparagus).
Dipstick Urinalysis
False-positive and false-negative results are
not unusual in dipstick urinalysis (Table 2).
The accuracy of this test in detecting micro-
scopic hematuria, significant proteinuria,
and UTI is summarized in Table 3.4-13
SPECIFIC GRAVITY
Urinary specific gravity (USG) correlates
with urine osmolality and gives important
insight into the patient’s hydration status. It
also reflects the concentrating ability of the
kidneys. Normal USG can range from 1.003
to 1.030; a value of less than 1.010 indicates
relative hydration, and a value greater than

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 Strength of Recommendations

Key clinical recommendation Label References

Patients with dipstick results of 3+ or greater may have significant proteinuria; further work-up is B 5
indicated.
Patients with microscopic hematuria (i.e., at least three red blood cells per high-power field in two C 19, 20
of three specimens) should be evaluated to exclude renal and urinary tract disease.
Exercise-induced hematuria is a relatively common, self-limited, and benign condition. Because C 30
results of repeat urinalysis after 48 to 72 hours should be negative in patients with this
condition, extended testing is not warranted.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented
evidence, usual practice, opinion, or case series. See page 1046 for more information.

1.020 indicates relative dehydration.14 Increased USG is
associated with glycosuria and the syndrome of inappro-
priate antidiuretic hormone; decreased USG is associated
with diuretic use, diabetes insipidus, adrenal insuffi-
ciency, aldosteronism, and impaired renal function.14 In
patients with intrinsic renal insufficiency, USG is fixed at
1.010—the specific gravity of the glomerular filtrate.
URINARY PH
Urinary pH can range from 4.5 to 8 but normally is
slightly acidic (i.e., 5.5 to 6.5) because of metabolic activ-
ity. Ingestion of proteins and acidic fruits (e.g., cranber-
ries) can cause acidic urine, and diets high in citrate can
cause alkaline urine.15-17 Urinary pH generally reflects the
serum pH, except in patients with renal tubular acidosis
(RTA). The inability to acidify urine to a pH of less than
5.5 despite an overnight fast and administration of an
acid load is the hallmark of RTA. In type I (distal) RTA,
the serum is acidic but the urine is alkaline, secondary
to an inability to secrete protons into the urine. Type II
(proximal) RTA is characterized by an inability to reab-
sorb bicarbonate. This situation initially results in alkaline
urine, but as the filtered load of bicarbonate decreases,
the urine becomes more acidic.
Determination of urinary pH is useful in the diag-
nosis and management of UTIs and calculi. Alkaline

TABLE 1
Common Causes of Abnormal Urine Coloration

Color Pathologic causes Food and drug causes

Cloudy Phosphaturia, pyuria, chyluria, lipiduria, Diet high in purine-rich foods (hyperuricosuria)
hyperoxaluria
Brown Bile pigments, myoglobin Fava beans
Levodopa (Larodopa), metronidazole (Flagyl), nitrofurantoin
(Furadantin), some antimalarial agents
Brownish-black Bile pigments, melanin, methemoglobin Cascara, levodopa, methyldopa (Aldomet), senna
Green or blue Pseudomonal UTI, biliverdin Amitriptyline (Elavil), indigo carmine, IV cimetidine (Tagamet),
IV promethazine (Phenergan), methylene blue, triamterene
(Dyrenium)
Orange Bile pigments Phenothiazines, phenazopyridine (Pyridium)
Red Hematuria, hemoglobinuria, myoglobinuria, Beets, blackberries, rhubarb
porphyria Phenolphthalein, rifampin (Rifadin)
Yellow Concentrated urine Carrots
Cascara

UTI = urinary tract infection; IV = intravenous.

Adapted with permission from Hanno PM, Wein AJ, Malkowicz SB. Clinical manual of urology. 3d ed. New York: McGraw-Hill, 2001:75.

