Management of hematuria is aimed at treating secondary causes of hematuria. If hematuria is a result of a UTI, treatment with antibiotics is usually initiated and urine testing repeated after 6 weeks. If hematuria is secondary to a kidney stone, then management depends on the size of the kidney stone. If the stone is small enough, usually less than 1 cm, then conservative management with analgesics and fluid hydration may be sufficient, however stones that are too bid may require removal by a urologist. Another common cause of hematuria is benign enlargement of the prostate (BPH), treatment is aimed at reducing the size of the bladder with medications like finasteride and symptomatic management with drugs like terazonsin or tamsulosin.

For people with exercise induced hematuria, management is conservative and involves cessation of strenuous activities and keeping hydrated. If the cause of hematuria is a result of malignancy, treatment and management depends on the type and stage of cancer and can involve chemotherapy, radiation or surgical resection of the tumor or organ involved.

The ideal treatment for IgAN would remove IgA from the glomerulus and prevent further IgA deposition. This goal still remains a remote prospect. There are a few additional caveats that have to be considered while treating IgA nephropathy. IgA nephropathy has a very variable course, ranging from a benign recurrent hematuria up to a rapid progression to chronic kidney failure. Hence the decision on which patients to treat should be based on the prognostic factors and the risk of progression. Also, IgA nephropathy recurs in transplants despite the use of ciclosporin, azathioprine or mycophenolate mofetil and steroids in these patients. There are persisting uncertainties, due to the limited number of patients included in the few controlled randomized studies performed to date, which hardly produce statistically significant evidence regarding the heterogeneity of IgA nephropathy patients, the diversity of study treatment protocols, and the length of follow-up.

Patients with isolated hematuria, proteinuria < 1 g/day and normal renal function have a benign course and are generally just followed up annually. In cases where tonsillitis is the precipitating factor for episodic hematuria, tonsillectomy has been claimed to reduce the frequency of those episodes. However, it does not reduce the incidence of progressive kidney failure. Also, the natural history of the disease is such that episodes of frank hematuria reduce over time, independent of any specific treatment. Similarly, prophylactic antibiotics have not been proven to be beneficial. Dietary gluten restriction, used to reduce mucosal antigen challenge, also has not been shown to preserve kidney function. Phenytoin has also been tried without any benefit.

A subset of IgA nephropathy patients, who have minimal change disease on light microscopy and clinically have nephrotic syndrome, show an exquisite response to steroids, behaving more or less like minimal change disease. In other patients, the evidence for steroids is not compelling. Short courses of high dose steroids have been proven to lack benefit. However, in patients with preserved renal function and proteinuria (1-3.5 g/day), a recent prospective study has shown that 6 months regimen of steroids may lessen proteinuria and preserve renal function. However, the risks of long-term steroid use have to be weighed in such cases. It should be noted that the study had 10 years of patient follow-up data, and did show a benefit for steroid therapy; there was a lower chance of reaching end-stage renal disease (renal function so poor that dialysis was required) in the steroid group. Importantly, angiotensin-converting enzyme inhibitors were used in both groups equally.

Cyclophosphamide had been used in combination with anti-platelet/anticoagulants in unselected IgA nephropathy patients with conflicting results. Also, the side effect profile of this drug, including long term risk of malignancy and sterility, made it an unfavorable choice for use in young adults. However, one recent study, in a carefully selected high risk population of patients with declining GFR, showed that a combination of steroids and cyclophosphamide for the initial 3 months followed by azathioprine for a minimum of 2 years resulted in a significant preservation of renal function. Other agents such as mycophenolate mofetil, ciclosporin and mizoribine have also been tried with varying results.

A study from Mayo Clinic did show that long term treatment with omega-3 fatty acids results in reduction of progression to kidney failure, without, however, reducing proteinuria in a subset of patients with high risk of worsening kidney function. However, these results have not been reproduced by other study groups and in two subsequent meta-analyses. However, fish oil therapy does not have the drawbacks of immunosuppressive therapy. Also, apart from its unpleasant taste and abdominal discomfort, it is relatively safe to consume.

The events that tend to progressive kidney failure are not unique to IgA nephropathy and non-specific measures to reduce the same would be equally useful. These include low-protein diet and optimal control of blood pressure. The choice of the antihypertensive agent is open as long as the blood pressure is controlled to desired level. However, Angiotensin converting enzyme inhibitors and Angiotensin II receptor antagonists are favoured due to their anti-proteinuric effect.

The aim of the medical treatment is to slow the progression of chronic kidney disease by reducing blood pressure and albumin levels. The current published guidelines define ideal BP of <130/80 mmHg for patients with hypertensive nephropathy; studies show that anything higher or lower than this can increase cardiovascular risk. According to the African American Study of Kidney Disease (AASK) trial, after an additional 5 years follow-up upon completion of the 10-year trial, up to 65% of the cohort had progressive nephropathy despite having controlled the mean systolic BP level <135 mmHg.

ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological treatments that can be used to lower BP to target levels; hence reducing neuropathy and proteinuria progression. The management plan should be individualized based on the condition of the patients including comorbidities and previous medical history.

