Avoidance is the primary treatment. Better alternatives are Nocturnal or Daily Dialysis, which are far more gentle processes for the new dialysis patient. Dialysis disequilibrium syndrome is a reason why hemodialysis initiation should be done gradually, i.e. it is a reason why the first few dialysis sessions are shorter and less aggressive than the typical dialysis treatment for end-stage renal disease patients.

Adenosine antagonists such as the methylxanthines theophylline and aminophylline, may help although studies have conflicting results.

N-acetylcysteine (NAC) by mouth twice a day, on the day before and of the procedure if creatinine clearance is estimated to be less than 60 mL/min [1.00 mL/s]) may reduce risk. Some authors believe the benefit is not overwhelming. A systematic review concluded that NAC is "likely to be beneficial" but did not recommend a specific dose.

Treatment is focused on preventing deposition of uric acid within the urinary system by increasing urine volume with potent diuretics such as furosemide. Raising the urinary pH to a level higher than 7 (alkalinization) is often difficult to attain, although sodium bicarbonate and/or acetazolamide are sometimes used in an attempt to increase uric acid solubility.

Dialysis (preferably hemodialysis) is started if the above measures fail.

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

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.

The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclophosphamide, and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.

The use of diuretics such as furosemide, is widespread and sometimes convenient in improving fluid overload. It is not associated with higher mortality (risk of death), nor with any reduced mortality or length of intensive care unit or hospital stay.

In terms of treatment/management for medullary cystic kidney disease, at present there are no specific therapies for this disease, and there are no specific diets known to slow progression of the disease. However, management for the symptoms can be dealt with as follows: erythropoietin is used to treat anemia, and growth hormone is used when growth becomes an issue. Additionally, a renal transplant may be needed at some point.

Finally, foods that contain potassium and phosphate must be reduced

Early and aggressive treatment is required to control the disorder. Diuretic medications help rid the body of excess fluid. ACE inhibitor medications (like Captopril and others) and non-steroidal anti-inflammatory drugs (like indomethacin) are used to slow the spilling of protein (albumin) in the urine. Antibiotics may be needed to control infections. Patients may also take iron supplements, potassium chloride, thyroxine and other vitamins to replenish what minerals the kidneys have leaked out.

Most patients will undergo regular and frequent albumin infusion (often daily) to replace what kidneys have lost. Infusions are performed via IV so a central venous catheter will need to be surgically inserted into patients chest or groin.

Dietary modifications may include the restriction of sodium and use of dietary supplements as appropriate for the nature and extent of malnutrition. Fluids may be restricted to help control swelling.

Many patients have a gastrostomy tube (g-tube) inserted for medication and/or feeds. Some patients develop oral aversions and will use the tube for all feeds. Other patients eat well and only use the tube for medicine or supplemental feeds. The tube is also useful for patients needing to drink large amounts of fluids around the time of transplant.

Patient will require removal of the kidneys (one at the time or both), dialysis, and ultimately a kidney transplant.

Currently, the only clinical/pharmacological treatment available for ADPKD consists in reducing the speed in gain of total kidney volume (TKV) with aquaretics (i.e. tolvaptan), which can alleviate pain while giving the patients a better quality of life for over a mean of 3 years. After this period, patients can restart gaining TKV at pre-treatment rates and may eventually have to go through dialysis and kidney transplant. Paliative treatment modalities involve symptomatic medications (non-opioid and opioid analgesics) for abdominal/retroperitoneal pain. Before the advent of aquaretic medication, the only option for analgesic-resistant pain were simple or complex surgical procedures (i.e. renal cyst aspiration, cyst decortication, renal denervation and nephrectomy), which can result in complications inherent to surgery.

In 2014, Japan was the first country in the world to approve a pharmacological treatment for ADPKD followed by Canada and Europe, which approved the drug tolvaptan for ADPKD patients in the beginning of 2015. Tolvaptan, an aquaretic drug, is a vasopressin receptor 2 (V2) antagonist. Pre-clinical studies had suggested that the molecule cAMP could be involved in the enlargement of ADPKD cysts, and studies on rodents confirmed the role of vasopressin in increasing the levels of cAMP in the kidney, which laid the basis for the conduction of clinical studies. Because data from the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP) led by Mayo Clinic showed that total kidney volume (TKV) predicted the risk of developing renal insufficiency in patients with ADPKD, the TEMPO 3:4 trial, which enrolled patients from 129 sites worldwide from 2007 to 2009, evaluated TKV as a primary end-point to test the efficacy of tolvaptan in ADPKD patients. That study showed a significant decrease in the ratio of TKV increase and deterring of renal function decline in ADPKD patients after treatment with tolvaptan; however, because laboratory test results regarding liver function appeared elevated in a percentage of patients enrolled in that study, the approval of the drug was either delayed by regulatory agencies or, as in case of the US, altogether denied.