1154 American Family Physician www.aafp.org/afp Volume 71, Number 6 ◆ March 15, 2005
 Urinalysis

TABLE 2
Causes of False-Positive and False-Negative Urinalysis Results

Dipstick test False positive False negative

Bilirubin Phenazopyridine (Pyridium) Chlorpromazine (Thorazine), selenium

Blood Dehydration, exercise, hemoglobinuria, Captopril (Capoten), elevated specific gravity, pH < 5.1,
menstrual blood, myoglobinuria proteinuria, vitamin C
Glucose Ketones, levodopa (Larodopa) Elevated specific gravity, uric acid, vitamin C
Ketones Acidic urine, elevated specific gravity, mesna Delay in examination of urine
(Mesnex), phenolphthalein, some drug
metabolites (e.g., levodopa)
Leukocyte Contamination Elevated specific gravity, glycosuria, ketonuria, proteinuria,
esterase some oxidizing drugs (cephalexin [Keflex], nitrofurantoin
[Furadantin], tetracycline, gentamicin), vitamin C
Nitrites Contamination, exposure of dipstick to air, Elevated specific gravity, elevated urobilinogen levels,
phenazopyridine nitrate reductase-negative bacteria, pH < 6.0, vitamin C
Protein Alkaline or concentrated urine, phenazopyridine, Acidic or dilute urine, primary protein is not albumin
quaternary ammonia compounds
Specific gravity* Dextran solutions, IV radiopaque dyes, proteinuria Alkaline urine
Urobilinogen Elevated nitrite levels, phenazopyridine —

IV = intravenous.
*—False-positive results are caused by false elevation; false-negative results are caused by false depression.

TABLE 3
Accuracy of Urinalysis for Disease Detection

Condition Test Results Sensitivity (%) Specificity (%) PPV NPV

Microscopic Dipstick ≥ 1+ blood 91 to 100 65 to 99 NA NA

hematuria4
Significant Dipstick ≥ 3+ protein 96 87 NA NA
proteinuria5
Culture-confirmed Dipstick Abnormal leukocyte 72 to 97 41 to 86 43 to 56 82 to 91
UTI6-13 esterase
Abnormal nitrites 19 to 48 92 to 100 50 to 83 70 to 88
Abnormal leukocyte 46 to 100 42 to 98 52 to 68 78 to 98
esterase or nitrites
≥ 3+ protein 63 to 83 50 to 53 53 82
≥ 1+ blood 68 to 92 42 to 46 51 88
Any of the above 94 to 100 14 to 26 44 100
abnormalities
Microscopy > 5 WBCs per HPF 90 to 96 47 to 50 56 to 59 83 to 95
> 5 RBCs per HPF 18 to 44 88 to 89 27 82
Bacteria (any amount) 46 to 58 89 to 94 54 to 88 77 to 86

PPV = positive predictive value; NPV = negative predictive value; NA = not applicable; UTI = urinary tract infection; WBCs = white blood cells;
HPF = high-powered field; RBCs = red blood cells.
Information from references 4 through 13.

