Signs and Symptoms
Toddlers diarrhea is characterized by three or more watery stools per day that persist for 2–4 weeks or more. Newborns and infants may normally have soft and frequent stools; however, any noticeable changes in stool frequency or form (i.e. watery) can indicate toddlers diarrhea. Other symptoms may include chills, fever, abdominal pain or cramping, nausea, and/or vomiting. Undigested food and/or mucus may also be observed in stools. More serious symptoms may include bloody stools, weight loss, greasy stools, and/or severe abdominal pain.Aside from these signs and symptoms, infants and children present as healthy individuals with appropriate weight gain (considering sufficient calorie intake), active lifestyles, and normal appetites. Complications
Possible complications associated with toddlers diarrhea include malabsorption and dehydration.Malabsorption affects the small intestine and results in the impaired absorption of important nutrients from an infant or childs diet, leading to malnutrition. Malabsorption is indicated by symptoms of bloating, appetite changes, weight loss, and/or gas.Dehydration occurs when there is not enough fluid intake to compensate for increased loss of fluid and electrolytes that may result from chronic diarrhea. Dehydration is indicated by symptoms of thirst, absence of tears when crying, infrequent urination, dry mouth, and/or decreased energy. Cause
Diarrhea happens when the amount of fluids absorbed in the intestine does not match the amount secreted. The imbalance can be achieved in two ways: an excess of secretion or a lack of absorption. Thus, diarrhea can be categorized into secretory diarrhea, an excess of secretion, or osmotic diarrhea which is a lack of absorption.
The impairment of Na transport in the distal convoluted tubule induces natriuresis and water loss, while increasing the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Amiloride also increases distal tubular calcium reabsorption and has been used as a therapy for idiopathic hypercalciuria. A combination of 25 mg of chlorthalidone plus 5 mg of amiloride daily led to a substantial reduction in urine calcium in Dents patients, but urine pH was "significantly higher in patients with Dent’s disease than in those with idiopathic hypercalciuria (P < 0.03), and supersaturation for uric acid was consequently lower (P < 0.03)." For patients with osteomalacia, vitamin D or derivatives have been employed, apparently with success. Some lab tests on mice with CLC-5-related tubular damage showed a high-citrate diet preserved kidney function and delayed progress of kidney disease. History
Dents disease was first described by Charles Enrique Dent and M. Friedman in 1964, when they reported two unrelated British boys with rickets associated with renal tubular damage characterized by hypercalciuria, hyperphosphaturia, proteinuria, and aminoaciduria. This set of symptoms was not given a name until 30 years later, when the nephrologist Oliver Wrong more fully described the disease. Wrong had studied with Dent and chose to name the disease after his mentor. Dents disease is a genetic disorder caused by mutations in the gene CLCN5, which encodes a kidney-specific voltage-gated chloride channel, a 746-amino-acid protein (CLC-5) with 12 to 13 transmembrane domains. It manifests itself through low-molecular-weight proteinuria, hypercalciuria, aminoaciduria and hypophosphataemia.