Lab result explainedBlood count (CBC)Last updated November 11, 2026

Haptoglobin blood test: what low and high haptoglobin levels mean

Haptoglobin (Hp) · Hemolysis work-up (often ordered with LDH, bilirubin, reticulocyte count and a Coombs test) · reported in mg/dL (some labs report g/L; 1 g/L = 100 mg/dL)

Haptoglobin is a protein made by the liver whose job is to catch hemoglobin that leaks into the bloodstream when red blood cells break apart. A haptoglobin blood test is the standard way to check for hemolysis, the premature destruction of red cells. Normal in adults is roughly 30 to 200 mg/dL (0.3 to 2.0 g/L), with each lab printing its own limits. When red cells are being destroyed faster than usual, haptoglobin is used up quicker than the liver can replace it, so the level drops, often to below 30 mg/dL and sometimes to undetectable.

A low haptoglobin is the result most people are looking up, and it is a clue rather than a diagnosis. The usual reasons are an immune attack on red cells (autoimmune hemolytic anemia), an inherited red cell problem such as G6PD deficiency, sickle cell disease or hereditary spherocytosis, mechanical damage from a heart valve or a clotting disorder, a reaction to a transfusion or a drug, or a severe vitamin B12 deficiency. Liver disease, oral estrogen and a common inherited variant that produces little or no haptoglobin can also lower it without any hemolysis at all, and newborns have almost none for the first months of life.

A high haptoglobin is far less specific. Haptoglobin is an acute-phase protein, so infection, inflammation, cancer, steroid medicines and nephrotic syndrome all push it up, and that rise can hide hemolysis by keeping the level in the normal range. For that reason haptoglobin is almost never read on its own: it is interpreted with LDH, indirect bilirubin, the reticulocyte count, the blood smear and, when hemolysis is confirmed, a direct Coombs test to find out whether the immune system is responsible.

Hp at a glance

What it is: a liver-made protein that binds free hemoglobin released from destroyed red blood cells; the complex is cleared by the liver and spleen within minutes.
Normal (adults): about 30–200 mg/dL (0.3–2.0 g/L). Labs differ; many print 41–165 or 50–220 mg/dL. Newborns normally have very little until around 6 months.
Low haptoglobin (below 30 mg/dL, especially below 25 or undetectable) suggests hemolysis: autoimmune, inherited, mechanical, drug- or transfusion-related, or severe B12 deficiency. Liver disease, estrogen and an inherited low-haptoglobin variant also lower it.
A low haptoglobin with a high LDH is about 90 percent specific for hemolysis; a normal haptoglobin with a normal LDH makes significant hemolysis unlikely (about 92 percent sensitive).
High haptoglobin usually reflects inflammation, infection, steroids or nephrotic syndrome; it can mask hemolysis.
Next step: LDH, bilirubin, reticulocyte count and blood smear; if hemolysis is confirmed, a direct Coombs test, and then G6PD, hemoglobin electrophoresis or other targeted tests depending on the pattern.

Have your whole report? Paste it into the free Lab Explainer

Every marker explained in plain language, in context with the others, with questions to bring to your appointment. No account needed.

What Hp measures

Red cells normally live about 120 days and are recycled quietly inside macrophages in the spleen and liver. When cells rupture inside blood vessels, or when extravascular destruction is heavy enough that some hemoglobin escapes, free hemoglobin appears in plasma. Free hemoglobin is toxic: it scavenges nitric oxide, damages the kidney and generates oxidative stress. Haptoglobin binds it almost irreversibly, and the haptoglobin-hemoglobin complex is removed through the CD163 receptor on macrophages within about 10 to 30 minutes. Each haptoglobin molecule is destroyed along with the hemoglobin it carries, and the liver needs days to make more, which is why ongoing hemolysis empties the pool.

The lab measures haptoglobin protein by immunoturbidimetry or nephelometry on a serum sample. The test does not distinguish between the three inherited haptoglobin types (Hp 1-1, 2-1 and 2-2); people with the 2-2 type run somewhat lower baseline levels and have a lower binding capacity. A small number of people, more often of East Asian or West African ancestry, carry a deletion that produces little or no haptoglobin from birth, and they will test undetectable for life without any red cell destruction.

Because haptoglobin is also an acute-phase reactant that rises two- to four-fold with inflammation, the same sample should be read against markers of inflammation (CRP) and liver function. A normal haptoglobin in someone with high CRP does not exclude hemolysis, and a low haptoglobin in someone with cirrhosis or a very large bruise does not prove it. No fasting is needed, but recent vigorous endurance exercise, a transfusion, intravenous immunoglobulin or starting oral estrogen can shift the result and should be mentioned.

Normal range for Hp

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (mg/dL (some labs report g/L; 1 g/L = 100 mg/dL))	Notes
Adults, typical reference range	About 30–200 mg/dL (0.3–2.0 g/L)	Labs differ widely: 41–165, 34–200 and 50–220 mg/dL are all in use. Use the limits printed on your report.
Low, consistent with hemolysis	Below 30 mg/dL	Below 25 mg/dL had 83 percent sensitivity and 96 percent specificity for hemolytic disease in the classic study; the lower the value, the stronger the signal.
Undetectable	Below about 10 mg/dL (reported as less than the assay limit)	Active hemolysis until proven otherwise, unless the person has had an undetectable level since birth (inherited anhaptoglobinemia) or has severe liver failure.
Low haptoglobin plus raised LDH	Haptoglobin under 25 mg/dL with LDH above the reference range	About 90 percent specific for hemolysis. Both normal makes significant hemolysis unlikely (about 92 percent sensitive for ruling it out).
Newborns and infants under about 6 months	Often 0–10 mg/dL	Normal at this age; haptoglobin is not a useful hemolysis marker in young infants. Adult values are reached between 6 and 12 months.
Haptoglobin 2-2 phenotype	Lower half of the range, sometimes just under the lower limit	An inherited variant present in roughly a third of people of European ancestry; not a sign of hemolysis, though it matters for interpreting borderline values.
High (acute-phase response)	Above the lab's upper limit, commonly 200–400 mg/dL	Infection, inflammation, tissue injury, cancer, corticosteroids, androgens, nephrotic syndrome. A high value can mask simultaneous hemolysis.

High haptoglobin

A high haptoglobin almost always means the liver has increased production as part of an inflammatory response, in the same way CRP, ferritin and fibrinogen rise. Infection, autoimmune disease, surgery, a heart attack, burns and many cancers can double or quadruple it. On its own it says little about red cells and is not a disease marker; a raised value in someone who feels well is usually unremarkable and is simply repeated once the inflammatory trigger has settled.

The practical importance of a high haptoglobin is what it can hide. If someone has hemolysis and inflammation at the same time, which is common in autoimmune hemolytic anemia, lupus, lymphoma, sepsis or after surgery, the acute-phase rise can hold haptoglobin in the normal or even high range despite ongoing red cell destruction. In that setting clinicians lean on LDH, bilirubin, reticulocytes, the blood smear and the Coombs test instead, or follow the trend over days: a haptoglobin that is falling from a high value while CRP stays up is meaningful.

Haptoglobin also rises in nephrotic syndrome, where the liver overproduces many proteins to compensate for urinary losses, and with corticosteroids, anabolic steroids or androgens, which stimulate its synthesis directly. Biliary obstruction and, to a modest degree, obesity and older age are associated with higher values.

Common causes

Infection and acute inflammation
Bacterial and viral infections, pneumonia, urinary infection and abscesses raise haptoglobin within 24 to 48 hours, typically to 2 to 4 times baseline, in parallel with CRP.
Chronic inflammatory and autoimmune disease
Rheumatoid arthritis, inflammatory bowel disease, vasculitis and polymyalgia rheumatica keep haptoglobin elevated in proportion to disease activity.
Tissue injury: surgery, trauma, burns, heart attack
Any significant tissue damage triggers an acute-phase response; after cardiac surgery the picture is complicated, because the bypass circuit also destroys red cells and consumes haptoglobin.
Cancer
Lymphoma, lung, breast, ovarian and gastrointestinal cancers often raise haptoglobin through tumor-related interleukin-6; it is not a cancer screening test.
Nephrotic syndrome
Heavy protein loss in the urine prompts the liver to overproduce haptoglobin, fibrinogen and lipoproteins; haptoglobin is one of the proteins that rises rather than falls.
Corticosteroids, anabolic steroids and androgens
Prednisone, dexamethasone, testosterone and related drugs increase hepatic haptoglobin synthesis, so a high value on these medicines is expected and can mask hemolysis.
Biliary obstruction and cholestatic liver disease
Blocked bile flow is associated with higher haptoglobin, in contrast to cirrhosis, where production falls.
Obesity, diabetes and older age
Fat tissue produces small amounts of haptoglobin and low-grade inflammation raises hepatic output, so values drift up modestly with weight and age.