March 15, 2005 ◆ Volume 71, Number 6 www.aafp.org/afp American Family Physician 1155
 TABLE 4
Common Causes of Hematuria
Glomerular causes
Familial causes
Fabry’s disease
Hereditary nephritis (Alport’s syndrome)
Nail-patella syndrome
Thin basement-membrane disease
Primary glomerulonephritis
Focal segmental glomerulonephritis
Goodpasture’s disease
Henoch-Schönlein purpura
IgA nephropathy (Berger’s disease)
Mesangioproliferative glomerulonephritis
Postinfectious glomerulonephritis
Rapidly progressive glomerulonephritis
Secondary glomerulonephritis
Hemolytic-uremic syndrome
Systemic lupus nephritis
Thrombotic thrombocytopenic purpura
Vasculitis
NSAIDs = nonsteroidal anti-inflammatory drugs.
Adapted with permission from Ahmed Z, Lee J. Asymptomatic urinary abnormalities. Hematuria and proteinuria. Med Clin North Am 1997;81:644.
urine in a patient with a UTI suggests the presence of a
urea-splitting organism, which may be associated with
magnesium-ammonium phosphate crystals and can
form staghorn calculi. Uric acid calculi are associated
with acidic urine.
HEMATURIA
According to the American Urological Association, the
presence of three or more red blood cells (RBCs) per
high-powered field (HPF) in two of three urine samples
is the generally accepted definition of hematuria.18-20 The
dipstick test for blood detects the peroxidase activity
of erythrocytes. However, myoglobin and hemoglobin
also will catalyze this reaction, so a positive test result
may indicate hematuria, myoglobinuria, or hemoglobin-
uria. Visualization of intact erythrocytes on microscopic
examination of the urinary sediment can distinguish
hematuria from other conditions. Microscopic exami-
nation also may detect RBC casts or dysmorphic RBCs.
Hematuria is divided into glomerular, renal (i.e., nonglo-
merular), and urologic etiologies (Table 4).21
Glomerular Hematuria. Glomerular hematuria typi-
cally is associated with significant proteinuria, erythro-
1156 American Family Physician
Renal causes Urologic causes
Arteriovenous malformation Benign prostatic hyperplasia
Hypercalciuria Cancer (kidney, ureteral, bladder,
Hyperuricosuria prostate, and urethral)
Loin pain-hematuria syndrome Cystitis/pyelonephritis
Malignant hypertension Nephrolithiasis
Medullary sponge kidney Prostatitis
Metabolic causes Schistosoma haematobium infection
Papillary necrosis Tuberculosis
Polycystic kidney disease Other causes
Renal artery embolism Drugs (e.g., NSAIDs, heparin,
Renal vein thrombosis warfarin [Coumadin],
cyclophosphamide [Cytoxan])
Sickle cell disease or trait
Trauma (e.g., contact sports,
Tubulointerstitial causes
running, Foley catheter)
Vascular cause
cyte casts, and dysmorphic RBCs. However, 20 percent
of patients with biopsy-proven glomerulonephritis
present with hematuria alone.22 IgA nephropathy (i.e.,
Berger’s disease) is the most common cause of glomeru-
lar hematuria.
Renal (Nonglomerular) Hematuria. Nonglomerular
hematuria is secondary to tubulointerstitial, renovascu-
lar, or metabolic disorders. Like glomerular hematuria, it
often is associated with significant proteinuria; however,
there are no associated dysmorphic RBCs or erythrocyte
casts. Further evaluation of patients with glomerular
and nonglomerular hematuria should include determi-
nation of renal function and 24-hour urinary protein or
spot urinary protein-creatinine ratio.
Urologic Hematuria. Urologic causes of hematuria
include tumors, calculi, and infections. Urologic hematu-
ria is distinguished from other etiologies by the absence
of proteinuria, dysmorphic RBCs, and erythrocyte casts.
Even significant hematuria will not elevate the protein
concentration to the 2+ to 3+ range on the dipstick test.23
Up to 20 percent of patients with gross hematuria have
urinary tract malignancy; a full work-up with cystoscopy
and upper-tract imaging is indicated in patients with this
www.aafp.org/afp Volume 71, Number 6 ◆ March 15, 2005

TABLE 5
Common Causes of Proteinuria
Transient proteinuria
Congestive heart failure
Dehydration
Emotional stress
Exercise
Fever
Orthostatic (postural) proteinuria
Seizures
Persistent proteinuria
Primary glomerular causes
Focal segmental glomerulonephritis
IgA nephropathy (i.e., Berger’s disease)
IgM nephropathy
Membranoproliferative glomerulonephritis
Membranous nephropathy
Minimal change disease
NSAIDs = nonsteroidal anti-inflammatory drugs; ACE = angiotensin-converting enzyme; HIV = human immunodeficiency virus.
Adapted with permission from Ahmed Z, Lee J. Asymptomatic urinary abnormalities. Hematuria and proteinuria. Med Clin North Am 1997;81:650.
condition.24 In patients with asymptomatic microscopic
hematuria (without proteinuria or pyuria), 5 to 22 per-
cent have serious urologic disease, and 0.5 to 5 percent
have a genitourinary malignancy.25-29
Exercise-induced hematuria is a relatively common,
benign condition that often is associated with long-
distance running. Results of repeat urinalysis after
48 to 72 hours should be negative in patients with this
condition.30
PROTEINURIA
In healthy persons, the glomerular capillary wall is per-
meable only to substances with a molecular weight of
less than 20,000 Daltons. Once filtered, low–molecular-
weight proteins are reabsorbed and metabolized by the
proximal tubule cells. Normal urinary proteins include
albumin, serum globulins, and proteins secreted by
the nephron. Proteinuria is defined as urinary protein
excretion of more than 150 mg per day (10 to 20 mg
per dL) and is the hallmark of renal disease. Microal-
buminuria is defined as the excretion of 30 to 150 mg
of protein per day and is a sign of early renal disease,
particularly in diabetic patients.
The reagent on most dipstick tests is sensitive to albu-
min but may not detect low concentrations of γ-globu-
lins and Bence Jones proteins. Dipstick tests for trace
March 15, 2005 ◆ Volume 71, Number 6
Urinalysis
Secondary glomerular causes Tubular causes
Alport’s syndrome Aminoaciduria
Amyloidosis Drugs (e.g., NSAIDs,
Collagen vascular diseases antibiotics)
(e.g., systemic lupus erythematosus) Fanconi syndrome
Diabetes mellitus Heavy metal ingestion
Drugs (e.g., NSAIDs, penicillamine Hypertensive nephrosclerosis
[Cuprimine], gold, ACE inhibitors) Interstitial nephritis
Fabry’s disease Overflow causes
Infections (e.g., HIV, syphilis, hepatitis, Hemoglobinuria
post-streptococcal infection)
Multiple myeloma
Malignancies (e.g., lymphoma, solid Myoglobinuria
tumors)
Sarcoidosis
Sickle cell disease
amounts of protein yield positive results at concentra-
tions of 5 to 10 mg per dL—lower than the threshold for
clinically significant proteinuria.15 A result of 1+ cor-
responds to approximately 30 mg of protein per dL and
is considered positive; 2+ corresponds to 100 mg per dL,
3+ to 300 mg per dL, and 4+ to 1,000 mg per dL.31,32
Dipstick urinalysis reliably can predict albuminuria with
sensitivities and specificities of greater than 99 percent.4
Asymptomatic proteinuria is associated with significant
renal disease in less than 1.5 percent of patients.4,33
Proteinuria can be classified as transient or persistent
(Table 5).21 In transient proteinuria, a temporary change
in glomerular hemodynamics causes the protein excess;
these conditions follow a benign, self-limited course.34,35
Orthostatic (postural) proteinuria is a benign condition
that can result from prolonged standing; it is confirmed
by obtaining a negative urinalysis result after eight hours
of recumbency.
Persistent proteinuria is divided into three general
categories: glomerular, tubular, and overflow. In glo-
merular proteinuria, the most common type, albumin is
the primary urinary protein. Tubular proteinuria results
when malfunctioning tubule cells no longer metabolize
or reabsorb normally filtered protein. In this condi-
tion, low–molecular-weight proteins predominate over
albumin and rarely exceed 2 g per day. In overflow pro-
www.aafp.org/afp American Family Physician 1157
teinuria, low–molecular-weight proteins overwhelm the
ability of the tubules to reabsorb filtered proteins.
Further evaluation of persistent proteinuria usually
includes determination of 24-hour urinary protein excre-
tion or spot urinary protein-creatinine ratio, microscopic
examination of the urinary sediment, urinary protein
electrophoresis, and assessment of renal function.32
GLYCOSURIA
Glucose normally is filtered by the glomerulus, but it is
