There is as yet inadeqaute data from randomised controlled trials.

Treatment with HAART and ACE inhibitors/Angiotensin receptor blockers has been shown to be beneficial and should be given to all patients unless otherwise contra-indicated. General renoprotective measures and the treatment of the complications of nephrotic syndrome and kidney failure are adjunctive.

Corticosteroid treatment can be useful in patients who do not respond to the above treatment. There is some evidence that ciclosporin might be helpful in selective cases, however further trials are required on both steroids and ciclosporin before these drugs can become standardised treatment if at all.

Treatment of secondary membranous nephropathy is guided by the treatment of the original disease. For treatment of idiopathic membranous nephropathy, the treatment options include immunosuppressive drugs and non-specific anti-proteinuric measures. Recommended first line therapy often includes: cyclophosphamide alternating with a corticosteroid.

Perhaps the most difficult aspect of membranous glomerulonephritis is deciding which people to treat with immunosuppressive therapy as opposed to simple "background" or anti-proteinuric therapies. A large part of this difficulty is due to a lack of ability to predict which people will progress to end-stage renal disease, or renal disease severe enough to require dialysis. Because the above medications carry risk, treatment should not be initiated without careful consideration as to risk/benefit profile. Of note, corticosteroids (typically Prednisone) alone are of little benefit. They should be combined with one of the other 5 medications, each of which, along with prednisone, has shown some benefit in slowing down progression of membranous nephropathy. It must be kept in mind, however, that each of the 5 medications also carry their own risks, on top of prednisone.

The twin aims of treating membranous nephropathy are first to induce a remission of the nephrotic syndrome and second to prevent the development of endstage renal failure. A meta-analysis of four randomized controlled studies comparing treatments of membranous nephropathy showed that regimes comprising chlorambucil or cyclophosphamide, either alone or with steroids, were more effective than symptomatic treatment or treatment with steroids alone in inducing remission of the nephrotic syndrome.

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.

It is not known whether ACE inhibitors or other treatments affect hearing loss. For those with classic Alport syndrome, hearing aids are often required in teenage or young adult years.

There is currently no treatment for CHILD syndrome so any treatment would target the symptoms currently present. Emoillents like Lac-Hydran (ammonium lactate) and Ureaphil (urea) are used to treat scaly patches on the skin. A pediatric orthopedic surgeon can evaluate any underdevelopment in the bones and treat them if necessary.

There is a compound that is a topical liquid that can calm lesions down on older adults and make them go away on younger children. The mixture was made by Dr. Amy Paller at Children's Hospital. It is mixed as follows: to make 250 ml: Grind up lovastatin tablets 5g (10-20-40-80 mg); mix with cholesterol NF powder (NDC# 51927-1203-00, PCCA) 5g; mix with preserved water while mixing (eventually mixing for 1/2 hour with electronic mortar and pestle) to bring to full volume with preserved water. 8 oz

The treatment of kidney damage may reverse or delay the progression of the disease. Kidney damage is treated by prescribing drugs:

- Corticosteroids: the result is a decrease in the proteinuria and the risk of infection as well as a resolution of the edema. Prednisone is usually prescribed at a dose of 60 mg/m² of body surface area/day in a first treatment for 4–8 weeks. After this period the dose is reduced to 40 mg/m² for a further 4 weeks. Patients suffering a relapse or children are treated with prednisolone 2 mg/kg/day till urine becomes negative for protein. Then, 1.5 mg/kg/day for 4 weeks. Frequent relapses treated by: cyclophosphamide or nitrogen mustard or cyclosporin or levamisole. Patients can respond to prednisone in a number of different ways:

- Corticosteroid sensitive patient or early steroid-responder: the subject responds to the corticosteroids in the first 8 weeks of treatment. This is demonstrated by a strong diuresis and the disappearance of edemas, and also by a negative test for proteinuria in three urine samples taken during the night.

- Corticosteroid resistant patient or late steroid-responder: the proteinuria persists after the 8-week treatment. The lack of response is indicative of the seriousness of the glomerular damage, which could develop into chronic kidney failure.

- Corticosteroid tolerant patient: complications such as hypertension appear, patients gain a lot of weight and can develop aseptic or avascular necrosis of the hip or knee, cataracts and thrombotic phenomena and/or embolisms.

- Corticosteroid dependent patient: proteinuria appears when the dose of corticosteroid is decreased or there is a relapse in the first two weeks after treatment is completed.

The susceptibility testing in vitro to glucocorticoids on patient's peripheral blood mononuclear cells is associated with the incidence of not optimal clinical responses: the most sensitive patients in vitro have shown a higher incidence of corticodependence, while the most resistant patients in vitro showed a higher incidence of ineffective therapy.

- Immunosupressors (cyclophosphamide): only indicated in recurring nephrotic syndrome in corticosteroid dependent or intolerant patients. In the first two cases the proteinuria has to be negated before treatment with the immunosuppressor can begin, which involves a prolonged treatment with prednisone. The negation of the proteinuria indicates the exact moment when treatment with cyclophosphamide can begin. The treatment is continued for 8 weeks at a dose of 3 mg/kg/day, the immunosuppression is halted after this period. In order to be able to start this treatment the patient should not be suffering from neutropenia nor anaemia, which would cause further complications. A possible side effect of the cyclophosphamide is alopecia. Complete blood count tests are carried out during the treatment in order to give advance warning of a possible infection.

Management of sickle nephropathy is not separate from that of overall patient management. In addition, however, the use of ACE inhibitors has been associated with improvement of the hyperfiltration glomerulopathy. Three-year graft and patient survival in kidney transplant recipients with sickle nephropathy is lower when compared to those with other causes of end-stage kidney disease.

Treating proteinuria mainly needs proper diagnosis of the cause.

The most common cause is diabetic nephropathy; in this case, proper glycemic control may slow the progression. Medical management consists of angiotensin converting enzyme (ACE) inhibitors, which are typically first-line therapy for proteinuria. In patients whose proteinuria is not controlled with ACE inhibitors, the addition of an aldosterone antagonist (i.e., spironolactone) or angiotensin receptor blocker (ARB) may further reduce protein loss. Caution must be used if these agents are added to ACE inhibitor therapy due to the risk of hyperkalemia.

Proteinuria secondary to autoimmune disease should be treated with steroids or steroid-sparing agent plus the use of ACE inhibitors.

Drug regimens prescribed for lupus nephritis include mycophenolate mofetil (MMF), intravenous cyclophosphamide with corticosteroids, and the immune suppressant azathioprine with corticosteroids. MMF and cyclophosphamide with corticosteroids are equally effective in achieving remission of the disease. MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy. Individuals with lupus nephritis have a high risk for B-cell lymphoma (which begins in the immune system cells).

The objective of this treatment is to treat the imbalances brought about by the illness: edema, hypoalbuminemia, hyperlipemia, hypercoagulability and infectious complications.

- Edema: a return to an unswollen state is the prime objective of this treatment of nephrotic syndrome. It is carried out through the combination of a number of recommendations:

- Rest: depending on the seriousness of the edema and taking into account the risk of thrombosis caused by prolonged bed rest.

- Medical nutrition therapy: based on a diet with the correct energy intake and balance of proteins that will be used in synthesis processes and not as a source of calories. A total of 35 kcal/kg body weight/day is normally recommended. This diet should also comply with two more requirements: the first is to not consume more than 1 g of protein/kg body weight/ day, as a greater amount could increase the degree of proteinuria and cause a negative nitrogen balance. Patients are usually recommended lean cuts of meat, fish, and poultry. The second guideline requires that the amount of water ingested is not greater than the level of diuresis. In order to facilitate this the consumption of salt must also be controlled, as this contributes to water retention. It is advisable to restrict the ingestion of sodium to 1 or 2 g/day, which means that salt cannot be used in cooking and salty foods should also be avoided. Foods high in sodium include seasoning blends (garlic salt, Adobo, season salt, etc.) canned soups, canned vegetables containing salt, luncheon meats including turkey, ham, bologna, and salami, prepared foods, fast foods, soy sauce, ketchup, and salad dressings. On food labels, compare milligrams of sodium to calories per serving. Sodium should be less than or equal to calories per serving.