In addition, there are lifestyle changes that can be made. Weight reduction, exercise, reducing salt intake can be done to manage hypertensive nephropathy.

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.

Surgery (autotransplantation) is thought by some to be of benefit in selected individuals and advocated in some centres, but usually considered the last resort.

Physicians discourage surgery, as LPHS symptoms often re-occur after autotransplantation.

Another treatment that has been known to help LPHS sufferers with their daily pain is a Spinal Cord Stimulator.

Nephropexy was performed in the past to stabilize the kidney, but presently surgery is not recommended in asymptomatic patients. Laparoscopic nephropexy has recently become available for selected symptomatic patients.

The treatment of LPHS varies considerably from centre to centre. As the condition is rare and poorly understood, a widely adopted standard of care is not existent.

Treatment of loin pain-hematuria syndrome (LPHS) typically consists of pain management. Narcotics or oral opioids may be prescribed to help control pain. Patients with severe pain may need high-dose opioids daily or almost daily. Occasionally, people with LPHS require hospitalization for intravenous opioid therapy and control of nausea. Other treatments may include denervation, autotransplantation, renal neurectomy, or nephrectomy. Unfortunately symptoms often recur following these procedures. Limited evidence suggests that drugs that inhibit angiotensin may reduce the frequency and severity of episodes of loin pain and gross hematuria.

Pain management with opiate and non-opiate analgesia is common. Angiotensin converting enzyme inhibitors are thought to be beneficial, as they reduce intraglomerular pressure and, presumably, reduce renal tubular congestion with RBCs.

Possible treatment regimens

Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control:also a renal biopsy may be needed to be performed at some point. A low-sodium diet may be needed when hypertension is present. In individuals with oliguric acute kidney injury, the amount of potassium should be controlled.

Therapy for rapidly progressive glomerulonephritis is done via corticosteroids and cyclophosphamide. The predictor of kidney survival is serum creatinine value. The substitution of azathioprine for cyclophosphamide after a 90-day initial period is another option.Plasmapheresis can be used for patients who present with severe renal failure.

Aggressive treatment of high blood lipids is warranted. Low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start. Replacement of erythropoietin and calcitriol, two hormones processed by the kidney, is often necessary in people with advanced disease. Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin. A target hemoglobin level of 9–12 g/dL is recommended. The normalization of hemoglobin has not been found to be of benefit. It is unclear if androgens help with anemia. Phosphate binders are also used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease. Although the evidence for them is limited, phosphodiesterase-5 inhibitors and zinc show potential for helping men with sexual dysfunction.

At stage 5 CKD, renal replacement therapy is usually required, in the form of either dialysis or a transplant.

It is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis, while others reject that antibiotics can prevent acute proliferative glomerulonephritis.

Most patients with thin basement membrane disease need only reassurance. Indeed, this disease was previously referred to as "benign familial hematuria" because of its usually benign course. Angiotensin converting enzyme inhibitors have been suggested to reduce the episodes of hematuria, though controlled studies are lacking. Treating co-existing hypercalciuria and hyperuricosuria will also be helpful in reducing hematuria.

The molecular basis for thin basement membrane disease has yet to be elucidated fully; however, defects in the gene encoding the a4 chain of type IV collagen have been reported in some families.

Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression. They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD. Furthermore, ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD. Aggressive blood pressure lowering decreases peoples risk of death.

Although the use of ACE inhibitors and ARBs represents the current standard of care for people with CKD, people progressively lose kidney function while on these medications, as seen in the IDNT and RENAL studies, which reported a decrease over time in estimated GFR (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines) in people treated by these conventional methods.

Initial treatment is with adequate hydration, alkalization of the urine with citrate supplementation or acetazolamide, and dietary modification to reduce salt and protein intake (especially methionine). If this fails then patients are usually started on chelation therapy with an agent such as penicillamine. Tiopronin is another agent.

Once renal stones have formed, however, the first-line treatment is ESWL (Extracorporeal shock wave lithotripsy). If ESWL do not work efficiently surgery can be necessary. Both endoscopic surgery and conventional open-abdominal surgery have proven to be effective treatment modalities for patients with more advanced disease. Adequate hydration is the foremost aim of treatment to prevent cysteine stones. The goal is to increase the urine volume because the concentration of cystine in the urine is reduced which prevents cystine from precipitating from the urine and forming stones. People with cystine stones should consume 5 to 7 liters a day. The rationale behind alkalizing the urine is that cystine tends to stay in solution and causes no harm. In order to alkalize the urine, sodium biocarbonate has been used. One must be careful in alkalizing their urine because it could lead to other forms of stones in process of preventing cystine stones. Penicillamine is a drug that acts to form a complex with cystine that is 50 times more soluble than cystine itself. Percutaneous nephrolithotripsy (PNL) is performed via a port created by puncturing the kidney through the skin and enlarging the access port to 1 cm in diameter. Most of the time, cystine stones are too dense to be broken up by shock (ESWL) so PNL is needed.

Videos of surgery are available on various websites that show stone removal by percutaneous nephrolithotomy.

