Wearing of broad protective glasses with side shields is recommended for people at risk for such injuries. Treatment
A presumptive diagnosis of fungal keratitis requires immediate empirical therapy. Natamycin ophthalmic suspension is the drug of choice for filamentous fungal infection. Fluconazole ophthalmic solution is recommended for Candida infection of the cornea. Amphotericin B eye drops may be required for non-responding cases, but can be quite toxic and requires expert pharmacist for preparation. Other medications have also been tried with moderate success. An updated Cochrane Review published in 2015 looking at the best treatment for fungal keratitis could not draw any conclusions as the studies included used different medications. The review did find that "people receiving natamycin were less likely to  develop a hole in their cornea and need a transplant." Prognosis
The infection typically takes a long time to heal, since the fungus itself is slow growing. Corneal perforation can occur in patients with untreated or partially treated infectious keratitis and requires surgical intervention in the form of corneal transplantation. Epidemiology
This disease is quite common in the tropics and with large agrarian population. India has a high number of cases with fungal keratitis, but poor reporting system prevents accurate data collection. Florida in US regularly reports cases of fungal keratitis, with Aspergillus and Fusarium spp. as the most common causes. According to the Global Action Fund for Fungal Infections, every year there are around 1 million cases of blindness due to fungal keratitis.
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.