- Medication: The pharmacological treatment of edema is based on the prescription of diuretic drugs (especially loop diuretics, such as furosemide). In severe cases of edema (or in cases with physiological repercussions, such as scrotal, preputial or urethral edema) or in patients with one of a number of severe infections (such as sepsis or pleural effusion), the diuretics can be administered intravenously. This occurs where the risk from plasmatic expansion is considered greater than the risk of severe hypovolemia, which can be caused by the strong diuretic action of intravenous treatment. The procedure is the following:

- Hypoalbuminemia: is treated using the medical nutrition therapy described as a treatment for edema. It includes a moderate intake of foods rich in animal proteins.

- Hyperlipidaemia: depending of the seriousness of the condition it can be treated with medical nutrition therapy as the only treatment or combined with drug therapy. The ingestion of cholesterol should be less than 300 mg/day, which will require a switch to foods that are low in saturated fats. Avoid saturated fats such as butter, cheese, fried foods, fatty cuts of red meat, egg yolks, and poultry skin. Increase unsaturated fat intake, including olive oil, canola oil, peanut butter, avocadoes, fish and nuts. In cases of severe hyperlipidaemia that are unresponsive to nutrition therapy the use of hypolipidemic drugs, may be necessary (these include statins, fibrates and resinous sequesters of bile acids).

- Thrombophilia: low molecular weight heparin (LMWH) may be appropriate for use as a prophylactic in some circumstances, such as in asymptomatic patients that have no history of suffering from thromboembolism. When the thrombophilia is such that it leads to the formation of blood clots, heparin is given for at least 5 days along with oral anticoagulants (OAC). During this time and if the prothrombin time is within its therapeutic range (between 2 and 3), it may be possible to suspend the LMWH while maintaining the OACs for at least 6 months.

- Infectious complications: an appropriate course of antibacterial drugs can be taken according to the infectious agent.

In addition to these key imbalances, vitamin D and calcium are also taken orally in case the alteration of vitamin D causes a severe hypocalcaemia, this treatment has the goal of restoring physiological levels of calcium in the patient.

- Achieving better blood glucose level control if the patient is diabetic.

- Blood pressure control. ACE inhibitors are the drug of choice. Independent of their blood pressure lowering effect, they have been shown to decrease protein loss.

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome in children and adolescents, as well as a leading cause of kidney failure in adults. It is also known as "focal glomerular sclerosis" or "focal nodular glomerulosclerosis". It accounts for about a sixth of the cases of nephrotic syndrome. (Minimal change disease (MCD) is by far the most common cause of nephrotic syndrome in children: MCD and primary FSGS may have a similar cause.)

Treatment depends on the grade (I-III) but typically consist of cortisone, rituximab and chemotherapy (etoposide, vincristine, cyclophosphamide, doxorubicin). Methotrexate has been seen to induce LYG. Interferon alpha has been used by the US National Cancer Institute with varying results. In recent years hematopoietic stem cell transplantation has been performed on LYG-patients with relative good success; a 2013 study identifying 10 cases found that 8 patients survived the treatment and were disease free several years later. Two of the disease free patients later died, one from suicide and one from graft versus host disease after a second transplantation 4 years later. The remaining two patients died from sepsis after the transplantation.

Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). Because of the significant side effects of long-term high-dose prednisone use, the starting dose is tapered over several weeks to a dose which controls symptoms while limiting the side effects of steroids.

Promising results are achieved with mycophenolate and tocilizumab. If treatment is not kept to a high standard, long-term damage or death can occur.

For patients who do not respond to steroids may require revascularization, either via vascular bypass or angioplasty and stenting. Outcomes following revascularization vary depending on the severity of the underlying disease

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

There are no prospective randomized controlled trials studying therapies for relapsing polychondritis. Evidence for efficacy of treatments is based on case reports and series of small groups of patients.

For mild cases limited to joint pain or arthritis, oral nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. Other treatments typically involve medications to suppress the immune system. Corticosteroids are frequently used for more serious disease. Steroid-sparing medications such as azathioprine or methotrexate may be used to minimize steroid doses and limit the side effects of steroids. For severe disease cyclophosphamide is often given in addition to high dose intravenous steroids.

More specifically, glomerulosclerosis can refer to:

- Focal segmental glomerulosclerosis

- Nodular glomerulosclerosis (diabetic)

There is currently no specific treatment for megalencephaly, however periodic head measurements may be assessed to determine the rate of brain growth.

Those individuals who develop neurological disorders may be prescribed anti-epileptic drugs for seizures. Studies have shown that reducing epilepsy can increase cell apoptosis and reduce the proliferation of neurons that ultimately leads to brain overgrowth.