In February 2017, an article was published in Nature Medicine entitled 'Alpha lipoic acid treatment prevents cystine urolithiasis in a mouse model of cystinuria', suggesting that a high dose of the readily available antioxidant, alpha-lipoic acid at 2,700 mg/67 kg body weight daily reduced the incidence of stones. The effects were dose dependent. The results are unprecedented for cystinuria. A clinical trial is underway based on this mouse model.

Management is focused on removing the infectious source. The shunt is removed immediately and antibiotics are begun. The infected shunt, typically a ventriculoatrial shunt, may be replaced with a ventriculoperitoneal shunt.

Microscopic hematuria does not discolor the urine and is thus found incidentally on urinalysis or light microscopy. It is defined as greater than three red blood cells per high powered field. In many of these cases, no source or cause is found. Any part of the kidneys or urinary system can cause microscopic hematuria. Causes can be separated into glomerular, arising from the filtering system of the kidney, and non-glomerular, arising from the kidney (outside the glomerulus), ureters, urinary bladder, prostate, or urethra.

Analgesics may be needed for the abdominal and joint pains. It is uncertain as to whether HSP needs treatment beyond controlling the symptoms. Most patients do not receive therapy because of the high spontaneous recovery rate. Steroids are generally avoided. However, if they are given early in the disease episode, the duration of symptoms may be shortened, and abdominal pain can improve significantly. Moreover, the chance of severe kidney problems may be reduced. A systematic review of randomized clinical trials did not find any evidence that steroid treatment (prednisone) is effective at decreasing the likelihood of developing long-term kidney disease.

Evidence of worsening kidney damage would normally prompt a kidney biopsy. Treatment may be indicated on the basis of the appearance of the biopsy sample; various treatments may be used, ranging from oral steroids to a combination of intravenous methylprednisolone (steroid), cyclophosphamide and dipyridamole followed by prednisone. Other regimens include steroids/azathioprine, and steroids/cyclophosphamide (with or without heparin and warfarin). Intravenous immunoglobulin (IVIG) is occasionally used.

There is no evidence from randomized clinical trials that treating children who have HSP with antiplatelet agent prevents persistent kidney disease. There is also no evidence from randomized clinical trials that treating children or adults with cyclophosphamide prevents severe kidney disease. Heparin treatment is not justified.

Treatment/management of nephritis depends on what has provoked the inflammation of the kidney(s). In the case of lupus nephritis, hydroxychloroquine could be used.

According to the United States Renal Data System (USRDS), hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%.

Haemodialysis is recommended for patients who progress to end-stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes.

Patient prognosis is dependent on numerous factors including age, ethnicity, blood pressure and glomerular filtration rate. Changes in lifestyle factors, such as reduced salt intake and increased physical activity have been shown to improve outcomes but are insufficient without pharmacological treatment.

Although plasma exchange/infusion (PE/PI) is frequently used, there are no controlled trials of its safety or efficacy in aHUS. Even though PE/PI often partially controls some of the hematological manifestations of aHUS in some patients, its effectiveness has not been demonstrated in terms of inducing total disease remission. PE/PI is associated with significant safety risks, including risk of infection, allergic reactions, thrombosis, loss of vascular access, and poor quality of life. Importantly, terminal complement activation has been shown to be chronically present on the surface of platelets in patients with aHUS who appear to be clinically well while receiving chronic PE/PI.

Before the introduction of eculizumab (INN and USAN, trade name Soliris), a monoclonal antibody that is a first-in-class terminal complement inhibitor, management options for patients with aHUS were extremely limited. Guidelines issued by the European Paediatric Study Group for HUS recommend rapid administration of plasma exchange or plasma infusion (PE/PI), intensively administered daily for 5 days and then with reducing frequency. However, the American Society for Apheresis offers a "weak" recommendation for plasma exchange to treat aHUS, due to the "low" or "very low" quality of evidence supporting its use. Although some patients experienced improvements in red blood cell and platelet counts, plasma therapies generally did not result in full remission.

This is relatively straightforward. It involves correction of the acidemia with oral sodium bicarbonate, sodium citrate or potassium citrate. This will correct the acidemia and reverse bone demineralisation. Hypokalemia and urinary stone formation and nephrocalcinosis can be treated with potassium citrate tablets which not only replace potassium but also inhibit calcium excretion and thus do not exacerbate stone disease as sodium bicarbonate or citrate may do.

Nephropathy can be associated with some therapies used to treat cancer. The most common form of kidney disease in cancer patients is Acute Kidney Injury (AKI) which can usually be due to volume depletion from vomiting and diarrhea that occur following chemotherapy or occasionally due to kidney toxicities of chemotherapeutic agents. Kidney failure from break down of cancer cells, usually after chemotherapy, is unique to onconephrology. Several chemotherapeutic agents, for example Cisplatin, are associated with acute and chronic kidney injuries. Newer agents such as anti Vascular Endothelial Growth Factor (anti VEGF) are also associated with similar injuries, as well as proteinuria, hypertension and thrombotic microangiopathy.

The long-term use of lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, is known to cause nephropathy.

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