Symptoms that can go with it

Usually none from the haptoglobin itself; symptoms belong to the underlying inflammation
Fever, chills and feeling unwell with infection
Joint pain and morning stiffness, abdominal pain or bloody diarrhea with inflammatory disease
Swelling of the legs and frothy urine with nephrotic syndrome
Weight loss, night sweats or new lumps, which need investigation
Pallor, jaundice or dark urine despite a normal or high haptoglobin, which raises the possibility of masked hemolysis

Low haptoglobin

A low haptoglobin means the protein is being consumed faster than the liver makes it, and the usual reason is that red blood cells are being destroyed early. Haptoglobin falls most dramatically with intravascular hemolysis, where cells rupture inside the circulation: a mechanical heart valve, paroxysmal nocturnal hemoglobinuria, a G6PD crisis, a severe transfusion reaction, malaria, or the small-vessel clotting disorders TTP, HUS and DIC. It also falls, though less reliably, with extravascular hemolysis in the spleen, which is how warm autoimmune hemolytic anemia, hereditary spherocytosis and sickle cell disease destroy cells. Values under 25 mg/dL, and particularly undetectable values, make hemolysis likely; a high LDH and indirect bilirubin, a rising reticulocyte count and abnormal cells on the smear confirm it.

Not every low haptoglobin is hemolysis. Severe vitamin B12 or folate deficiency and thalassemia major destroy red cell precursors inside the bone marrow (ineffective erythropoiesis), which drops haptoglobin and raises LDH in a way that looks exactly like hemolysis until the MCV, B12 level and smear are checked. Cirrhosis and acute liver failure reduce production. Oral estrogen and pregnancy lower it modestly. A large hematoma being reabsorbed, cardiopulmonary bypass, an ECMO circuit or a long-distance run can each deplete it for a day or two. Newborns have little haptoglobin for months, and a small number of people inherit a gene deletion and have none at all, which is harmless.

The size of the drop matters less than the company it keeps. A haptoglobin of 20 mg/dL with normal hemoglobin, LDH, bilirubin and reticulocytes in someone who feels well is most often a laboratory-range or inherited finding and is simply repeated. The same value with a falling hemoglobin, jaundice, dark urine or a high LDH is hemolysis and is worked up promptly, because autoimmune hemolysis, TTP and transfusion reactions can become dangerous within days.

Common causes

Autoimmune hemolytic anemia (warm or cold)
Antibodies coat red cells, which are destroyed in the spleen (warm IgG) or by complement in the circulation (cold agglutinins). Haptoglobin is low or absent, LDH and indirect bilirubin high, reticulocytes raised and the direct Coombs test positive. May be primary or triggered by lupus, lymphoma, chronic lymphocytic leukemia, infection or drugs.
Inherited red cell disorders
G6PD deficiency (hemolysis after fava beans, infection or oxidant drugs), hereditary spherocytosis, pyruvate kinase deficiency, sickle cell disease and thalassemia all lower haptoglobin, chronically or in crises.
Mechanical destruction
Mechanical heart valves (especially older or leaking ones), left ventricular assist devices, cardiopulmonary bypass and ECMO shear red cells, as does prolonged foot-strike in marathon running and march hemoglobinuria.
Microangiopathic hemolysis: TTP, HUS, DIC, HELLP, malignant hypertension
Small-vessel clots slice red cells into fragments (schistocytes). Haptoglobin is undetectable, platelets are low and LDH is very high. These are emergencies.
Transfusion reactions
An acute reaction to incompatible blood, or a delayed reaction 3 to 14 days after transfusion when an old antibody re-forms, consumes haptoglobin; the direct Coombs test is positive.
Drug-induced hemolysis
Ceftriaxone, piperacillin, dapsone, primaquine, rasburicase, methyldopa, nitrofurantoin, ribavirin and some chemotherapy and immunotherapy drugs can cause immune or oxidative hemolysis.
Paroxysmal nocturnal hemoglobinuria (PNH)
An acquired stem cell disorder in which complement destroys cells inside vessels; haptoglobin is undetectable, urine is dark in the morning and clots are a major risk. Diagnosed by flow cytometry.
Infection
Malaria, babesiosis, Clostridium perfringens sepsis, mycoplasma (cold agglutinins) and infectious mononucleosis can all produce hemolysis.
Ineffective erythropoiesis: B12 or folate deficiency, thalassemia major, myelodysplasia
Red cell precursors die in the marrow, releasing hemoglobin and LDH. Severe B12 deficiency can give an undetectable haptoglobin and an LDH in the thousands; the MCV is usually high and the reticulocyte count low, which separates it from true hemolysis.
Reduced production and non-hemolytic causes
Cirrhosis and acute liver failure, oral estrogen and pregnancy, large hematomas being reabsorbed, early infancy, and the inherited anhaptoglobinemia deletion. None of these need a hemolysis work-up if the other markers are normal.

