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Results for “AMINOACIDURIA, RENAL”

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At least 451 records · Page 25Linked to original sources
PubMed1980

Hyperaminoaciduria in mild phosphate diabetes in adults.

Quantitative urinary amino acid excretion has been studied in 23 adult patients with mild phosphate diabetes (MPD), in 22 adult control patients with various renal disorders and in 15 children, 7--19 years old, with atopic disorders (normal controls). Statistically significant increases in urinary excretion of glutamine (p < 0.01), glycine (p < 0.01) and cystine (p < 0.05) were found in the MPD patients compared to the normal controls. The urinary excretion of glutamine was significantly increased while the increases in cystine and glycine excretions were non-significant when MPD patients were compared to the control patients. In addition to clinical signs and analyses of plasma and urinary phosphate, a quantitative evaluation of urinary amino acids might be a tool in the diagnosis of MPD. The significance of the increased urinary amino acid excretion in MPD is discussed.

Adult↗
PubMed1973

Lowes syndrome.

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Ammonia↗
PubMedDate not supplied

Congenital renal tubular dysfunction associated with maternal sniffing of organic solvents.

Two cases of neonatal renal tubular dysfunction and metabolic acidosis due to maternal sniffing of a product containing toluene are reported. Both mothers had been sniffing regularly throughout their pregnancies. The infants were dysmature and had some dysmorphic features. They had hyperchloraemic acidosis and exhibited amino-aciduria. The metabolic changes were however transient. It is suggested that the sniffing of toluene containing solvents during pregnancy may change membrane permeability in both the proximal as well as distal renal tubules and may also enhance liver enzyme activity in the foetus.

Abnormalities, Drug-Induced↗
PubMed1967

Amino acid transport: evidence for genetic control of two types in human kidney.

A mutation affecting renal transport of proline, hydroxyproline, and glycerine occurs in man. In the presumed homozygote there is still significant residual transport of these compounds; however, this remaining function is saturated at normal concentrations of substrate in the plasma and is not inhibited by L-proline in the expected way. The presumed heterozygote has partial loss of a transport system common to the three substrates, which becomes saturated at high concentrations of substrate and is inhibited by L-proline. Two different types of transport systems are proposed: a common system and systems with lower capacity and greater specificity. The two types of transport appear to be controlled by separate genes.

Absorption↗