almost completely reabsorbed in the proximal tubule.
Glycosuria occurs when the filtered load of glucose
exceeds the ability of the tubule to reabsorb it (i.e., 180 to
200 mg per dL). Etiologies include diabetes mellitus,
Cushing’s syndrome, liver and pancreatic disease, and
Fanconi’s syndrome.
KETONURIA
Ketones, products of body fat metabolism, normally are
not found in urine. Dipstick reagents detect acetic acid
through a reaction with sodium nitroprusside or nitro-
ferricyanide and glycine. Ketonuria most commonly is
associated with uncontrolled diabetes, but it also can
occur during pregnancy, carbohydrate-free diets, and
starvation.
NITRITES
Nitrites normally are not found in urine but result when
bacteria reduce urinary nitrates to nitrites. Many gram-
negative and some gram-positive organisms are capable of
this conversion, and a positive dipstick nitrite test indicates
that these organisms are present in significant numbers
(i.e., more than 10,000 per mL). This test is specific but
The Authors
JEFF A. SIMERVILLE, M.D., is a fifth-year resident in urology at
Georgetown University Medical Center, Washington, D.C. He
received his medical degree from Georgetown University School
of Medicine.
WILLIAM C. MAXTED, M.D., is professor of urology at Georgetown
University School of Medicine, where he received his medical
degree and completed a residency in urology.
JOHN J. PAHIRA, M.D., is professor of urology at Georgetown
University School of Medicine. He received his medical degree
from Pennsylvania State University Milton S. Hershey Medical
Center College of Medicine, Hershey, and a residency in urology at
the Hospital of the University of Pennsylvania, Philadelphia.
Address correspondence to Jeff A. Simerville, M.D., 6641 Wakefield
Dr., #411, Alexandria, VA 22307 (e-mail: jsimerville@cox.net).
Reprints are not available from the authors.
1158 American Family Physician www.aafp.org/afp
not highly sensitive. Thus, a positive result is helpful, but a
negative result does not rule out UTI.6 The nitrite dipstick
reagent is sensitive to air exposure, so containers should
be closed immediately after removing a strip. After one
week of exposure, one third of strips give false-positive
results, and after two weeks, three fourths give false-posi-
tive results.36 Non-nitrate–reducing organisms also may
cause false-negative results, and patients who consume a
low-nitrate diet may have false-negative results.
LEUKOCYTE ESTERASE
Leukocyte esterase is produced by neutrophils and may
signal pyuria associated with UTI. To detect significant
pyuria accurately, five minutes should be allowed for the
dipstick reagent strip to change color. Leukocyte casts
in the urinary sediment can help localize the area of
inflammation to the kidney.
Organisms such as Chlamydia and Ureaplasma urea-
lyticum should be considered in patients with pyuria and
negative cultures. Other causes of sterile pyuria include
balanitis, urethritis, tuberculosis, bladder tumors, viral
infections, nephrolithiasis, foreign bodies, exercise, glo-
merulonephritis, and corticosteroid and cyclophospha-
mide (Cytoxan) use.
BILIRUBIN AND UROBILINOGEN
Urine normally does not contain detectable amounts of
bilirubin. Unconjugated bilirubin is water insoluble and
cannot pass through the glomerulus; conjugated bili-
rubin is water soluble and indicates further evaluation
for liver dysfunction and biliary obstruction when it is
detected in the urine.
Normal urine contains only small amounts of urobi-
linogen, the end product of conjugated bilirubin after it
has passed through the bile ducts and been metabolized
in the intestine. Urobilinogen is reabsorbed into the por-
tal circulation, and a small amount eventually is filtered
by the glomerulus. Hemolysis and hepatocellular disease
can elevate urobilinogen levels, and antibiotic use and bile
duct obstruction can decrease urobilinogen levels.
Microscopic Urinalysis
Microscopic examination is an indispensable part of
urinalysis; the identification of casts, cells, crystals, and
bacteria aids in the diagnosis of a variety of conditions.
To prepare a urine specimen for microscopic analysis, a
fresh sample of 10 to 15 mL of urine should be centri-
fuged at 1,500 to 3,000 rpm for five minutes. The super-
natant then is decanted and the sediment resuspended
in the remaining liquid.37 A single drop is transferred to
a clean glass slide, and a cover slip is applied.
Volume 71, Number 6 ◆ March 15, 2005
 Urinalysis

