Although normally benign, idiopathic renal hypouricemia may increase the risk of exercise-induced acute renal failure.

Hypouricemia is common in vegetarians due to the low purine content of most vegetarian diets. Vegetarian diet has been found to result in mean serum uric acid values as low as 239 µmol/L (2.7 mg/dL). While a vegetarian diet is typically seen as beneficial with respect to conditions such as gout, care should be taken to avoid associated health conditions.

Transient hypouricemia sometimes is produced by total parenteral nutrition. Paradoxically, total parenteral nutrition may produce hypouricemia followed shortly by acute gout, a condition normally associated with hyperuricemia. The reasons for this are unclear.

Increased levels predispose for gout and, if very high, kidney failure. The metabolic syndrome often presents with hyperuricemia. Prognosis is good with regular consumption of Allopurinol.

People with gout, and by inference hyperuricemia, are significantly less likely to develop Parkinson's disease, unless they also require diuretics.

Low temperature is a commonly reported trigger of acute gout: an example would be a day spent standing in cold water, followed by an attack of gout the next morning. This is believed to be due to temperature-dependent precipitation of uric acid crystals in tissues at below normal temperature. Thus, one aim of prevention is to keep the hands and feet warm, and soaking in hot water may be therapeutic.

Treatment consists of addressing the cause, such as by removing an offending drug. There is no clear evidence that corticosteroids help.

Nutrition therapy consists of adequate fluid intake, which can require several liters of extra fluid.

The kidneys are the only body system that are directly affected by tubulointerstitial nephritis. Kidney function is usually reduced; the kidneys can be just slightly dysfunctional, or fail completely.

In chronic tubulointerstitial nephritis, the most serious long-term effect is kidney failure. When the proximal tubule is injured, sodium, potassium, bicarbonate, uric acid, and phosphate reabsorption may be reduced or changed, resulting in low bicarbonate, known as metabolic acidosis, low potassium, low uric acid known as hypouricemia, and low phosphate known as hypophosphatemia. Damage to the distal tubule may cause loss of urine-concentrating ability and polyuria.

In most cases of acute tubulointerstitial nephritis, the function of the kidneys will return after the harmful drug is not taken anymore, or when the underlying disease is cured by treatment. If the illness is caused by an allergic reaction, a corticosteroid may speed the recovery kidney function; however, this is often not the case.

Chronic tubulointerstitial nephritis has no cure. Some patients may require dialysis. Eventually, a kidney transplant may be needed.

Studies indicate that persons with symptomatic haemochromatosis have somewhat reduced life expectancy compared to the general population. This is mainly due to excess mortality from cirrhosis and liver cancer. Patients who were treated with phlebotomy lived longer than those who weren't. Patients without liver disease or diabetes had similar survival rate to the general population.

Where venesection is not possible, long-term administration of desferrioxamine mesylate is useful. Desferrioxamine is an iron-chelating compound, and excretion induced by desferrioxamine is enhanced by administration of Vitamin C. It cannot be used during pregnancy or breast-feeding due to risk of defects in the child.

MDM is most common on the Dalmatian island of Mljet (or "Meleda"), thought to be because of a founder effect. It is of autosomal recessive inheritance. It may be caused by a mutation on the "SLURP1" gene, located on chromosome 8.

Meleda disease (MDM) or "mal de Meleda", also called Mljet disease, keratosis palmoplantaris and transgradiens of Siemens, (also known as "Acral keratoderma," "Mutilating palmoplantar keratoderma of the Gamborg-Nielsen type," "Palmoplantar ectodermal dysplasia type VIII", and "Palmoplantar keratoderma of the Norrbotten type") is an extremely rare autosomal recessive congenital skin disorder in which dry, thick patches of skin develop on the soles of the hands and feet, a condition known as palmoplantar hyperkeratosis.

Experimentation has shown that manipulating the levels of thyroid hormone can be considered as a strategy to promote remyelination and prevent irreversible damage in Multiple sclerosis patients. N-cadherin agonists have been identified and observed to stimulate neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease. It has been shown that intranasal administration of aTf (apotransferrin) can protect myelin and induce remyelination.

