Treatment includes spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.

Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.

Where an underlying neoplasm is the cause, treatment of this condition is indicated in order to reduce progression of symptoms. For cases without a known cause, treatment involves suppression of the immune system with corticosteroid treatment, intravenous immunoglobulin, immunosuppressive agents like Rituximab, Cellcept, or Imuran or plasmapheresis.

As of today, no agreed-upon treatment of Dent's disease is known and no therapy has been formally accepted. Most treatment measures are supportive in nature:

- Thiazide diuretics (i.e. hydrochlorothiazide) have been used with success in reducing the calcium output in urine, but they are also known to cause hypokalemia.

- In rats with diabetes insipidus, thiazide diuretics inhibit the NaCl cotransporter in the renal distal convoluted tubule, leading indirectly to less water and solutes being delivered to the distal tubule. The impairment of Na transport in the distal convoluted tubule induces natriuresis and water loss, while increasing the reabsorption of calcium in this segment in a manner unrelated to sodium transport.

- Amiloride also increases distal tubular calcium reabsorption and has been used as a therapy for idiopathic hypercalciuria.

- A combination of 25 mg of chlorthalidone plus 5 mg of amiloride daily led to a substantial reduction in urine calcium in Dent's patients, but urine pH was "significantly higher in patients with Dent’s disease than in those with idiopathic hypercalciuria (P < 0.03), and supersaturation for uric acid was consequently lower (P < 0.03)."

- For patients with osteomalacia, vitamin D or derivatives have been employed, apparently with success.

- Some lab tests on mice with CLC-5-related tubular damage showed a high-citrate diet preserved kidney function and delayed progress of kidney disease.

Idiopathic hypoglycemia is, literally, a medical condition in which the glucose level in the blood (blood glucose) is abnormally low due to an undeterminable cause. This is considered an incomplete and unsatisfactory diagnosis by physicians and is rarely used by endocrinologists, as it implies an unfinished diagnostic evaluation. In general, the more severe the hypoglycemia and the more clearly it is proven, the less likely it is to remain "idiopathic".

"Idiopathic hypoglycemia" can also be a synonym for reactive hypoglycemia or for hypoglycemia that is not diagnosed by a physician and does not fulfill the Whipple triad criteria. A more precise term for that condition is idiopathic postprandial syndrome.

Medications that are sometimes required include estrogen replacement therapy in postmenopausal women and bisphosphonates. Bisphosphonates may improve bone turnover.

Newer medications termed "calcimimetics" used in secondary hyperparathyroidism are now being used in primary hyperparathyroidism. Calcimimetics reduce the amount of parathyroid hormone released by the parathyroid glands. They are recommended in patients in whom surgery is inappropriate.

Treatment is usually surgical removal of the gland(s) containing adenomas, but medication may also be required.

Treatment may involve surgery, which is currently the only recommended intervention. Surgery should include the removal of even small nodules, to prevent the recurrence of the scrotal calcinosis.

In endocrinology, the terms 'primary' and 'secondary' are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, "i.e.", the tumor's location. Hyperaldosteronism can also be caused by plant poisoning, where the patient has been exposed to too much licorice. Licorice is a perennial herb that is used in making candies and in cooking other desserts because of its sweet taste. It contains the chemical glycyrrhizin, which has medicinal uses, but at higher levels it can be toxic. It has the potential for causing problems with sodium and potassium in the body. It also interferes with the enzyme in the kidneys that converts cortisol to cortisone.

Flumazenil is the only GABA receptor antagonist on the market as of Jan 2013, and it is currently manufactured only as an intravenous formulation. It is approved by the FDA for use in anesthesia reversal and benzodiazepine overdose. However, given its pharmacology, researchers consider it to be a promising medication in the treatment of idiopathic hypersomnia. Results of a small, double-blind, randomized, controlled clinical trial were published in November 2012. This research showed that flumazenil provides relief for most patients whose CSF contains the unknown "somnogen" that enhances the function of GABA receptors, making them more susceptible to the sleep-inducing effect of GABA. For one patient, daily administration of flumazenil by sublingual lozenge and topical cream has proven effective for several years. A 2014 case report also showed improvement in idiopathic hypersomnia symptoms after treatment with a continuous subcutaneous flumazenil infusion. The supply of generic flumazenil was initially thought to be too low to meet the potential demand for treatment of idiopathic hypersomnia. However, this scarcity has eased, and dozens of patients are now being treated with flumazenil off-label.

There is some evidence of the existence of a so-called "adrenergic postprandial syndrome": the glycemia is normal, and the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient.

