Visible hematuria causes brown or red discoloration of the urine that is visible to the naked eye. It can be painful or painless.

The most worrisome cause of painless, visible blood in the urine is kidney or bladder cancer, especially in a person wth risk factors such as male sex, age over 35, history of smoking, chronic bladder inflammation, and occupational exposures (to aromatic amines and aniline dyes) Between 80-90% of people with bladder cancer initially presented with visible hematuria.

Other causes include

- Exercise-induced hematuria–occurs in up to 30% of long distance runners and often resolves a few days after running cessation

Microscopic hematuria is a medical condition in which urine contains small amounts of blood; the blood quantity is too low to change the color of the urine (otherwise, it is known as gross hematuria). While not dangerous in itself, it may be a symptom of kidney disease, such as IgA nephropathy or Sickle cell trait, which should be monitored by a doctor.

The American Urological Association (AUA) recommends a definition of microscopic hematuria as three or more red blood cells per high-power microscopic field in urinary sediment from two of three properly collected urinalysis specimens.

Most patients with thin basement membrane disease are incidentally discovered to have microscopic hematuria on urinalysis. The blood pressure, kidney function, and the urinary protein excretion are usually normal. Mild proteinuria (less than 1.5 g/day) and hypertension are seen in a small minority of patients. Frank hematuria and loin pain should prompt a search for another cause, such as kidney stones or loin pain-hematuria syndrome. Also, there are no systemic manifestations, so presence of hearing impairment or visual impairment should prompt a search for hereditary nephritis such as Alport syndrome.

Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules.

Nephroptosis is asymptomatic in most patients. However, nephroptosis can be characterized by violent attacks of colicky flank pain, nausea, chills, hypertension, hematuria and proteinuria. Patients with symptomatic nephroptosis often complain of sharp pains that radiate into the groin. Many patients also suggest a weighing feeling on the abdomen. Pain is typically relieved by lying down ( flank pain on standing that is relieved on lying down, the probable cause to pain is that movement of the kidney causes intermittent renal tract obstruction ). The attack of colic pain is called 'Dietl's crisis' or 'renal paroxysm'.

Hemorrhagic cystitis or Haemorrhagic cystitis is defined by lower urinary tract symptoms that include dysuria, hematuria, and hemorrhage. The disease can occur as a complication of cyclophosphamide, ifosfamide and radiation therapy. In addition to hemorrhagic cystitis, temporary hematuria can also be seen in bladder infection or in children as a result of viral infection.

Minimal change disease is characterised as a cause of nephrotic syndrome without visible changes in the glomerulus on microscopy. Minimal change disease typically presents with edema, an increase in proteins passed from urine and decrease in blood protein levels, and an increase in circulating lipids (i.e., nephrotic syndrome) and is the most common cause of the nephrotic syndrome in children. Although no changes may be visible by light microscopy, changes on electron microscopy within the glomerules may show a fusion of the foot processes of the podocytes (cells lining the basement membrane of the capillaries of glomerulus). It is typically managed with corticosteroids and does not progress to chronic kidney disease.

Thin basement membrane disease must be differentiated from the other two common causes of glomerular hematuria, IgA nephropathy and Alport syndrome. The history and presentation are helpful in this regard:

- In Alport syndrome, there is often a family history of kidney failure, which may be associated with hearing impairment. Also, males tend to be more affected as Alport syndrome is X-linked in most cases.

- In IgA nephropathy, episodes of frank hematuria are more common, and a family history is less common.

A kidney biopsy is the only way to diagnose thin basement membrane disease. It reveals thinning of the glomerular basement membrane from the normal 300 to 400 nanometers (nm) to 150 to 250 nm. However, a biopsy is rarely done in cases where the patient has isolated microscopic hematuria, normal kidney function, and no proteinuria. The prognosis is excellent in this setting unless the clinical manifestations progress, as occurs in most males and some females with Alport syndrome and many patients with IgA nephropathy.

The classic presentation (in 40–50% of the cases) is episodic hematuria, which usually starts within a day or two of a non-specific upper respiratory tract infection (hence "synpharyngitic"), as opposed to post-streptococcal glomerulonephritis, which occurs some time (weeks) after initial infection. Less commonly gastrointestinal or urinary infection can be the inciting agent. All of these infections have in common the activation of mucosal defenses and hence IgA antibody production. Groin pain can also occur. The gross hematuria resolves after a few days, though microscopic hematuria may persist. These episodes occur on an irregular basis every few months and in most patients eventually subsides, although it can take many years. Renal function usually remains normal, though rarely, acute kidney failure may occur (see below). This presentation is more common in younger adults.

A smaller proportion (20-30%), usually the older population, have microscopic hematuria and proteinuria (less than 2 gram/day). These patients may not have any symptoms and are only clinically found if a physician decides to take a urine sample. Hence, the disease is more commonly diagnosed in situations where screening of urine is compulsory (e.g., schoolchildren in Japan).