TABLE 6
Urinary Casts and Associated Pathologic
Conditions

Type of cast Composition Associated conditions

Hyaline Mucoproteins Pyelonephritis, chronic renal

disease
May be a normal finding
Erythrocyte Red blood Glomerulonephritis
cells May be a normal finding in
patients who play contact
sports
Leukocyte White blood Pyelonephritis,
Figure 1. Squamous epithelial cells (arrows) and leukocytes cells glomerulonephritis,
(200 X). interstitial nephritis, renal
inflammatory processes
Epithelial Renal tubule Acute tubular necrosis,
cells interstitial nephritis,
eclampsia, nephritic
syndrome, allograft
rejection, heavy metal
ingestion, renal disease
Granular Various cell Advanced renal disease
types
Waxy Various cell Advanced renal disease
types
Fatty Lipid-laden Nephrotic syndrome, renal
renal tubule disease, hypothyroidism
cells
Broad Various cell End-stage renal disease
types

Figure 2. Convoluted renal tubule cells (200 X). Information from reference 38.

CELLS
Leukocytes may be seen under low- and high-power
magnification (Figure 1). Men normally have fewer than
two white blood cells (WBCs) per HPF; women nor-
mally have fewer than five WBCs per HPF.
Epithelial cells often are present in the urinary sedi-
ment. Squamous epithelial cells are large and irregu-
larly shaped, with a small nucleus and fine granular
cytoplasm; their presence suggests contamination.
The presence of transitional epithelial cells is normal.
These cells are smaller and rounder than squamous
cells, and they have larger nuclei. The presence of
renal tubule cells indicates significant renal pathol-
ogy (Figure 2). Erythrocytes are best visualized under
high-power magnification. Dysmorphic erythrocytes,
which have odd shapes because of their passage
through an abnormal glomerulus, suggest glomerular
disease.
CASTS
Casts in the urinary sediment may be used to localize
disease to a specific location in the genitourinary tract
(Table 6).38 Casts, which are a coagulum of Tamm-
Horsfall mucoprotein and the trapped contents of tubule
lumen, originate from the distal convoluted tubule or
collecting duct during periods of urinary concentration
or stasis, or when urinary pH is very low. Their cylindri-
cal shape reflects the tubule in which they were formed
and is retained when the casts are washed away. The pre-
dominant cellular elements determine the type of cast:
hyaline, erythrocyte, leukocyte, epithelial, granular,
waxy, fatty, or broad (Figure 3).
CRYSTALS
Crystals may be seen in the urinary sediment of healthy
patients (Figure 4). Calcium oxalate crystals have a
refractile square “envelope” shape that can vary in size.

March 15, 2005 ◆ Volume 71, Number 6 www.aafp.org/afp American Family Physician 1159
 A C

B D

Figure 3. Urinary casts. (A) Hyaline cast (200 X); (B) erythrocyte cast (100 X); (C) leukocyte cast (100 X); (D) granular cast
(100 X).

Uric acid crystals are yellow to orange-brown and may
be diamond- or barrel-shaped. Triple phosphate crystals
may be normal but often are associated with alkaline
urine and UTI (typically associated with Proteus spe-
cies). These crystals are colorless and have a characteris-
tic “coffin lid” appearance. Cystine crystals are colorless,
have a hexagonal shape, and are present in acidic urine,
which is diagnostic of cystinuria.
ony count as low as 100 CFU per mL suggests UTI, and
antibiotics should be considered. The presence of bacte-
ria in a properly collected male urine specimen is sug-
gestive of infection, and a culture should be obtained.
The authors indicate that they do not have any conflicts of interest.
Sources of funding: none reported.
Figures 1 through 4 reprinted from the National Institutes of Health
Clinical Center Department of Laboratory Medicine, Bethesda, Md.

BACTERIURIA
Gram-negative streptococci and staphylococci can be
distinguished by their characteristic appearance under
high-powered magnification.
Gram staining can help guide antibiotic therapy, but
it is not indicated in routine outpatient practice. Clean-
catch specimens from female patients frequently are
contaminated by vaginal flora. In these patients, five
bacteria per HPF represents roughly 100,000 colony-
forming units (CFU) per mL, the classic diagnostic
criterion for asymptomatic bacteriuria and certainly
compatible with a UTI. In symptomatic patients, a col-
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A C

B D

Figure 4. Urinary crystals. (A) Calcium oxalate crystals (arrows; 100 X); (B) uric acid crystals (100 X); (C) triple phosphate
crystals with amorphous phosphates (400 X); (D) cystine crystals (100 X).

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12. Semeniuk H, Church D. Evaluation of the leukocyte esterase and nitrite
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13. Leman P. Validity of urinalysis and microscopy for detecting urinary tract
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14. Kavouras SA. Assessing hydration status. Curr Opin Clin Nutr Metab
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15. Sheets C, Lyman JL. Urinalysis. Emerg Med Clin North Am 1986;4:
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18. Mariani AJ, Mariani MC, Macchioni C, Stams UK, Hariharan A, Moriera A.
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Volume 71, Number 6 ◆ March 15, 2005
 Stool analysis

Color of stool
Color of stool interpretation
Brown, dark brown,
Normal color
yellow brown
Gray color Ingestion of chocolate or Cocoa. steatorrhea
Iron or bismuth ingestion, bleeding from the upper
Very dark brown
GI tract.
Red color Diet high in meat.
Green or yellow-green Diet high in spinach, green vegetables.
Yellow or yellow-green diarrhea
Black and tarry bleeding of upper GI tract from tumors.
tumors, hemorrhoids, fissure, or inflammatory
Maroon or pink
process.
Clay-colored biliary obstruction.
Pale color with greasy
pancreatic deficiency leading to malabsorption.
appearance

Consistency of stool

Consistency Interpretation
small round hard stool habitual constipation.

