In one study, hypouricemia was found in 4.8% of hospitalized women and 6.5% of hospitalized men. (The definition was less than 0.14 mmol l-1 for women and less than 0.20 mmol l-1 in men.)

Genetic mutations known to cause hypouricemia are of two kinds: mutations causing xanthine oxidase deficiency, which reduces the production of uric acid; and mutations causing abnormal kidney function that increases the excretion of uric acid. Collectively known as familial renal hypouricemia, these latter mutations are of two types, involving defects of "pre"secretory and "post"secretory reabsorption.

A genetic mutation in Dalmatian dogs causes hypouricemia due to a kidney defect that interferes with reabsorption of uric acid. A similar mutation has been reported in a human brother and sister.

In humans, loss-of-function mutations in the gene URAT1 are associated with presecretory reabsorption defects.

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.

In Dalmatian dogs, a lack of uricase (a genetic trait fixed in this breed) contributes to hyperuricemia and corresponding hyperuricosuria.

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.

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.

Interstitial nephritis (or tubulo-interstitial nephritis) is a form of nephritis affecting the interstitium of the kidneys surrounding the tubules, i.e., is inflammation of the spaces between renal tubules. This disease can be either acute, meaning it occurs suddenly, or chronic, meaning it is ongoing and eventually ends in kidney failure.

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.

Haemochromatosis is one of the most common heritable genetic conditions in people of northern European extraction with a prevalence of 1 in 200. The disease has a variable penetration and about 1 in 10 people of this demographic carry a mutation in one of the genes regulating iron metabolism, the most common allele being the C282Y allele in the "HFE" gene. The prevalence of mutations in iron metabolism genes varies in different populations. A study of 3,011 unrelated white Australians found that 14% were heterozygous carriers of an HFE mutation, 0.5% were homozygous for an "HFE" mutation, and only 0.25% of the study population had clinically relevant iron overload. Most patients who are homozygous for HFE mutations will not manifest clinically relevant haemochromatosis (see Genetics above). Other populations have a lower prevalence of both the genetic mutation and the clinical disease.

Genetic studies suggest the original haemochromatosis mutation arose in a single person, possibly of Celtic ethnicity, who lived 60–70 generations ago. At that time when dietary iron may have been scarcer than today, the presence of the mutant allele may have provided an evolutionary or natural selection reproductive advantage by maintaining higher iron levels in the blood.

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.

Incidence of demyelinating diseases vary from disorder to disorder. Some conditions, such as Tabes dorsalis appear predominantly in males and begins in mid-life. Optic neuritis on the other hand, occurs preferentially in females typically between the ages of 30 and 35. Other conditions such as multiple sclerosis vary in prevalence depending on the country and population. This condition can appear in children as well as adults.

Prognosis depends on the condition itself. Some conditions such as multiple sclerosis depend on the subtype of the disease and various attributes of the patient such as age, sex, initial symptoms and the degree of disability the patient experiences. Life expectancy in Multiple sclerosis patients is 5 to 10 years lower than unaffected people. MS is an inflammatory demyelinating disease of the

central nervous system (CNS) that develops in genetically susceptible individuals after exposure to unknown environmental trigger(s). The bases for MS are unknown but are strongly suspected to involve immune reactions against autoantigens, particularly myelin proteins. The most accepted hypothesis is that dialogue between T-cell receptors and myelin antigens leads to an immune attack on the myelin-oligodendrocyte complex. These interactions between active T cells and myelin antigens provoke a massive destructive inflammatory response and promotes continuing proliferation of T and B cells and macrophage activation, which sustains secretion of inflammatory mediators. Other conditions such as central pontine myelinolysis have about a third of patients recover and the other two thirds experience varying degrees of disability. There are cases, such as transverse myelitis where the patient can begin recovery as early as 2 to 12 weeks after the onset 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.

Minor cases of demodectic mange usually do not cause much itching but might cause pustules on the dog's skin, redness, scaling, leathery, hair loss, warm to the touch, or any combination of these. It most commonly appears first on the face, around the eyes, or at the corners of the mouth, and on the forelimbs and paws. May be misdiagnosed as a "hot spot" or other skin ailment.

In the more severe form, hair loss can occur in patches all over the body and might be accompanied by crusting, pain, enlarged lymph nodes, and deep skin infections.

Demodectic mange is transmitted from host to host through direct contact. Typically animals become infected through nursing from their mother. Demodex mites are host-adapted; there is no zoonotic potential in either canine or feline demodicosis. These mites ("Demodex canis") thrive only on their specific hosts (dogs). The transmission of these mites from mother to pup is normal (which is why the mites are normal inhabitants of the dog's skin), but some individuals are sensitive to the mites due to a cellular immune deficiency, underlying disease, stress, or malnutrition, which can lead to the development of clinical demodectic mange.

Some breeds appear to have an increased risk of mild cases as young dogs, including the Afghan Hound, American Staffordshire Terrier, Boston Terrier, Boxer, Chihuahua, Chow Chow, Shar Pei, Collie, Dalmatian, Doberman Pinscher, Bulldog, French Bulldog, English Bull Terrier, Miniature Bull Terrier, German Shepherd Dog, Great Dane, Old English Sheepdog, American Pit Bull Terrier, West Highland White Terrier, Rat Terrier, Yorkshire Terrier, dachshund and Pug.