Urinary incontinence as a consequence of an insufficient urethral closure mechanism (urethral sphincter mechanism incompetence, USMI) or an impaired storing capacity of the urinary bladder is a considerable side effect of castration in the female dog. Different factors such as breed, body weight and time of spaying have an impact on the risk of urinary incontinence. Loss of urine while the patient is recumbent is the most typical symptom which is first observed at a mean time of 2.8 years after castration. Diagnosis is obtained by excluding other causes, whereas a precise patient history is particularly helpful. Therapy is aimed at increasing the closing pressure of the urethra and/or the compliance of the urinary bladder. Usually success can be achieved by medical therapy, thus surgical intervention is normally not required. In addition to urinary incontinence, coat changes can be observed as an undesirable effect of castration in certain dog breeds. To date, the pathophysiology of decreased urethral closing pressure, altered storing function of the urinary bladder and coat changes induced by castration are still not fully understood. Apart from the well-known hypothesis of estrogen deficiency, altered secretion of the hypothalamic and pituitary hormones GnRH, FSH and LH due to castration may have an influence. In addition to a-adrenergic medication, Flavoxate and Estriol, depot formulations of GnRH analogues have been successfully used to treat urinary incontinence. These depot formulations have also been described for the treatment of coat changes due to spaying.