There is no proven therapy for the CFHR5 nephropathy, although research is currently underway to develop ways of preventing kidney failure developing in those affected.

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.

Increase the water intake to prevent oxalates to precipitate .

Minimize dietary intake of oxalates by restricting the intake of leafy vegetables , sesame seeds , tea , cocoa , beet root , spinach , rhubarb , etc.

Treatment of analgesic nephropathy begins with the discontinuation of analgesics, which often halts the progression of the disease and may even result in normalization of kidney function.

The management of this condition can be done via-improvement of any electrolyte imbalance, as well as, hypertension and anemia treatment as the individuals condition warrants.

There is no FDA-approved treatment. However, it has been shown that mild to moderate dietary restrictions slow the progression of autosomal dominant polycystic kidney disease (ADPKD).

If and when the disease progresses enough in a given case, the nephrologist or other practitioner and the patient will have to decide what form of renal replacement therapy will be used to treat end-stage kidney disease (kidney failure, typically stage 4 or 5 of chronic kidney disease).

That will either be some form of dialysis, which can be done at least two different ways at varying frequencies and durations (whether it is done at home or in the clinic depends on the method used and the patient's stability and training) and eventually, if they are eligible because of the nature and severity of their condition and if a suitable match can be found, unilateral or bilateral kidney transplantation.

A Cochrane Review study of autosomal dominant polycystic kidney disease made note of the fact that it is important at all times, while avoiding antibiotic resistance, to control infections of the cysts in the kidneys, and if affected, the liver, when needed for a certain duration to combat infection, by using, quote: "bacteriostatic and bacteriocidal drugs".

The optimal treatment is prevention. Rigorous and continuous control of phosphate and calcium balance most probably will avoid the metabolic changes which may lead to calciphylaxis.

There is no specific treatment. Of the treatments that exist, none are internationally recognized as the standard of care. An acceptable treatment could include:

- Dialysis (the number of sessions may be increased)

- Intensive wound care

- Clot-dissolving agents (tissue plasminogen activator)

- Hyperbaric oxygen

- Maggot larval debridement

- Adequate pain control

- Correction of the underlying plasma calcium and phosphorus abnormalities (lowering the Ca x P product below 55 mg2/dL2)

- Sodium thiosulfate

- Avoiding (further) local tissue trauma (including avoiding all subcutaneous injections, and all not-absolutely-necessary infusions and transfusions)

- Urgent parathyroidectomy: The efficacy of this measure remains uncertain although calciphylaxis is associated with frank hyperparathyroidism. Urgent parathyroidectomy may benefit those patients who have uncontrollable plasma calcium and phosphorus concentrations despite dialysis. Also, cinacalcet can be used and may serve as an alternative to parathyroidectomy.

- Patients who receive kidney transplants also receive immunosuppression. Considering lowering the dose of or discontinuing the use of immunosuppressive drugs in people who have received kidney transplants and continue to have persistent or progressive calciphylactic skin lesions can contribute to an acceptable treatment of calciphylaxis.

- A group has reported plasma exchange effective and propose a serum marker and perhaps mediator (calciprotein particles)

In addition to measures for chronic kidney disease (CKD) of any cause, there is evidence that ACE inhibitors can slow the deterioration of kidney function in Alport syndrome, delaying the need for dialysis or transplantation. The development of proteinuria has been recommended as an indication for commencing treatment.

Once kidney failure has developed, patients usually do well on dialysis or with a kidney transplant. Very rarely the Alport molecule in the donor kidney causes an aggressive immune response in the recipient, 'Alport post-transplant anti-GBM disease'.

Gene therapy has been frequently discussed, but delivering it to the podocytes in the glomerulus that normally produce the type IV collagen in the glomerular basement membrane is challenging.

