aminoaciduria


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aminoaciduria

 [ah-me″no-as″ĭ-du´re-ah]
an excess of amino acids in the urine; it may be either the overflow type caused by excessive levels in the blood, or the renal type caused by defective transport mechanisms in the renal tubules. Many types are called by the name of the amino acid plus the suffix -uria, such as cystinuria, lysinuria, and tryptophanuria.

a·mi·no·ac·i·du·ri·a

(ă-mē'nō-as-i-dyū'rē-ă),
Excretion of amino acids in the urine, especially in excessive amounts.
Synonym(s): hyperaminoaciduria
[amino acid + G. ouron, urine]

aminoaciduria

/ami·no·ac·id·u·ria/ (-as″ĭ-du´re-ah) an excess of amino acids in the urine.

aminoaciduria

(ə-mē′nō-ăs′ĭ-do͝or′ē-ə, -dyo͝or′-, ăm′ə-)
n.
A disorder of protein metabolism in which excessive amounts of amino acids are excreted in the urine.

aminoaciduria

[amē′nō·as′idoo͡r′ē·ə]
the abnormal presence of amino acids in the urine that usually indicates an inborn error of metabolism, as in cystinuria. Formerly called acidaminuria.

a·mi·no·ac·i·du·ri·a

(ă-mē'-nō-as'i-dyūr'ē-ă)
Excretion of amino acids in the urine, especially in excessive amounts.
[amino acid + G. ouron, urine]

aminoaciduria

The presence of amino acids in the urine. This occurs in a group of disorders that feature abnormal protein METABOLISM.

Aminoaciduria

A condition confirmed by laboratory tests where high levels of amino acids are found in the urine.

aminoaciduria

an excess in the urine of amino acids. Occurs in fanconi's syndrome, a familial renal disease of Norwegian elkhounds and Basenji dogs, and as a predisposing factor in the development of cystine uroliths.
References in periodicals archive ?
Glucosuria and aminoaciduria were noted to appear abruptly after three weeks of injections, and the complete expression of the Fanconi syndrome (i.
The primary findings associated with chronic cadmium exposures in animals as well as humans were proteinuria, glucosuria, aminoaciduria, and progressive reduction in the glomerular filtration rate which was identified by the significantly increased serum creatinine and beta 2-microglobulin concentrations.
In cases associated with Fanconi syndrome, the most classical presentation includes tubular dysfunction with aminoaciduria, phosphaturia, and glucosuria.
Normalization of serum 25(OH)D and calcium and increase in urinary calcium excretion with disappearance of aminoaciduria are the important biochemical indices of healing osteomalacia.
The manifestations of Cd nephrotoxicity include proteinuria, calciuria, aminoaciduria, glycosuria, and tubular necrosis (IPCS 1992; Jarup et al.