Since there are very few treatment methods focused on managing megalencephaly, future research is targeted at inhibiting mutation of the pathway. However, this next step could be met with several complications as understanding the underlying mechanism of the mutation is a difficult task. The genetic coding that initiates a single mutation is sporadic and patterns are hard to detect in many cases.

Even thought very little research has been done to create inhibitors of the PI3K-AKT pathway, several pharmaceutical companies have begun to focus their interests in designing a prevention method for this purpose.

Chronic allograft nephropathy, abbreviated CAN and also known as sclerosing/chronic allograft nephropathy, is the leading cause of kidney transplant failure and happens month to years after the transplant.

Ask-Upmark kidneys are a cause of secondary hypertension that can be curable.

Glomerulosclerosis, also known as glomerular sclerosis, refers to a hardening of the glomerulus in the kidney. It is a general term to describe scarring of the kidneys' tiny blood vessels, the glomeruli, the functional units in the kidney that filter urine from the blood.

Proteinuria (large amounts of protein in urine) is one of the signs of glomerulosclerosis. Scarring disturbs the filtering process of the kidneys and allows protein to leak from the blood into urine. However, glomerulosclerosis is one of many causes of proteinuria. A kidney biopsy (removal of tiny part of kidney with a needle) may be necessary to determine whether a patient has glomerulosclerosis or another kidney problem. About 15 percent of people with proteinuria turn out to have glomerulosclerosis.

Both children and adults can develop glomerulosclerosis and it can result from different types of kidney conditions. One frequently encountered type of glomerulosclerosis is caused by diabetes. Drug use or infections may cause focal segmental glomerulosclerosis (FSGS), a very chronic kidney condition. FSGS may also occur in patients with AIDS but most are of unknown cause.

Early stages of glomerulosclerosis may not produce any symptoms but the most important warning sign is proteinuria, usually discovered in routine medical exams. Losing large amounts of protein may cause swelling in the ankles and accumulation of fluid in the abdomen.

Scarred glomeruli cannot be repaired and many patients with glomerulosclerosis get worse over time until their kidneys fail. This condition is called end-stage renal disease (ESRD) and the patients must begin dialysis treatment or receive a kidney transplant. ESRD may be reached within a year or up to ten or more of diagnosis of glomerulosclerosis but time will vary.

Treatments for glomerulosclerosis depend on what caused the scarring of the glomeruli. This is determined by renal biopsy. Immunosuppressive drugs stop proteinuria in some patients, but once the treatments have ended proteinuria will continue. The drugs may sometimes damage the patient's kidneys even more.

Controlling the patient's blood pressure may control the progression of kidney failure. ACE inhibitors, a type of blood pressure medicine, preserve kidney function in patients with diabetes. ACE inhibitors may also slow down kidney failure for patients without diabetes. Low protein diets may also lighten the work done by kidneys to process waste. Some patients will need to control their cholesterol through diet or both diet and medicine.

AIP often completely resolves with steroid treatment. The failure to differentiate AIP from malignancy may lead to unnecessary pancreatic resection, and the characteristic lymphoplasmacytic infiltrate of AIP has been found in up to 23% of patients undergoing pancreatic resection for suspected malignancy who are ultimately found to have benign disease. In this subset of patients, a trial of steroid therapy may have prevented a Whipple procedure or complete pancreatectomy for a benign disease which responds well to medical therapy. "This benign disease resembles pancreatic carcinoma both clinically and radiographically. The diagnosis of autoimmune pancreatitis is challenging to make. However, accurate and timely diagnosis may preempt the misdiagnosis of cancer and decrease the number of unnecessary pancreatic resections." Autoimmune pancreatitis responds dramatically to corticosteroid treatment.

If relapse occurs after corticosteroid treatment or corticosteroid treatment is not tolerated, immunomodulators may be used. Immunomodulators such as azathioprine, and 6-mercaptopurine have been shown to extend remission of autoimmune pancreatitis after corticosteroid treatment. If corticosteroid and immunomodulator treatments are not sufficient, rituximab may also be used. Rituximab has been shown to induce and maintain remission.

Renal segmental hypoplasia, also Ask-Upmark kidney, is a kidney with a partially developed or atrophic renal cortex.

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