In a test tube model, clarithromycin (an antibiotic approved by the FDA for the treatment of infections) was found to return the function of the GABA system to normal in patients with idiopathic hypersomnia. Investigators therefore treated a few patients with off-label clarithromycin, and most felt their symptoms improved with this treatment. In order to help further determine whether clarithromycin is truly beneficial for the treatment of idiopathic hypersomnia, a small, double-blind, randomized, controlled clinical trial was completed in 2012. "In this pilot study, clarithromycin improved subjective sleepiness in GABA-related hypersomnia. Larger trials of longer duration are warranted." In 2013, a retrospective review evaluating longer-term clarithromycin use showed efficacy in a large percentage of patients with GABA-related hypersomnia. "It is important to note that the positive effect of clarithromycin is secondary to a benzodiazepine antagonist-like effect, not its antibiotic effects, and treatment must be maintained."

Many antiepileptic drugs are used for the management of canine epilepsy. Oral phenobarbital, in particular, and imepitoin are considered to be the most effective antiepileptic drugs and usually used as ‘first line’ treatment. Other anti-epileptics such as zonisamide, primidone, gabapentin, pregabalin, sodium valproate, felbamate and topiramate may also be effective and used in various combinations. A crucial part of the treatment of pets with epilepsy is owner education to ensure compliance and successful management.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

In terms of possible treatment for the condition of idiopathic sclerosing mesenteritis, medications such as corticosteroids, tamoxifen and thalidomide have been used.

Patients with ICOE-G need prophylactic treatment mainly with carbamazepine or other antiepileptic drugs licensed for focal seizures. A slow reduction in the dose of medication 2 or 3 years after the last visual or other minor or major seizure should be advised, but if visual seizures reappear, treatment should be restored.

Drug therapy can slow down progression and in some cases even improve the heart condition. Standard therapy may include salt restriction, ACE inhibitors, diuretics, and beta blockers. Anticoagulants may also be used for antithrombotic therapy. There is some evidence for the benefits of coenzyme Q10 in treating heart failure.

Artificial pacemakers may be used in patients with intraventricular conduction delay, and implantable cardioverter-defibrillators in those at risk of arrhythmia. These forms of treatment have been shown to prevent sudden cardiac death, improve symptoms, and reduce hospitalization in patients with systolic heart failure.

A 2014 meta-analysis of three small trials evaluating probiotics showed a slight improvement in management of chronic idiopathic constipation, but well-designed studies are necessary to know the true efficacy of probiotics in treating this condition.

Children with functional constipation often claim to lack the sensation of the urge to defecate, and may be conditioned to avoid doing so due to a previous painful experience. One retrospective study showed that these children did indeed have the urge to defecate using colonic manometry, and suggested behavioral modification as a treatment for functional constipation.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

To date, there is no known effective treatment for the non-proliferative form of macular telangiectasia type 2.

Treatment options are limited. No treatment has to date been shown to prevent progression. The variable course of progression of the disease makes it difficult to assess the efficacy of treatments. Retinal laser photocoagulation is not helpful. In fact, laser therapy may actually enhance vessel ectasia and promote intraretinal fibrosis in these individuals. It is hoped that a better understanding of the pathogenesis of the disease may lead to better treatments.

The use of vascular endothelial growth factor (VEGF) inhibitors, which have proven so successful in treating age-related macular degeneration, have not proven to be effective in non-proliferative MacTel type 2. Ranibizumab reduces the vascular leak seen on angiography, although microperimetry suggests that neural atrophy may still proceed in treated eyes.In proliferative stages (neovascularisation), treatment with Anti-VEGF can be helpful.

CNTF is believed to have neuroprotective properties and could thus be able to slow down the progression of MacTel type 2. It has been shown to be safe to use in MacTel patients in a phase 1 safety trial.

The most crucial aspect of managing patients with macular telangiectasia is recognition of the clinical signs. This condition is relatively uncommon: hence, many practitioners may not be familiar with or experienced in diagnosing the disorder. MacTel must be part of the differential in any case of idiopathic paramacular hemorrhage, vasculopathy, macular edema or focal pigment hypertrophy, especially in those patients without a history of retinopathy or contributory systemic disease.

Treatment options for macular telangiectasia type 1 include laser photocoagulation, intra-vitreal injections of steroids, or anti-vascular endothelial growth factor (anti-VEGF) agents. Photocoagulation was recommended by Gass and remains to date the mainstay of treatment. It seems to be successful in causing resolution of exudation and VA improvement or stabilization in selected patients. Photocoagulation should be used sparingly to reduce the chance of producing a symptomatic paracentral scotoma and metamorphopsia. Small burns (100–200 μm) of moderate intensity in a grid-pattern and on multiple occasions, if necessary, are recommended. It is unnecessary to destroy every dilated capillary, and, particularly during the initial session of photocoagulation, those on the edge of the capillary-free zone should be avoided.

