Rud syndrome is a poorly characterized disorder, probably of X-linked recessive inheritance, named after Einar Rud who described 2 patients with the case in 1927 and 1929. It was argued that all reported cases of Rud syndrome are genetically heterogeneous and significantly differ from the original case reports of Rud and that the designation Rud syndrome should be eliminated and that the patients with such diagnosis should be reassigned to other syndromes, such as Refsum disease and Sjögren-Larsson syndrome. Some consider Rud syndrome and Sjögren-Larsson syndrome the same entity and that Rud syndrome does not exist. Presentation
While inclusion criteria for Rud syndrome have varied considerably, the major manifestations include congenital ichthyosis, hypogonadism, small stature, mental retardation, and epilepsy. : 502 : 564  Ocular findings were inconsistently reported and included strabismus, blepharoptosis, blepharospasm, glaucoma, cataract, nystagmus, and retinitis pigmentosa. Other systemic includes metabolic, bony, neurologic, and muscular abnormalities. Diagnosis
Treatment
Eponym
In 1929, the Danish physician Einar Rud described a 22-year-old Danish male had ichthyosis, hypogonadism, short stature, epilepsy, anemia, and polyneuritis. In 1929, he described a 29-year-old female with ichthyosis, hypogonadism, partial gigantism, and diabetes mellitus. References


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Licorice and closely related plants are perennial shrubs, the roots of which are used in medicine as well as making candies and in cooking other desserts because of the sweet taste. Through inhibition of 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), glycyrrhizin allows cortisol to activate mineralocorticoid receptors in the kidney. This severely potentiates mineralocorticoid receptor-mediated renal sodium reabsorbtion, due to much higher circulating concentrations of cortisol compared to aldosterone. This, in turn, expands the extracellular volume, increases total peripheral resistance and increases arterial blood pressure. The condition is termed pseudohyperaldosteronism.Secondary hyperaldosterone can also be caused by a genetic mutation in the kidneys which causes sodium and potassium wasting. These conditions can be referred to syndromes such as Bartter Syndrome and Gitelman Syndrome. Treatment
Treatment includes removing the causative agent (such as licorice), a high-potassium, low-sodium diet (for primary) and high-sodium diet (for secondary), spironolactone and eplerenone, potassium-sparing diuretics that act as aldosterone antagonists, and surgery, depending on the cause. Secondary hyperaldosteronism may also be treated with cox2 inhibitors which cause water retention, sodium retention and potassium retention as well as raising blood pressure. Bartter and Gitleman syndrome tend to cause low blood pressure in significant populations and treatment with blood pressure medications tend to lower the blood pressure even more. Other animals
Cats can be affected by hyperaldosteronism. The most common signs in cats are muscle weakness and loss of eyesight, although only one of these signs may be present.