The treatment was approved in the DRC in December 2018. Funding
For current funding statistics, human African trypanosomiasis is grouped with kinetoplastid infections. Kinetoplastids refer to a group of flagellate protozoa. Kinetoplastid infections include African sleeping sickness, Chagas disease, and Leishmaniasis. All together, these three diseases accounted for 4.4 million disability adjusted life years (DALYs) and an additional 70,075 recorded deaths yearly. For kinetoplastid infections, the total global research and development funding was approximately $136.3 million in 2012. Each of the three diseases, African sleeping sickness, Chagas disease, and Leishmaniasis each received approximately a third of the funding, which was about $36.8 million US dollars, $38.7 million US dollars, and $31.7 million US dollars, respectively.For sleeping sickness, funding was split into basic research, drug discovery, vaccines, and diagnostics. The greatest amount of funding was directed towards basic research of the disease; approximately $21.6 million US dollars was directed towards that effort. As for therapeutic development, approximately $10.9 million was invested.The top funder for kinetoplastid infection research and development are public sources. About 62% of the funding comes from high-income countries while 9% comes from low- and middle-income countries. High-income countries public funding is the largest contributor to the neglected disease research effort. However, in recent years, funding from high-income countries has been steadily decreasing; in 2007, high-income countries provided 67.5% of the total funding whereas, in 2012, high-income countries public funds only provided 60% of the total funding for kinetoplastid infections.
Nephrogenic diabetes insipidus, also known as renal diabetes insipidus, is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (also called vasopressin). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to antidiuretic hormone, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms
The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with polydipsia (excessive thirst) and polyuria (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension. On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, antidiuretic hormone levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms. Causes
Acquired
Nephrogenic diabetes insipidus is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis, polycystic kidney disease, electrolyte imbalance, or some other kidney defect.The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium.