Diet modification is often recommended as a first-line method of self-treatment for interstitial cystitis, though rigorous controlled studies examining the impact diet has on interstitial cystitis signs and symptoms are currently lacking. Individuals with interstitial cystitis often experience an increase in symptoms when they consume certain foods and beverages. Avoidance of these potential trigger foods and beverages such as caffeine-containing beverages including coffee, tea, and soda, alcoholic beverages, chocolate, citrus fruits, hot peppers, and artificial sweeteners may be helpful in alleviating symptoms. Diet triggers vary between individuals with IC; the best way for a person to discover his or her own triggers is to use an elimination diet. Sensitivity to trigger foods may be reduced if calcium glycerophosphate and/or sodium bicarbonate is consumed. The foundation of therapy is a modification of diet to help patients avoid those foods which can further irritate the damaged bladder wall.

The mechanism by which dietary modification benefits people with IC is unclear. Integration of neural signals from pelvic organs may mediate the effects of diet on symptoms of IC.

Bladder instillation of medication is one of the main forms of treatment of interstitial cystitis, but evidence for its effectiveness is currently limited. Advantages of this treatment approach include direct contact of the medication with the bladder and low systemic side effects due to poor absorption of the medication. Single medications or a mixture of medications are commonly used in bladder instillation preparations. DMSO is the only approved bladder instillation for IC/BPS yet it is much less frequently used in urology clinics.

A 50% solution of DMSO had the potential to create irreversible muscle contraction. However, a lesser solution of 25% was found to be reversible. Long-term use of DMSO is questionable, as its mechanism of action is not fully understood though DMSO is thought to inhibit mast cells and may have anti-inflammatory, muscle-relaxing, and analgesic effects. Other agents used for bladder instillations to treat interstitial cystitis include: heparin, lidocaine, chondroitin sulfate, hyaluronic acid, pentosan polysulfate, oxybutynin, and botulinum toxin A. Preliminary evidence suggests these agents are efficacious in reducing symptoms of interstitial cystitis, but further study with larger, randomized, controlled clinical trials is needed.

Some research suggests that cranberry (juice or capsules) may decrease the number of UTIs in those with frequent infections. A Cochrane review concluded that the benefit, if it exists, is small. Long-term tolerance is also an issue with gastrointestinal upset occurring in more than 30%. Cranberry juice is thus not currently recommended for this indication. As of 2015, probiotics require further study to determine if they are beneficial.

The evidence that preventive antibiotics decrease urinary tract infections in children is poor. However recurrent UTIs are a rare cause of further kidney problems if there are no underlying abnormalities of the kidneys, resulting in less than a third of a percent (0.33%) of chronic kidney disease in adults. Whether routine circumcisions prevents UTIs has not been well studied as of 2011.

In people who do not require hospitalization and live in an area where there is a low prevalence of antibiotic-resistant bacteria, an fluoroquinolone by mouth such as ciprofloxacin or levofloxacin is an appropriate initial choice for therapy. In areas where there is a higher prevalence of fluoroquinolone resistance, it is useful to initiate treatment with a single intravenous dose of a long-acting antibiotic such as ceftriaxone or an aminoglycoside, and then continuing treatment with a fluoroquinolone. Oral trimethoprim/sulfamethoxazole is an appropriate choice for therapy if the bacteria is known to be susceptible. If trimethoprim/sulfamethoxazole is used when the susceptibility is not known, it is useful to initiate treatment with a single intravenous dose of a long-acting antibiotic such as ceftriaxone or an aminoglycoside. Oral beta-lactam antibiotics are less effective than other available agents for treatment of pyelonephritis. Improvement is expected in 48 to 72 hours.

People with acute pyelonephritis that is accompanied by high fever and leukocytosis are typically admitted to the hospital for intravenous hydration and intravenous antibiotic treatment. Treatment is typically initiated with an intravenous fluoroquinolone, an aminoglycoside, an extended-spectrum penicillin or cephalosporin, or a carbapenem. Combination antibiotic therapy is often used in such situations. The treatment regimen is selected based on local resistance data and the susceptibility profile of the specific infecting organism(s).

During the course of antibiotic treatment, serial white blood cell count and temperature are closely monitored. Typically, the intravenous antibiotics are continued until the person has no fever for at least 24 to 48 hours, then equivalent antibiotics by mouth can be given for a total of 2–week duration of treatment. Intravenous fluids may be administered to compensate for the reduced oral intake, insensible losses (due to the raised temperature) and vasodilation and to optimize urine output. Percutaneous nephrostomy or ureteral stent placement may be indicated to relieve obstruction caused by a stone. Children with acute pyelonephritis can be treated effectively with oral antibiotics (cefixime, ceftibuten and amoxicillin/clavulanic acid) or with short courses (2 to 4 days) of intravenous therapy followed by oral therapy. If intravenous therapy is chosen, single daily dosing with aminoglycosides is safe and effective.

Treatment of xanthogranulomatous pyelonephritis involves antibiotics as well as surgery. Removal of the kidney is the best surgical treatment in the overwhelming majority of cases, although polar resection (partial nephrectomy) has been effective for some people with localized disease. Watchful waiting with serial imaging may be appropriate in rare circumstances.