Many major studies showing improvement in kidney function in patients with hepatorenal syndrome have involved expansion of the volume of the plasma with albumin given intravenously. The quantity of albumin administered intravenously varies: one cited regimen is 1 gram of albumin per kilogram of body weight intravenously on the first day, followed by 20 to 40 grams daily. Notably, studies have shown that treatment with albumin alone is inferior to treatment with other medications in conjunction with albumin; most studies evaluating pre-transplant therapies for HRS involve the use of albumin in conjunction with other medical or procedural treatment.

Midodrine is an alpha-agonist and octreotide is an analogue of somatostatin, a hormone involved in regulation of blood vessel tone in the gastrointestinal tract. The medications are respectively systemic vasoconstrictors and inhibitors of splanchnic vasodilation, and were not found to be useful when used individually in treatment of hepatorenal syndrome. However, one study of 13 patients with hepatorenal syndrome showed significant improvement in kidney function when the two were used together (with midodrine given orally, octreotide given subcutaneously and both dosed according to blood pressure), with three patients surviving to discharge. Another nonrandomized, observational study of individuals with HRS treated with subcutaneous octreotide and oral midodrine showed that there was increased survival at 30 days.

The vasopressin analogue ornipressin was found in a number of studies to be useful in improvement of kidney function in patients with hepatorenal syndrome, but has been limited in its use, as it can cause severe ischemia to major organs. Terlipressin is a vasopressin analogue that has been found in one large study to be useful for improving kidney function in patients with hepatorenal syndrome with a lesser incidence of ischemia but is not available in the United States. A key criticism of all of these medical therapies has been heterogeneity in the populations investigated and the use of kidney function, instead of mortality, as an outcome measure.

Other agents that have been investigated for use in treatment of HRS include pentoxifylline, acetylcysteine, and misoprostol. The evidence for all of these therapies is based on either case series, or in the case of pentoxifylline, extrapolated from a subset of patients treated for alcoholic hepatitis.

Patients will require dialysis to compensate for the function of their kidneys.

Treatment involves having the person stop taking any calcium supplements and any other alkali agents they have been taking, and hydration.

In severe cases, hospitalization may be required, in which case saline may be administered intravenously.

If kidney failure is advanced then treatment for that is required, namely chronic dialysis.

Congenital nephrotic syndrome can be successfully controlled with early diagnosis and aggressive treatment including albumin infusions, nephrectomy, medications and ultimately a kidney transplant. Most children live fairly normal life post-transplant but will spend significant time hospitalised pre-transplant and have numerous surgeries to facilitate treatment.

Due to the protein (albumin) losses many patients have reduced muscle tone and may experience delays in certain physical milestones such as sitting, crawling and walking. Similarly many patients experience growth delays due to protein loss. Delays vary from mild to significant but most patients experience growth spurts once they receive their transplanted kidney. Physical therapy may be useful for the child to strengthen muscle tone.

Undiagnosed cases are often fatal in the first year due to blood clots, infections or other complications.

Over time, kidney failure can develop and most men with the disease will eventually require dialysis or kidney transplantation. For reasons which are not understood, women with the disease, although they often have blood in their urine, only rarely develop kidney failure. The disease has been shown to recur following kidney transplantation, however in most cases the kidney transplant has a normal lifespan.

The definitive treatment for hepatorenal syndrome is liver transplantation, and all other therapies can best be described as bridges to transplantation. While liver transplantation is by far the best available management option for HRS, the mortality of individuals with HRS has been shown to be as high as 25% within the first month after transplantation. Individuals with HRS and evidence of greater hepatic dysfunction (quantified as MELD scores above 36) have been found to be at greatest risk of early mortality after liver transplantation. A further deterioration of kidney function even after liver transplantation in individuals with HRS has been demonstrated in several studies; however, this is transient and thought to be due to the use of medications with toxicity to the kidneys, and specifically the introduction of immunosuppressants such as tacrolimus and cyclosporine that are known to worsen kidney function. Over the long-term, however, individuals with HRS who are the recipients of liver transplants almost universally recover kidney function, and studies show that their survival rates at three years are similar to those who have received liver transplants for reasons other than HRS.

In anticipation of liver transplantation (which may be associated with considerable in-hospital delay), several other strategies have been found to be beneficial in preserving kidney function. These include the use of intravenous albumin infusion, medications (for which the best evidence is for analogues of vasopressin, which causes splanchnic vasoconstriction), radiological shunts to decrease pressure in the portal vein, dialysis, and a specialized albumin-bound membrane dialysis system termed molecular adsorbents recirculation system (MARS) or liver dialysis.