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

Pyuria is the condition of urine containing white blood cells or pus. Defined as the presence of 6-10 or more neutrophils per high power field of unspun, voided mid-stream urine. It can be a sign of a bacterial urinary tract infection. Pyuria may be present in the people with sepsis, or in an older people with pneumonia.

Sterile pyuria, is urine which contains white blood cells while appearing sterile by standard culturing techniques. It is often caused by sexually transmitted infections, such as gonorrhea, or viruses which will not grow in bacterial cultures. Sterile pyuria is listed as a side effect from some medications such as paracetamol (acetaminophen). Its occurrence is also associated with certain disease processes, such as Kawasaki disease and genitourinary tuberculosis. However, there are many known causes, including systemic or infectious disease, structural and physiological reasons, intrinsic kidney pathology, or drugs.

Pyonephrosis is sometimes a complication of kidney stones, which can be a source of persisting infection. It may also occur spontaneously. It can occur as a complication of hydronephrosis or pyelonephritis.

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.

Pyonephrosis (Greek "pyon" "pus" + "nephros" "kidney") is an infection of the kidneys' collecting system. Pus collects in the renal pelvis and causes distension of the kidney. It can cause kidney failure.

Signs and symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day. It can cause high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back. There is often associated vomiting.

Chronic pyelonephritis causes persistent flank or abdominal pain, signs of infection (fever, unintentional weight loss, malaise, decreased appetite), lower urinary tract symptoms and blood in the urine. Chronic pyelonephritis can in addition cause fever of unknown origin. Furthermore, inflammation-related proteins can accumulate in organs and cause the condition AA amyloidosis.

Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.

Pyelonephritis that has progressed to urosepsis may be accompanied by signs of septic shock, including rapid breathing, decreased blood pressure, shivering, and occasionally delirium.

Bacteriuria is the presence of bacteria in urine. It is divided into two main types, those with symptoms (urinary tract infection) and those without (asymptomatic bacteriuria). Diagnosis is by urinalysis or urine culture. "Escherichia coli" is the most common bacterium found. Most people without symptoms should not be tested for the condition. Differential diagnosis include contamination.

If symptoms are present treatment is generally with antibiotics. Bacteriuria without symptoms generally does not require treatment. Exceptions include during pregnancy, those who have had a recent kidney transplant, young children with significant vesicoureteral reflux, and in those undergoing surgery of the urinary tract.

Bacteriuria without symptoms is present in about 3% of otherwise healthy middle aged women. Among those in nursing homes rates are as high as 50% among women and 40% in men. In those with a long term indwelling urinary catheter rates are 100%. Up to 10% of women have a urinary tract infection in a given year and half of women having at least one infection at some point in their lives.

Symptomatic bacteriuria is bacteriuria with the accompanying symptoms of a urinary tract infection (such as frequent urination, painful urination, fever, back pain). Symptomatic bacteriuria can be indicative of a urinary tract infection like pyelonephritis or cystitis. The most common type of bacteriuria associated with urinary tract infections is "Escherichia coli" which is a gram-negative rod-shaped bacteria.

Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.

The BUN:Cr in postrenal azotemia is initially >15. The increased nephron tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine. Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.

Pyelonephritis is inflammation of the kidney, typically due to a bacterial infection. Symptoms most often include fever and flank tenderness. Other symptoms may include nausea, burning with urination, and frequent urination. Complications may include pus around the kidney, sepsis, or kidney failure.

It is typically due to a bacterial infection, most commonly "Escherichia coli". Risk factors include sexual intercourse, prior urinary tract infections, diabetes, structural problems of the urinary tract, and spermicide use. The mechanism of infection is usually spread up the urinary tract. Less often infection occurs through the bloodstream. Diagnosis is typically based on symptoms and supported by urinalysis. If there is no improvement with treatment, medical imaging may be recommended.