Unfortunately mesna is ineffective as a treatment once hemorrhagic cystitis has developed. Although rare, once a case of radiation-induced hemorrhagic cystitis is diagnosed there is no empirically-proven treatments to heal this type of condition, which can severely degrade a patient's quality of life and might possibly lead to renal failure with risk of death.

Viral hemorrhagic cystitis in children generally spontaneously resolves within a few days.

The first step in the treatment of HC should be directed toward clot evacuation. Bladder outlet obstruction from clots can lead to urosepsis, bladder rupture, and renal failure. Clot evacuation can be performed by placing a wide-lumen bladder catheter at bedside. The bladder can be irrigated with water or sodium chloride solution. The use of water is preferable because water can help with clot lysis. Care must be taken to not overdistend the bladder and cause a perforation.. Hyperbaric oxygen (HBO2) therapy has been proven to be effective in treating radiation-induced hemorrhagic cystitis.

Causes of hemorrhagic cystitis include chemotherapy (e.g. cyclophosphamide, Ifosfamide), radiation, or infection. Ifosfamide is the most common cause of hemorrhagic cystitis. Radiation-induced hemorrhagic cystitis develops in similar or smaller patient numbers when compared to cyclophosphamide-induced cases.

Adenovirus (particularly serotypes 11 and 21 of subgroup B) is the most common cause of acute viral hemorrhagic cystitis in children, though it can result from BK virus as well. A chemical hemorrhagic cystitis can develop when vaginal products are inadvertently placed in the urethra. Gentian violet douching to treat candidiasis has resulted in hemorrhagic cystitis when the drug was misplaced in the urethra, but this hemorrhagic cystitis resolved spontaneously with cessation of treatment. Accidental urethral placement of contraceptive suppositories has also caused hemorrhagic cystitis in several patients. The bladder irritation was thought to be caused by the spermicidal detergent nonoxynol-9. In the acute setting, the bladder can be copiously irrigated with alkalinized normal saline to minimize bladder irritation.

Although hemorrhagic cystitis post-transplantation/bone marrow transplantation is not technically infectious, a short discussion is in order for completeness. Patients undergoing therapy to suppress the immune system are at risk for hemorrhagic cystitis due to either the direct effects of chemotherapy or activation of dormant viruses in the kidney, ureter, or bladder.

Urinary catheters should be inserted using aseptic technique and sterile equipment (including sterile gloves, drape, sponges, antiseptic and sterile solution), particularly in an acute care setting. Hands should be washed before and after catheter insertion. Overall, catheter use should be minimized in all patients, particularly those at higher risk of CAUTI and mortality (e.g. the elderly or those with impaired immunity).

In addition to traditional IC therapies, diet modification remains a core self care strategy as foods that are irritating to the bladder dramatically worsen the symptoms that patients may experience. Foods high in acid and/or caffeine (such as all coffees, regular teas, green teas, sodas, diet sodas, artificial sweeteners and most fruit juices) should be avoided. The daily goal of patients should be to soothe rather than irritate the bladder wall.

Treatment involves avoiding the trigger if that can be determined.

In a small minority of cases of urethral syndrome, treatment with antibiotics is effective, which indicates that in some cases it may be caused by bacterial infection which does not show up in either urinalysis or urine culture. For chronic urethral syndrome, a long term, low-dose antibiotic treatment is given on a continuous basis or after intercourse each time if intercourse appears to trigger symptoms.

As low oestrogen may also be considered a source for urethral syndrome, hormone replacement therapy, and oral contraceptive pill (birth-control pills) containing oestrogen are also used to treat the symptoms of this condition in women.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

Even when caught early, aggressive treatment is required (Bobba). Antibiotics are proven to cure Emphysematous cystitis over time and reduce the amount of gas inside the bladder wall. Prognosis is poor if antibiotics are not used to treat the patient. Additional treatment consists of urinary drainage and good control of blood glucose. The treatment of underlying comorbid diseases, such as diabetes, is extremely important because they can intensify the infection (Gheonea, Bondari). Hyperbaric oxygen is an effective treatment, and has cured some cases in as little as 48 hours. Although it is unclear as to how gas formation occurs in emphysematous cystitis, it’s dependant on whether or not the patient has contributing diseases (Mccabe). Gas formation in diabetic patients diagnosed with Emphysematous cystitis has been determined to occur due to the production of carbon dioxide as a result of the fermentation of the high concentrations of glucose. Gas formation in nondiabetic patients is most likely due the breaking down of urinary lactulose and tissue proteins. Inflammation caused by infection increases pressure and decreases circulation, which provides the perfect environment for bacteria to produce gas (Sereno).

Bacteria and yeast, including those naturally occurring as part of the human microbiome, can travel along urinary catheters and cause an infection in the bladder, kidneys, and other organs connected to the urinary tract.

CAUTI can lead to complications such as prostatitis, epididymitis, and orchitis in men, and cystitis, pyelonephritis, gram-negative bacteremia, endocarditis, vertebral osteomyelitis, septic arthritis, endophthalmitis, and meningitis in all patients. Complications associated with CAUTI cause discomfort to the patient, prolonged hospital stay, and increased cost and mortality. It has been estimated that more than 13,000 deaths are associated with UTIs annually. Estimated > 560,000 nosocomial UTIs annually.

Asymptomatic bacteriuria generally does not require treatment. Exceptions include during pregnancy and in those undergoing surgery of the urinary tract. Children with vesicoureteral reflux or others with structural abnormalities of the urinary tract.

There is no indication to treat asymptomatic bacteriuria in diabetics, renal transplant recipients, and in those with spinal cord injuries.

The overuse of antibiotic therapy to treat asymptomatic bacteriuria increases the risk of diarrhea, antimicrobial resistance, and infection due to Clostridium difficile. Other effects include increased financial burdens and overreporting of mandated catheter-associated urinary tract infection.

Emphysematous cystitis is a rare type of infection of the bladder wall by gas-forming bacteria or fungi. The most frequent offending organism is "E. coli". Other gram negative bacteria, including "Klebsiella" and "Proteus" are also commonly isolated. Fungi, such as "Candida", have also been reported as causative organisms. "Citrobacter" and "Enterococci" have also been found to cause Emphysematous cystitis (Mokabberi). Although it is a rare type of bladder infection, it is the most common type of all gas-forming bladder infections (Mccabe). The condition is characterized by the formation of air bubbles in and around the bladder wall. The gas found in the bladder consists of nitrogen, hydrogen, oxygen, and carbon dioxide. The disease most commonly affects elderly diabetic and immunocompromised patients (Sereno). The first case was identified in a post-mortem examination in 1888 (Nemati, Basra).

Symptomatic bacteriuria is typically treated as a urinary tract infection with antibiotics. Common choices include nitrofurantoin, and trimethoprim/sulfamethoxazole.

Eosinophilic cystitis is a rare condition where eosinophiles are present in the bladder wall. Signs and symptoms are similar to a bladder infection. Its cause is not entirely clear; however, may be linked to food allergies, infections, and medications among others.

In recent years the prognosis for CP/CPPS has improved with the advent of multimodal treatment, phytotherapy, protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control, and chronic pain therapy.

In a preliminary 2005 open label study of 16 treatment-recalcitrant CPPS patients, controversial entities known as nanobacteria were proposed as a cause of prostatic calcification and symptoms found in CPPS. Patients were treated with EDTA (to dissolve the calcifications) and 3 months of tetracycline (a calcium-leaching antibiotic with anti-inflammatory effects, used here to kill the "pathogens"), and half had significant improvement in symptoms. Scientists have expressed strong doubts about whether nanobacteria are living organisms. Research in 2008 showed that "nanobacteria" are merely tiny lumps of abiotic limestone.

Phytotherapeutics such as quercetin and flower pollen extract have been studied in small clinical trials; the evidence is insufficient to judge safety or efficacy.

The evidence supporting a viral cause of prostatitis and chronic pelvic pain syndrome is weak. Single case reports have implicated herpes simplex virus (HSV) and cytomegalovirus (CMV) but a study using PCR failed to demonstrate the presence of viral DNA in patients with chronic pelvic pain syndrome undergoing radical prostatectomy for localized prostate cancer. The reports implicating CMV must be interpreted with caution because in "all" cases the patients were immunocompromised. For HSV the evidence is weaker still and there is only one reported case and the causative role of the virus was not proven, and there are no reports of successful treatments using antiviral drugs such as aciclovir.

Due to the concomitant presence of bladder disorders, gastrointestinal disorders, and mood disorders, research has been conducted to understand whether CP/CPPS might be caused by problems with the hypothetical bladder-gut-brain axis.

Research has been conducted to understand how chronic bladder pain affects the brain, using techniques like MRI and functional MRI; as of 2016 it appeared that people with CP/CPPS have increased grey matter in the primary somatosensory cortex, the Insular cortex, the insular cortex, and the anterior cingulate cortex, and in the central nucleus of the amygdala; studies in rodents have shown that blocking the metabotropic glutamate receptor 5 which is expressed in the central nucleus of the amygdala, can block bladder pain.

Bladder tamponade is obstruction of the bladder outlet due to heavy blood clot formation within it. It generally requires surgery. Such heavy bleeding is usually due to bladder cancer.

Cystitis is a urinary bladder inflammation that results from any one of a number of distinct syndromes. It is most commonly caused by a bacterial infection in which case it is referred to as a urinary tract infection.

Glomerulation refers to bladder hemorrhages which are thought to be associated with some types of interstitial cystitis (IC).

The presence of glomerulations, also known as petechial hemorrhages, in the bladder suggests that the bladder wall has been damaged, irritated and/or inflamed. In fact, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Diagnostic Criteria for IC, developed in 1987, required the presence of glomerulations or Hunner's Ulcers to make a firm diagnosis of IC and is still used, today, to determine patient eligibility for some clinical trials. Research conducted by Waxman, however, determined that the hydrodistention procedure itself may have created these tiny broken blood vessels. Thus, a diagnosis of IC is now based upon other, less invasive methods, such as the PUF questionnaire.