Very rarely (5% each), the presenting history is:

- Nephrotic syndrome (3-3.5 grams of protein loss in the urine, associated with a poorer prognosis)

- Acute kidney failure (either as a complication of the frank hematuria, when it usually recovers, or due to rapidly progressive glomerulonephritis which often leads to chronic kidney failure)

- Chronic kidney failure (no previous symptoms, presents with anemia, hypertension and other symptoms of kidney failure, in people who probably had longstanding undetected microscopic hematuria and/or proteinuria)

A variety of systemic diseases are associated with IgA nephropathy such as liver failure, celiac disease, rheumatoid arthritis, reactive arthritis, ankylosing spondylitis and HIV. Diagnosis of IgA nephropathy and a search for any associated disease occasionally reveals such an underlying serious systemic disease. Occasionally, there are simultaneous symptoms of Henoch–Schönlein purpura; see below for more details on the association. Some HLA alleles have been suspected along with complement phenotypes as being genetic factors.

This is characterised by forms of glomerulonephritis in which the number of cells is not changed. These forms usually result in the nephrotic syndrome. Causes include:

Loin Pain Hematuria Syndrome ", aka "LPHS, is the combination of debilitating unilateral or bilateral flank pain and microscopic or macroscopic amounts of blood in the urine that is otherwise unexplained.

Loin pain-hematuria syndrome (LPHS) is a poorly defined disorder characterized by recurrent or persistent loin (flank) pain and hematuria that appears to represent glomerular bleeding. Most patients present with both manifestations, but some present with loin pain or hematuria alone. Pain episodes are rarely associated with low-grade fever and dysuria, but urinary tract infection is not present. The major causes of flank pain and hematuria, such as nephrolithiasis and blood clot, are typically not present. Renal arteriography may suggest focally impaired cortical perfusion, while renal biopsy may show interstitial fibrosis and arterial sclerosis.

The pain is typically severe, and narcotic therapy is often prescribed as a way to manage chronic pain. Sleep can be difficult because the supine position increases pressure on the flank. The onset of pain is often associated with nausea and vomiting, making pain management by oral opiates complicated.

Most types of RPGN are characterized by severe and rapid loss of kidney function featuring severe hematuria (blood in the urine), red blood cell casts in the urine, and proteinuria (protein in the urine), sometimes exceeding 3 g protein/24 h, a range associated with nephrotic syndrome. Some patients also experience hypertension (high blood pressure) and edema. Severe disease is characterized by pronounced oliguria or anuria, which portends a poor prognosis.

Among the signs and symptoms of acute proliferative glomerulonephritis are the following:

- Hematuria:

- Oliguria

- Edema

- Hypertension

- Fever, headache, malaise, anorexia, nausea.

Cystinuria is a cause of persistent kidney stones. It is a disease involving the defective transepithelial transport of cystine and dibasic amino acids in the kidney and intestine, and is one of many causes of kidney stones. If not treated properly, the disease could cause serious damage to the kidneys and surrounding organs, and in some rare cases death. The stones may be identified by a positive nitroprusside cyanide test. The crystals are usually hexagonal, translucent, white. Upon removal, the stones may be pink or yellow in color, but later they turn to greenish due to exposure to air. Cystinuria is usually asymptomatic when no stone is formed. However, once a stone is formed, or if stone production is severe or frequent, symptoms may be present:

- Nausea/vomiting

- Dull ache or "colicky" pain

- Chronic pain

- Hematuria

- Obstructive syndromes like hydronephrosis

- Infective syndromes like pyelonephritis

Cystinurics can also experience chronic pain in one, or both, kidneys due to the scars that the jagged edges of the stones can leave or damage from multiple stone removal surgeries. This can leave a cystinuric in constant pain which often requires medical intervention, such as long-term use of analgesics or surgical procedures, including T11, T12 or T13 nerve blocks (although, these procedures are often not successful, they can provide some relief). Aside from the chronic pain, a cystinuric will often have severe breakthrough pain from passing stones. People with cystinuria pass stones monthly, weekly, or daily, and need ongoing care. Cystinurics have an increased risk for chronic kidney disease and since kidney damage or poor function is often present in cystinurics, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or over the counter (OTC) medications should be used with caution.

Cystine stones are often not visible on most x-rays, CT's, and ultrasounds. This does not mean the cystinuric doesn't have a stone. It takes a trained eye and experience to spot a cystine stone. It is not unusual for a cystinuric to pass a stone, or stones, after being released from the hospital with a CT or x-ray result of no stones in the kidneys.

Urine odor in cystinuria has a smell of rotten eggs due to the increase in cystine.

Diagnosis is made by history and examination.

In immunocompromised patients, pus is present in the urine but often no organism can be cultured. In children, polymerase chain reaction sequencing of urine can detect fragments of the infectious agent.

The procedure differs somewhat for women and men. Laboratory testing of urine samples now can be performed with dipsticks that indicate immune system responses to infection, as well as with microscopic analysis of samples. Normal human urine is sterile. The presence of bacteria or pus in the urine usually indicates infection. The presence of hematuria, or blood in the urine, may indicate acute UTIs, kidney disease, kidney stones, inflammation of the prostate (in men), endometriosis (in women), or cancer of the urinary tract. In some cases, blood in the urine results from athletic training, particularly in runners.

Signs and symptoms of chronic kidney disease, including loss of appetite, nausea, vomiting, itching, sleepiness or confusion, weight loss, and an unpleasant taste in the mouth, may develop.

The histopathology is characterized by interstitial fibrosis, tubular atrophy,

fibrotic intimal thickening of arteries and glomerulosclerosis.

Histologically, IgA nephropathy may show mesangial widening and focal and segmental inflammation. Diffuse mesangial proliferation or crescentic glomerulonephritis may also be present. Immunoflourescence shows mesangial deposition of IgA often with C3 and properdin and smaller amounts of other immunoglobulins (IgG or IgM). Early components of the classical complement pathway (C1q or C4) are usually not seen. Electron microscopy confirms electron-dense deposits in the mesangium that may extend to the subendothelial area of adjacent capillary walls in a small subset of cases, usually those with focal proliferation.

The cause of LPHS is not known. One theory proposes that it is caused by a thin glomerular basement membrane and red blood cell (RBC) renal tubular congestion that leads to swelling of the kidney and distension of the renal fascia resulting in pain.

Researchers have hypothesized that the syndrome may be due to blood vessel diseases of the kidney, spasms of the kidney vessels, or other bleeding disorders (coagulopathy).

The hematuria in LPHS may be due to an abnormal (thick or thin) glomerular basement membrane. The glomerular basement membrane is a tissue in the kidney that filters the blood. An abnormal glomerular basement membrane may allow red blood cells into the urinary space. Because kidney stones are so common in people with LPHS, crystals in the kidney tubules may also play a part in bleeding and pain.

Other speculations on cause include

- IgA nephropathy. This is a condition in which small amount of a type of normal antibody (called IgA) get stuck in the kidney as it passes through in the bloodstream. This is a chronic condition, which sometimes goes away on its own but occasionally can cause damage to the kidneys. A related condition called IgM nephropathy can sometimes cause pain.

- Thin membrane disease. In this condition the membrane that filters the blood to make urine is too thin, and blood can pass across it in very small amounts. In a few cases of this condition, there is pain in the kidneys, usually occurring in attacks every so often. Although this condition can be painful, kidney failure does not seem to occur in the long term, so that the only real problem is the symptoms.

- Infection. In some cases, loin pain-haematuria syndrome occurs after a bladder infection with involvement of the kidney. Even when the infection has been treated and bugs can no longer be found in the urine, pain may persist for 6 months, or even longer in some cases.

- "Classic loin pain-haematuria syndrome". Some patients have none of the above diagnoses. In these cases there may be minor abnormalities on a kidney biopsy. Angiogram tests to look at the blood vessels in the kidney may show abnormal blood flow, perhaps causing a cramp like pain. The cause is not fully understood. It certainly is [more common] in women than in men, and there may be hormonal influences. Some women find the pain is worse at different times of their menstrual cycle, or comes on during pregnancy, or if they are taking [oral contraceptives].

It has also been reported to be caused by microscopic granules of calcium oxylate into the glomerulus itself, causing blood vessels to rupture and increase the distention of the renal capsule.

This condition may persist for some years, and can be lifelong. Damage to the kidneys leading to kidney failure does not occur. However, because LPHS is unusual in patients older than 60 years, some clinicians believe that LPHS eventually resolves.

At this time no cure has been found for this disease. LPHS is a debilitating disease due to chronic pain and the inability to know how to control the glomerular aspect. The pain of LPHS can be worsened by acts as simple as riding in the car and undertaking daily activities. Many people with this disease are unable to maintain employment due to the debilitating pain.

CAN is characterized by a gradual decline in kidney function and, typically, accompanied by high blood pressure and hematuria.

Nephritis is often caused by infections, and toxins, but is most commonly caused by autoimmune disorders that affect the major organs like kidneys.

- Pyelonephritis is inflammation that results from a urinary tract infection that reaches the renal pelvis of the kidney.

- Lupus nephritis is inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system.

- "Athletic nephritis" is nephritis resulting from strenuous exercise. Bloody urine after strenuous exercise may also result from march hemoglobinuria, which is caused by trauma to red blood cells, causing their rupture, which leads to the release of hemoglobin into the urine.

Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function, (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months) with glomerular crescent formation seen in at least 50% or 75% of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars).

Microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. The majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. In the case of glomerular damage occurring in HN, hematuria can occur as well.

Nephroptosis (also called floating kidney or renal ptosis) is an abnormal condition in which the kidney drops down into the pelvis when the patient stands up. It is more common in women than in men. It has been one of the most controversial conditions among doctors in both its diagnosis and its treatments.