Symptoms that can go with it

Fatigue, breathlessness on exertion and pallor as hemoglobin falls
Yellowing of the eyes or skin (jaundice) from indirect bilirubin
Dark, tea- or cola-colored urine, especially first thing in the morning, with intravascular hemolysis
Back, abdominal or flank pain during a hemolytic episode
An enlarged spleen, felt as fullness under the left ribs, in chronic extravascular hemolysis
Fever, chills and a racing heart with a transfusion reaction or infection-triggered hemolysis
Confusion, bruising, pinpoint rash or very little urine with TTP or HUS, which are emergencies
None at all when the low value is inherited, from estrogen or from liver disease

Read it alongside

LDH (lactate dehydrogenase) — released from ruptured red cells; low haptoglobin with high LDH is the core hemolysis pattern, and the combination is about 90 percent specific.
Bilirubin, total and direct — hemolysis raises indirect (unconjugated) bilirubin; a mostly direct rise points to the liver or bile ducts instead.
Reticulocyte count — rises within days as the marrow responds to red cell loss; a low reticulocyte count with low haptoglobin suggests ineffective erythropoiesis (B12 or folate deficiency) or marrow failure rather than hemolysis.
Hemoglobin, MCV and MCHC — show whether anemia is present and hint at the cause: a high MCHC favors spherocytosis or autoimmune hemolysis, a high MCV favors B12 deficiency.
Peripheral blood smear — spherocytes, bite cells, sickle cells or fragmented cells (schistocytes) each point to a specific cause; schistocytes with low platelets are an emergency.
Direct Coombs test (DAT) — positive when antibodies or complement coat the red cells; separates immune from non-immune hemolysis.
CRP — a high CRP warns that an acute-phase rise may be masking hemolysis; haptoglobin should then be read with LDH and bilirubin rather than alone.
G6PD test, hemoglobin electrophoresis, vitamin B12 — ordered once hemolysis is confirmed and the Coombs test is negative, to find the inherited or nutritional cause.

What usually happens next

If haptoglobin is low, expect LDH, total and direct bilirubin, a reticulocyte count, a CBC and a blood smear on the same or a repeat sample; together these confirm or exclude hemolysis within a day.
If hemolysis is confirmed, a direct Coombs test comes next. A positive result points to autoimmune, drug-induced or transfusion-related hemolysis; a negative result leads to G6PD testing, hemoglobin electrophoresis, a review of heart valves and medicines, and sometimes flow cytometry for PNH.
If haptoglobin is low but LDH, bilirubin, reticulocytes and hemoglobin are all normal, the usual plan is to repeat it in a few weeks, note any oral estrogen, liver disease or heavy exercise, and consider an inherited low-haptoglobin variant; no treatment is needed.
If haptoglobin is high, the question is what inflammation is driving it; CRP, a white cell count and a history of infection, surgery or steroid use usually answer it, and the value is rechecked when well.
Useful questions to ask: is this hemolysis or something that mimics it, is it immune or non-immune, is it acute or chronic, and do I need to stop a medicine or avoid a trigger?

Diet, lifestyle and natural levers with evidence

What can move Hp once the cause is known. Nothing here replaces finding the cause.

Avoid known hemolysis triggers if you have G6PD deficiency

Strong evidence

In people with G6PD deficiency, fava beans, naphthalene mothballs, henna and oxidant drugs such as primaquine, dapsone, rasburicase, nitrofurantoin and sulfonamides provoke hemolysis that drops haptoglobin to undetectable within 1 to 3 days. Strict avoidance is the single measure that keeps haptoglobin, LDH and hemoglobin normal; there is no supplement that offsets the exposure.