Much of the research referenced in this section has been conducted in 2012 and represents very new information about demyelinating diseases and potential therapies for them.

Treatment typically involves improving the patient's quality of life. This is accomplished through the management of symptoms or slowing the rate of demyelination. Treatment can include medication, lifestyle changes (i.e. quit smoking, adjusting daily schedules to include rest periods and dietary changes), counselling, relaxation, physical exercise, patient education and, in some cases, deep brain thalamic stimulation (in the case of tremors). The progressive phase of MS appears driven by the innate immune system, which will directly contribute to the neurodegenerative changes that occur in progressive MS. Until now, there are no therapies that specifically target innate immune cells in MS. As the role of innate immunity in MS becomes better defined, it may be possible to better treat MS by targeting the innate immune system.

Treatments are patient-specific and depend on the symptoms that present with the disorder, as well as the progression of the condition.

For demodectic mange, properly performed deep skin scrapings generally allow the veterinarian to identify the microscopic mites. Acetate tape impression with squeezing has recently found to be a more sensitive method to identify mites. It was originally thought that because the mite is a normal inhabitant of the dog's skin, the presence of the mites does not conclusively mean the dog suffers from demodex. Recent research, however, found that demodex mite can hardly be found on clinically normal dogs, meaning that the presence of any number of mites in a sample is very likely to be significant. In breeds such as the West Highland White Terrier, relatively minor skin irritation which would otherwise be considered allergy should be carefully scraped because of the predilection of these dogs to demodectic mange. Skin scrapings may be used to follow the progress of treatment in demodectic mange.

Alternatively, plasma levels of zinc and copper have been seen to be decreased in dogs suffering with demodicosis. This may be due to inflammation involved in the immune response of demodicosis which can lead to oxidative stress resulting in dogs suffering from demodicosis to exhibit higher levels of antioxidant productivity. The catalases involved in the antioxidant pathway require the trace minerals zinc and copper. Dogs with demodicosis show a decrease in plasma copper and zinc levels due to the increased demand for antioxidant activity. Therefore, this may be considered as a potential marker for demodicosis.

Localized demodectic mange is considered a common puppyhood ailment, with roughly 90% of cases resolving on their own with no treatment. Minor, localized cases should be left to resolve on their own to prevent masking of the more severe generalized form. If treatment is deemed necessary Goodwinol, a rotenone-based insecticide ointment is often prescribed, but it can be irritating to the skin. Demodectic mange with secondary infection is treated with antibiotics and medicated shampoos.

In more severe generalized cases, Amitraz is a parasiticidal dip that is licensed for use in many countries (the only FDA approved treatment in the USA) for treating canine demodicosis. It is applied weekly or biweekly, for several weeks, until no mites can be detected by skin scrapings. Demodectic mange in dogs can also be managed with avermectins, although there are few countries which license these drugs, which are given by mouth, daily, for this use. Ivermectin is used most frequently; collie-like herding breeds often do not tolerate this drug due to a defect in the blood–brain barrier, though not all of them have this defect. Other avermectin drugs that can be used include doramectin and milbemycin.

Recent results suggest that the isoxazolines afoxolaner and fluralaner, given orally, are effective in treating dogs with generalised demodicosis.

Cats with "Demodex gatoi" must be treated with weekly or bi-weekly sulfurated lime rinses. "Demodex cati" are treated similarly to canine demodicosis. With veterinary guidance, localized demodectic mange can also be treated with a topical keratolytic and antibacterial agent, followed by a lime sulfur drip or a local application of Rotenone. Ivermectin may also be used. Generalized demodectic mange in cats is more difficult to treat. There are shampoos available that can help to clear dead skin, kill mites and treat bacterial infections. Treatment is in most cases prolonged with multiple applications.

Because of the possibility of the immune deficiency being an inherited trait, many veterinarians believe that all puppies with generalized demodex should be spayed or neutered and not reproduce. Females with generalized demodex should be spayed because the stress of the estrus cycle will often bring on a fresh wave of clinical signs.