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It is caused by abnormal transport of the amino acid cystine from lysosomes of all tissues, resulting in a massive intra-lysosomal cystine accumulation. Via an as yet unknown mechanism, lysosomal cystine appears to amplify apoptosis such that cells die inappropriately, leading to loss of renal epithelial cells, accounting for the renal Fanconi syndrome, and simlar loss in other tissues can account for the short stature, retinopathy, and other features of the disease.
There are three distinct types of cystinosis each with slightly different symptoms: nephropathic cystinosis, intermediate cystinosis, and non-nephropathic or ocular cystinosis. Infants affected by nephropathic cystinosis initially exhibit poor growth and particular kidney problems (sometimes called renal Fanconi syndrome). The kidney problems lead to the loss of important minerals, salts, fluids, and other nutrients. The loss of nutrients not only impairs growth, but may result in soft, bowed bones (hypophosphatemic rickets), especially in the legs. The nutrient imbalances in the body lead to increased urination, thirst, dehydration, and abnormally acidic blood (acidosis). By about age two years, cystine crystals may be present in the cornea. The buildup of these crystals in the eye causes an increased sensitivity to light (photophobia). Untreated children will experience complete kidney failure by about age 10 years. Other signs and symptoms that may occur in untreated patients include muscle deterioration, blindness, inability to swallow, diabetes, and thyroid and nervous system problems.
The signs and symptoms of intermediate cystinosis are the same as nephropathic cystinosis, but they occur at a later age. Intermediate cystinosis typically begins to affect individuals from age 12 years to age 15 years. Malfunctioning kidneys and corneal crystals are the main initial features of this disorder. If intermediate cystinosis is left untreated, complete kidney failure will occur, but usually not until the late teens to mid twenties.
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