Intravitreal injections of triamcinolone acetonide (IVTA) which have proved to be beneficial in the treatment of macular edema by their anti-inflammatory effect, their downregulation of VEGF production, and stabilization of the blood retinal barrier were reported anecdotally in the management of macular telangiectasia type 1. In two case reports, IVTA of 4 mg allowed a transitory reduction of retinal edema, with variable or no increase in VA. As expected with all IVTA injections, the edema recurred within 3–6 months, and no permanent improvement could be shown.14,15 In general, the effect of IVTA is short-lived and complications, mainly increased intraocular pressure and cataract, limit its use.

Indocyanine green angiography-guided laser photocoagulation directed at the leaky microaneurysms and vessels combined with sub-Tenon’s capsule injection of triamcinolone acetonide has also been reported in a limited number of patients with macular telangiectasia type 1 with improvement or stabilization of vision after a mean follow-up of 10 months.16 Further studies are needed to assess the efficacy of this treatment modality.

Recently, intravitreal injections of anti-VEGF agents, namely bevacizumab, a humanized monoclonal antibody targeted against pro-angiogenic, circulatory VEGF, and ranibizumab, a FDA-approved monoclonal antibody fragment that targets all VEGF-A isoforms, have shown improved visual outcome and reduced leakage in macular edema form diabetes and retinal venous occlusions. In one reported patient with macular telangiectasia type 1, a single intravitreal bevacizumab injection resulted in a marked increase in VA from 20/50 to 20/20, with significant and sustained decrease in both leakage on FA and cystoid macular edema on OCT up to 12 months. It is likely that patients with macular telangiectasia type 1 with pronounced macular edema from leaky telangiectasis may benefit functionally and morphologically from intravitreal anti-VEGF injections, but this warrants further studies.

Today, laser photocoagulation remains mostly effective, but the optimal treatment of macular telangiectasia type 1 is questioned, and larger series comparing different treatment modalities seem warranted. The rarity of the disease however, makes it difficult to assess in a controlled randomized manner.

However, these treatment modalities should be considered only in cases of marked and rapid vision loss secondary to macular edema or CNV. Otherwise, a conservative approach is recommended, since many of these patients will stabilize without intervention.

Acquired idiopathic generalized anhidrosis (AIGA) is characterized by generalized absence of sweating without other autonomic and neurologic dysfunction.

AIGA is classified into 3 subgroups: idiopathic pure sudomotor failure (IPSF), sweat gland failure (SGF), and sudomotor neuropathy, with each subgroup presenting a different pathogenesis.

Treatment for cerebrovascular disease may include medication, lifestyle changes and/or surgery, depending on the cause.

Examples of medications are:

- antiplatelets (aspirin, clopidogrel)

- blood thinners (heparin, warfarin)

- antihypertensives (ACE inhibitors, beta blockers)

- anti-diabetic medications.

Surgical procedures include:

- endovascular surgery and vascular surgery (for future stroke prevention).

Historically, papilledema was a potential contraindication to lumbar puncture, as it indicates a risk for tentorial herniation and subsequent death via cerebral herniation, however newer imaging techniques have been more useful at determining when and when not to conduct a lumbar puncture. Imaging by CT or MRI is usually performed to elicit whether there is a structural cause i.e., tumor. An MRA and MRV may also be ordered to rule out the possibility of stenosis or thrombosis of the arterial or venous systems.

The treatment depends largely on the underlying cause. However, the root cause of papilledema is the increased intracranial pressure (ICP). This is a dangerous sign, indicative of a brain tumor, CNS inflammation or idiopathic intracranial hypertension (IIH) that may become manifest in the near future.

Thus, a biopsy is routinely performed prior to the treatment in the initial stages of papilledema to detect whether a brain tumor is present. If detected, laser treatment, radiation and surgeries can be used to treat the tumor.

To decrease ICP, medications can be administered by increasing the absorption of Cerebrospinal fluid (CSF), or decreasing its production. Such medicines include diuretics like acetazolamide and furosemide. These diuretics, along with surgical interventions, can also treat IIH. In IIH, weight loss (even a loss of 10-15%) can lead to normalization of ICP.

Meanwhile, steroids can reduce inflammation (if this is a contributing factor to increased ICP), and may help to prevent vision loss. However, steroids have also been known to cause increased ICP, especially with a change in dosage. However, if a severe inflammatory condition exists, such as multiple sclerosis, steroids with anti-inflammatory effects such as Methylprednisolone and prednisone can help.

Other treatments include repeated lumbar punctures to remove excess spinal fluid in the cranium. The removal of potentially causative medicines including tetracyclines and vitamin A analogues may help decrease ICP; however, this is only necessary if the medication is truly felt to contribute to the ICP increase.