Hence, patients with a history of Fuchs dystrophy may be at a greater risk of corneal edema after ocular surgery as they have fewer functioning endothelial cells.FECD is classified into 4 stages, from early signs of guttae formation to end-stage subepithelial scarring. Diagnosis is made by biomicroscopic examination in the clinic. Other modalities, such as corneal thickness measurement (pachymetry), in-vivo confocal biomicroscopy, and specular microscopy can be used in conjunction.The exact pathogenesis is unknown but factors include endothelial cell apoptosis, sex hormones, inflammation, and aqueous humor flow and composition. Mutations in collagen VIII, a major component of Descemets membrane secreted by endothelial cells, have been linked to the early-onset FECD.As a genetically heterogeneous disease, the phenotype, or clinical experience of patients with Fuchs dystrophy may reflect the combination of genetic contributors to the disease. Some genetic lesions correlate with more severe disease and earlier onset. Therefore, some individuals may experience symptoms of the disease at a much earlier age, while others may not experience symptoms until late in life.Genes include:

Diagnosis
The diagnosis of Fuchs dystrophy is often made with slit lamp biomicroscopy. With direct illumination, the clinician can visualize guttae, the characteristic pathological changes in disease.Scheimpflug imaging, anterior segment optical coherence tomography, confocal microscopy, and specular microscopy are additional imaging techniques that can identify the presence of guttae and quantify the thickness of the cornea.
Frasier syndrome is a urogenital anomaly associated with the WT1 (Wilms tumor 1 gene) gene.It was first characterized in 1964. Presentation
Both males and females can have Frasier syndrome but their presentations can be different. Affected females usually have normal genitalia and gonads and have only the features of impaired renal function, which may not present until early childhood or even adolescence. Because females do not have all the features of the condition (e.g. gonadal dysgenesis), females are usually given the diagnosis of isolated nephrotic syndrome Medline ref. Frasier syndrome in some infants may therefore go unrecognized until the affected child presents with signs of renal impairment and further testing is undertaken to evaluate the cause. In infants with XY genotype it causes an intersex condition as a result of gonadal dysgenesis. Although males with Frasier syndrome have the typical male chromosome pattern (46,XY), they have gonadal dysgenesis, in which external genitalia may not look clearly male or clearly female (ambiguous genitalia) or the genitalia appear completely female. The internal reproductive organs (gonads) are typically undeveloped and referred to as streak gonads.Source These abnormal gonads are nonfunctional and often become cancerous, so they are usually removed surgically early in life. Renal features of the condition include progressive glomerulonephropathy (focal segmental glomerulosclerosis). Patients are also at increased risk of genito-urinary tumors (usually gonadoblastoma).The glomerulonephropathy presents later than in Denys-Drash syndrome, and the tumour risk phenotype is different; whilst Denys-Drash syndrome is associated with Wilms tumour, Frasier syndrome is associated with gonadoblastoma.