A kidney disorder where amino acids are present in the urine [Described 1927. After Guido Fanconi (b.1892), Professor of Paediatrics at the University of Zurich, Switzerland.]
A genetic disease associated with abnormal metabolism of cystine. Characterized by abnormal renal function, glycosuria, phosphaturia, amino aciduria, and bicarbonate wasting.
A rare metabolic disorder that is associated with the loss of a number of minerals or nutrients in the urine, including amino acids, glucose, and phosphate. It can lead to rickets and failure to grow in children. Fanconi syndrome may be inherited or acquired later in life. When Fanconi syndrome is acquired later in life, the kidney damage may be caused by exposure to agents such as cadmium, lead, mercury, and outdated tetracycline medications.
A disorder of the proximal kidney tubules, which may be inherited or acquired and is most common in children. It is characterized by the urinary excretion of large amounts of amino acids, glucose, and phosphates (though blood levels of these substances are normal). Symptoms may include osteomalacia, rickets, muscle weakness, and ‘cystinosis. Treatment is directed to the cause.
Within the domain of renal health, a specific disorder manifests wherein essential substances such as glucose, amino acids, uric acid, phosphate, and bicarbonate, instead of undergoing reabsorption into the bloodstream, are excreted in the urine. This aberration disrupts the normal physiological balance and functioning of the kidneys.
In the realm of medical conditions, there exists a rare disorder that arises as a consequence of either a deficiency in vitamin D or exposure to elevated levels of heavy metals. This condition disrupts the delicate equilibrium of the body and gives rise to distinctive symptoms and complications.
Fanconi’s syndrome is an uncommon kidney disorder, typically presenting in childhood. This condition results in the loss of vital chemicals like amino acids, phosphate, calcium, and potassium through urine. The implications of these losses can lead to failure to thrive, inhibited growth, and bone disorders like rickets.
Potential causes of this condition could be various rare genetic anomalies impacting body chemistry, or adverse reactions to certain medications, including outdated tetracycline.
In cases where an underlying chemical imbalance is identified and rectifiable, the affected child might regain normal growth patterns. Alternatively, undergoing a kidney transplant could also be a potential solution.