In comparison, the ENaC inhibitor triamterene is metabolized by the liver. Excretion
About 50% of amiloride is excreted unchanged by the kidneys, while around 40% is excreted in the feces (likely drug that wasnt absorbed). The half-life of amiloride in humans is between 6 and 9 hours, which may be prolonged in people with poor kidney function. Pharmacogenomics
A single nucleotide polymorphism (SNP) in the protein NEDD4L may impact how amiloride affects a persons blood pressure in people with high blood pressure. Chemistry
Amiloride is a pyrazinoylguanidine, composed of a substituted pyrazine ring structure with a carbonylguanidinium substituent. Amilorides pKa is 8.67, which is due to the guanidinium group. In high pH (alkaline, low hydrogen concentration) environments, the guanidinium group is deprotonated and the compound is rendered neutral, depleting its activity on sodium channels. Amiloride, as a pure substance, is highly fluorescent, with excitation wavelengths at 215, 288, and 360 nm, emitting light at 420 nm. History
Amiloride was first synthesized and discovered by the Merck Sharp and Dohme Research Laboratories in the late 1960s. The drug was discovered as part of a screening process of chemicals that reversed the effects of mineralocorticoids in vivo. Amiloride was the only drug in the screen that was capable of causing the excretion of sodium (natriuresis) without a concomitant urinary excretion of potassium (kaliuresis). Thousands of amiloride analogues have been studied since its initial discovery, which have been used to study the effects of sodium transporters.Amiloride was approved by the U.S. Food and Drug Administration (FDA) on October 5, 1981.
Because triphalangeal thumbs cannot easily oppose and do not possess many of the optimal qualities found in most opposable thumbs, they tend to cause the hand to be less effective in use and, therefore, prove to be more problematic in daily life. Cause
Malformations of the upper extremities can occur in the third to seventh embryonic week. In some cases the TPT is hereditary. In these cases, there is a mutation on chromosome 7q36. If the TPT is hereditary, it is mostly inherited as an autosomal dominant trait, non-opposable and bilateral. The sporadic cases are mostly opposable and unilateral. Syndromes
Triphalangeal thumb can occur in syndromes but it can also be isolated. The triphalangeal thumb can appear in combination with other malformations or syndromes.Syndromes include:

Holt-Oram syndrome
Aase syndrome
Diamond-Blackfan anemia
Townes-Brocks syndromeMalformations include:
Radial polydactyly
Syndactyly
Claw-like hand or foot

Diagnosis
Classifications
There are multiple classifications for the triphalangeal thumb. The reason for these different classifications is the heterogeneity in appearance of the TPT. The classification according to Wood  describes the shape of the extra phalanx: delta (Fig. 4), rectangular or full phalanx (Table 1). With the classification made by Buck-Gramcko a surgical treatment can be chosen (Table 1). Buck-Gramcko differentiates between six different shapes of the extra phalanx and associated malformations.Table 1: Classifications of Wood  and Buck-Gramcko

Treatment
The goals of surgical treatment are: reducing length of the thumb, creating a good functioning, a stable and non-deviated joint and improving the position of the thumb if necessary. Hereby improving function of the hand and thumb.