Pyelonephritis may be preventable by urination after sex and drinking sufficient fluids. Once present it is generally treatment with antibiotic, such as ciprofloxacin or ceftriaxone. Those with severe disease may required treatment in hospital. In those with certain structural problems of the urinary tract or kidney stones, surgery may be required.

Pyelonephritis is common. About 1 to 2 per 1,000 women are affected a year and just under 0.5 per 1,000 males. Young adult females are most often affected, followed by the very young and old. With treatment, outcomes are generally good in young adults. Among people over the age of 65 the risk of death is about 40%.

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.

The prognosis of hydronephrosis is extremely variable, and depends on the condition leading to hydronephrosis, whether one (unilateral) or both (bilateral) kidneys are affected, the pre-existing kidney function, the duration of hydronephrosis (acute or chronic), and whether hydronephrosis occurred in developing or mature kidneys.

For example, unilateral hydronephrosis caused by an obstructing stone will likely resolve when the stone passes, and the likelihood of recovery is excellent. Alternately, severe bilateral prenatal hydronephrosis (such as occurs with posterior urethral valves) will likely carry a poor long-term prognosis, because obstruction while the kidneys are developing causes permanent kidney damage even if the obstruction is relieved postnatally.

Hydronephrosis can be a cause of pyonephrosis - which is a urological emergency.

The signs and symptoms of hydronephrosis depend upon whether the obstruction is acute or chronic, partial or complete, unilateral or bilateral. Hydronephrosis that occurs acutely with sudden onset (as caused by a kidney stone) can cause intense pain in the flank area (between the hips and ribs). Historically, this type of pain has been described as "Dietl's crisis". Conversely, hydronephrosis that develops gradually will generally cause either attacks of a dull discomfort or no pain. Nausea and vomiting may also occur. An obstruction that occurs at the urethra or bladder outlet can cause pain and pressure resulting from distension of the bladder. Blocking the flow of urine will commonly result in urinary tract infections which can lead to the development of additional stones, fever, and blood or pus in the urine. If complete obstruction occurs, kidney failure may follow.

Blood tests may show impaired kidney function (elevated urea or creatinine) or electrolyte imbalances such as hyponatremia or hyperchloremic metabolic acidosis. Urinalysis may indicate an elevated pH due to the secondary destruction of nephrons within the affected kidney. Physical examination may detect a palpable abdominal or flank mass caused by the enlarged kidney.

Renal azotemia (acute kidney failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of kidney parenchymal damage. Causes include kidney failure, glomerulonephritis, acute tubular necrosis, or any other kind of kidney disease.

The BUN:Cr in renal azotemia is less than 15. In cases of kidney disease, glomerular filtration rate decreases, so nothing gets filtered as well as it normally would. However, in addition to not being normally filtered, what urea does get filtered is not reabsorbed by the proximal tubule as it normally would be. This results in lower levels of urea in the blood and higher levels of urea in the urine as compared to creatinine. Creatinine filtration decreases, leading to a higher amount of creatinine in the blood. Third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addison's Disease.

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.

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

In young children, the only symptom of a urinary tract infection (UTI) may be a fever. Because of the lack of more obvious symptoms, when females under the age of two or uncircumcised males less than a year exhibit a fever, a culture of the urine is recommended by many medical associations. Infants may feed poorly, vomit, sleep more, or show signs of jaundice. In older children, new onset urinary incontinence (loss of bladder control) may occur.

Because renal excretion is the primary means of eliminating acid from the body, there is consequently a tendency towards acidemia.

This leads to the clinical features of dRTA:

- Normal anion gap metabolic acidosis/acidemia

- Hypokalemia

- Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate).

- Nephrocalcinosis (deposition of calcium in the substance of the kidney)

- Bone demineralisation (causing rickets in children and osteomalacia in adults)

The symptoms and sequelae of dRTA are variable and range from being completely asymptomatic, to loin pain and hematuria from kidney stones, to failure to thrive and severe rickets in childhood forms as well as possible renal failure and even death.

dRTA commonly leads to sodium loss and volume contraction, which causes a compensatory increase in blood levels of aldosterone. Aldosterone causes increased resorption of sodium and loss of potassium in the collecting duct of the kidney, so these increased aldosterone levels cause the hypokalemia which is a common symptom of dRTA.