Watery Diarrhea
Pasty stools are due to high- 1. common bile duct obstruction
fat contents 2. Celiac disease.
 3. Cystic fibrosis

spastic bowel, rectal narrowing, stricture, or

Ribbon-like stool
partial obstruction.

Contents

Content Interpretation
1. Severe constipation.
2. Mucous colitis.
Pure mucous 3. Excessive straining of the stool.
4. emotionally unstable patient

1. Bacillary dysentery.
2. Ulcerative colitis.
3. Intestinal tuberculosis.
Mucous in diarrhea with
4. amoebiasis.
microscopically present with
5. Enteritis.
RBCs and WBCs
6. Acute diverticulitis.
7. ulcerating malignancy of the colon.

1. Malignancies of the colon.

Mucus with blood which is
clinging to stool
An excessive amount of mucus
Increased number of WBCs in
the stool
2. Inflammatory lesion of rectal canal.
1. Villous adenoma of the colon.
1. Bacillary dysentery.
2. chronic ulcerative colitis.
3. Shigellosis.
4. salmonella infection.
5. Yersinia infection.
6. Invasive E.coli diarrhea.
7. Fistula of anus or rectum.
8. Localized abscess.
9. Few WBCs are seen in amoebiasis.
10.WBCs may appear in typhoid.
 1. Cholera.
2. Viral diarrhea.
The absence of WBCs seen in 3. Drug-induced diarrhea.
4. Amoebic colitis.
some of the diarrhoeal
5. Non-invasive E.coli diarrhoea.
conditions
6. Parasitic infestation.
7. Toxigenic bacterial infection.

1. Hemorrhoids.
2. Cancer.
blood in stool 3. Dysentery.
4. Causes of occult blood

1. Gastrointestinal tumors., colon cancer

2. Inflammatory bowel disease.
3. Diverticulosis.
4. Varices.
5. Ischemic bowel disease.
6. Arteriovenous malformations of GI tract.
7. Haemorrhoids.
8. Blood swallowed from oral cavity or
Occult blood nasopharynx.
9. Adenoma.
10. Gastric carcinoma.
11. Peptic ulcer.
12. Gastritis.
13. Amyloidosis.
14. Kaposi’s sarcoma.

1. Malabsorption.
2. Deficiency of pancreatic digestive
Presence of Fat enzyme.
3. Deficiency of Bile.

Meat fibers. and muscle fibers defect in the digestion.

1. Malabsorption syndrome.
The increased amount of meat 2. A pancreatic functional defect like
fibers cystic fibrosis.
Ova and parasites

Multiple stool sample is needed to rule out the parasitic infestation, at least
three consecutive days. Normally no parasite or ova in the stool

Ova and Picture

Interpretation
parasites

Ascaris
Roundworms
lumbricoides.

Necator
Hookworm
americanus.

Enterobius
Pinworms
vermicularis.
Whipworm Trichuris trichiura.
Diphyllobothrium
latum, Taenia
Tapeworm
saginata, and
Taenia solium
Entamoeba
histolytica (an
Protozoa amoeba),
and
 Giardia lamblia (a
flagellate)

Stool test Result comment

Negative
Suggests abnormal
amounts of
Occult blood hemoglobin from
Positive excessive blood loss.
Suspect ulcers, polyps,
diverticulitis or
colorectal cancer
Negative
Parasitology
Parasite infection and
Positive
Dysbiosis
Negative
Campylobacter
specific antigen Active Campylobacter
positive
infection
Negative
Shiga Toxin E.coli
(STEC) Active Shiga Toxin
positive
E.coli (STEC)
 Negative Normal
Active Helicobacter
H. pylori Stool Antigen pylori infection or
positive
partially treated H.
pylori infection
Negative No further assesment
Clostridium difficile Active Clostridium
infection positive
difficile infection
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ACG LIVER CAMERTIES GUIDELINES 2017

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catalog/Clinical+and+Interpretive/8112
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