Infections also trigger episodes, so a low haptoglobin during an illness in someone with G6PD deficiency should still be checked rather than assumed.

Folic acid when hemolysis is chronic

Moderate evidence

Chronic hemolysis (sickle cell disease, spherocytosis, autoimmune hemolysis, mechanical valves) consumes folate as the marrow turns over red cells several times faster than normal, and 1 mg of folic acid a day is standard supportive care in hematology guidelines to prevent a second, megaloblastic anemia on top of the first. It supports red cell production; it does not raise haptoglobin or slow the hemolysis itself.

Check vitamin B12 before starting, since folic acid can mask B12 deficiency while nerve damage progresses.

Time the test away from endurance exercise

Moderate evidence

Running a marathon or a long hard run lowers haptoglobin measurably, sometimes to undetectable, through foot-strike hemolysis; studies of runners show the drop within hours and recovery over 1 to 3 days. Cycling and swimming cause much less. A low haptoglobin drawn within 48 hours of a long run is not interpretable and should simply be repeated after a few rest days.

Vitamin E if you have diabetes and the haptoglobin 2-2 genotype

Preliminary evidence

The haptoglobin 2-2 protein clears hemoglobin less efficiently, and in people with type 2 diabetes this genotype carries roughly twice the cardiovascular risk. In the ICARE trial of 1,434 Hp 2-2 diabetics, 400 IU of vitamin E a day halved the composite of heart attack, stroke and cardiovascular death over 18 months (2.2 versus 4.7 percent). Standard haptoglobin tests do not report genotype, the finding has not been replicated in a second large trial, and vitamin E showed no benefit in unselected populations.

Vitamin E at 400 IU or more increases bleeding with anticoagulants and was linked to slightly higher mortality in some meta-analyses; this is a conversation with your clinician, not a routine supplement.

When to see a clinician promptly

An undetectable or very low haptoglobin with dark urine, yellow eyes, breathlessness, a fast heart rate or dizziness: active hemolysis that can drop hemoglobin quickly, needs same-day assessment.
Low haptoglobin with a low platelet count, bruising, confusion, fever or reduced urine output: possible TTP or HUS, an emergency that is treated within hours.
Fever, back pain, chills or dark urine during or within two weeks after a blood transfusion.
Hemolysis starting within days of a new medicine, especially an antibiotic, antimalarial or gout drug, or after eating fava beans.
A persistently low haptoglobin with a high LDH, falling hemoglobin or an enlarged spleen, even without symptoms, to establish the cause.
Low haptoglobin in pregnancy with high blood pressure, headache or abdominal pain, which can signal HELLP syndrome.

Frequently asked questions

What is a normal haptoglobin level?

Most labs consider roughly 30 to 200 mg/dL (0.3 to 2.0 g/L) normal for adults, though the printed range varies from one lab to another; 41 to 165 and 50 to 220 mg/dL are both common. Values below the lower limit, and particularly below 25 mg/dL or undetectable, raise the question of hemolysis. Babies normally have very little haptoglobin until around 6 months of age.

What does a low haptoglobin mean?

It usually means red blood cells are being destroyed faster than normal (hemolysis), because haptoglobin is used up as it binds the hemoglobin they release. Causes include autoimmune hemolytic anemia, G6PD deficiency, sickle cell disease, spherocytosis, mechanical heart valves, transfusion or drug reactions and clotting disorders such as TTP. Severe B12 deficiency, liver disease, oral estrogen, pregnancy, recent long-distance running and an inherited low-haptoglobin variant also lower it without hemolysis, which is why LDH, bilirubin and a reticulocyte count are checked alongside.

Is a haptoglobin of 20 or 10 mg/dL dangerous?

The number alone is not dangerous; what matters is whether red cells are actually being destroyed and how fast. A value of 20 with normal hemoglobin, LDH and bilirubin in someone who feels well is often an inherited trait or a lab-range finding and is simply repeated. A value of 10 or undetectable with a high LDH, jaundice, dark urine or a falling hemoglobin is active hemolysis and needs prompt evaluation, since some causes can become serious within days.

Can haptoglobin be low without hemolysis?

Yes. The liver makes haptoglobin, so cirrhosis and liver failure lower it. Oral contraceptives, hormone therapy and pregnancy reduce it modestly. Severe vitamin B12 or folate deficiency and thalassemia destroy red cell precursors in the bone marrow and mimic hemolysis. A large bruise being reabsorbed, heart surgery and marathon running deplete it briefly. Infants have little for the first months of life, and a small number of people, more often of East Asian or West African ancestry, inherit a gene deletion and have none at all without any ill effect.

What does a high haptoglobin mean?

Haptoglobin is an acute-phase protein, so infection, inflammation, surgery, injury, cancer, corticosteroids, androgens and nephrotic syndrome all raise it, often to two to four times normal. A high value is rarely important in itself. Its main significance is that it can hide hemolysis: someone with both inflammation and red cell destruction may have a normal or high haptoglobin, so LDH, bilirubin, reticulocytes and a Coombs test are used instead in that situation.

Why are haptoglobin and LDH tested together?

They move in opposite directions during hemolysis: LDH leaks out of ruptured red cells and rises, while haptoglobin is consumed and falls. In the classic study, a haptoglobin under 25 mg/dL with a raised LDH was about 90 percent specific for hemolysis, and normal values of both made significant hemolysis unlikely (about 92 percent sensitive for excluding it). Either marker alone is less reliable, because LDH also rises with liver, muscle and heart injury and haptoglobin also falls with liver disease.

What is the difference between haptoglobin and a Coombs test?

Haptoglobin tells you whether red cells are being destroyed; it does not say why. The direct Coombs test (direct antiglobulin test) looks for antibodies or complement stuck to the red cells and tells you whether the immune system is responsible. The usual sequence is haptoglobin, LDH and bilirubin first to confirm hemolysis, then a Coombs test to split the causes into immune (autoimmune, drug, transfusion) and non-immune (inherited, mechanical, infectious).

How quickly does haptoglobin recover after hemolysis stops?

Once red cell destruction stops, the liver rebuilds the pool over several days; haptoglobin typically returns to the normal range within one to two weeks, which makes it a useful marker for confirming that a hemolytic episode has settled or that treatment of autoimmune hemolysis is working. If it stays undetectable, hemolysis is probably continuing at a low level even if the hemoglobin looks stable.

References

Haptoglobin (HP) test. MedlinePlus, US National Library of Medicine (2022)View source
Marchand A, Galen RS, Van Lente F. The predictive value of serum haptoglobin in hemolytic disease. JAMA (1980)
Shih AW, McFarlane A, Verhovsek M. Haptoglobin testing in hemolysis: measurement and interpretation. American Journal of Hematology (2014)
Körmöczi GF, Säemann MD, Buchta C, et al.. Influence of clinical factors on the haemolysis marker haptoglobin. European Journal of Clinical Investigation (2006)
Barcellini W, Fattizzo B. Clinical applications of hemolytic markers in the differential diagnosis and management of hemolytic anemia. Disease Markers (2015)
Levy AP, Asleh R, Blum S, et al.. Haptoglobin: basic and clinical aspects. Antioxidants and Redox Signaling (2010)
Overview of hemolytic anemia. Merck Manual Professional Version (2024)
Jäger U, Barcellini W, Broome CM, et al.. Diagnosis and treatment of autoimmune hemolytic anemia in adults: recommendations from the First International Consensus Meeting. Blood Reviews (2020)
Telford RD, Sly GJ, Hahn AG, Cunningham RB, Bryant C, Smith JA. Footstrike is the major cause of hemolysis during running. Journal of Applied Physiology (2003)
Milman U, Blum S, Shapira C, et al.. Vitamin E supplementation reduces cardiovascular events in a subgroup of middle-aged individuals with both type 2 diabetes mellitus and the haptoglobin 2-2 genotype: a prospective double-blinded clinical trial (ICARE). Arteriosclerosis, Thrombosis, and Vascular Biology (2008)
Hill A, DeZern AE, Kinoshita T, Brodsky RA. Paroxysmal nocturnal haemoglobinuria. Nature Reviews Disease Primers (2017)
Phillips J, Henderson AC. Hemolytic anemia: evaluation and differential diagnosis. American Family Physician (2018)

Related markers

Related conditions

Evidence guides

Worried about your number?

Ask AskMN what your Hp result could mean in the context of your other results, symptoms and medications. Free, unlimited, no account needed.

Ask about my Hp

This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.