Lower urinary tract infection is also referred to as a bladder infection. The most common symptoms are burning with urination and having to urinate frequently (or an urge to urinate) in the absence of vaginal discharge and significant pain. These symptoms may vary from mild to severe and in healthy women last an average of six days. Some pain above the pubic bone or in the lower back may be present. People experiencing an upper urinary tract infection, or pyelonephritis, may experience flank pain, fever, or nausea and vomiting in addition to the classic symptoms of a lower urinary tract infection. Rarely the urine may appear bloody or contain visible pus in the urine.

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.

An overview of types 1, 2, and 4 is presented below (type 3 is usually excluded from modern classifications):

Distal RTA (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of H+ secretion into lumen of nephron by the alpha intercalated cells of the medullary collecting duct of the distal nephron.

This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Because renal excretion is the primary means of eliminating from the body, there is consequently a tendency towards acidemia. There is an inability to excrete H while cannot be reclaimed by the cell, leading to acidemia (as builds up in the body) and hypokalemia (as cannot be reabsorbed by the alpha cell).

This leads to the clinical features of dRTA; In other words, the intercalated cells' apical H+/K+ antiporter is non-functional, resulting in proton retention and potassium excretion. Since calcium phosphate stones demonstrate a proclivity for deposition at higher pHs (alkaline), the substance of the kidney develops stones bilaterally; this does not occur in the other RTA types.

- Normal anion gap metabolic acidosis/acidemia

- Hypokalemia, Hypocalcemia, Hyperchloremia

- Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate).

- Nephrocalcinosis (deposition of calcium in the substance of the kidney)

- Bone demineralisation (causing rickets in children and osteomalacia in adults)

- Sjogren's syndrome

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:

Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction (papillary necrosis). Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

Also the sickle cell disease in young patients is characterized by renal hyperperfusion, glomerular hypertrophy, and glomerular hyperfiltration. Many of these individuals eventually develop a glomerulopathy leading to glomerular proteinuria (present in as many as 30%) and, in some, the nephrotic syndrome. Co-inheritance of microdeletions in the -globin gene (thalassemia) appear to protect against the development of nephropathy and are associated with lower mean arterial pressure and less protein in the urine.

Mild increases in the blood levels of nitrogen and uric acid can also develop. Advanced kidney failure and high blood urea levels occur in 10% of cases. Pathologic examination reveals the typical lesion of "hyperfiltration nephropathy" namely, focal segmental glomerular sclerosis. This finding has led to the suggestion that anemia-induced hyperfiltration in childhood is the principal cause of the adult glomerulopathy. Nephron loss secondary to ischemic injury also contributes to the development of azotemia in these patients.

In addition to the glomerulopathy described above, kidney complications of sickle cell disease include cortical infarcts leading to loss of function, persistent bloody urine, and perinephric hematomas. Papillary infarcts, demonstrable radiographically in 50% of patients with sickle trait, lead to an increased risk of bacterial infection in the scarred kidney tissues and functional tubule abnormalities. The presence of visible blood in the urine without pain occurs with a higher frequency in sickle trait than in sickle cell disease and likely results from infarctive episodes in the renal medulla. Functional tubule abnormalities such as nephrogenic diabetes insipidus result from marked reduction in vasa recta blood flow, combined with ischemic tubule injury. This concentrating defect places these patients at increased risk of dehydration and, hence, sickling crises. The concentrating defect also occurs in individuals with sickle trait. Other tubule defects involve potassium and hydrogen ion excretion, occasionally leading to high blood potassium, metabolic acidosis, and a defect in uric acid excretion which, combined with increased purine synthesis in the bone marrow, results in high blood uric acid levels.