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Background: Calcinosis cutis is an uncommon dermatopathy characterized by the deposition of minerals in the skin, usually involving collagen and elastic fibers in the dermis. Usually, it results from dystrophic calcification and can be generalized or focal. The dermatopathy may be primary or secondary to certain disorders, especially chronic proliferative otitis, foreign body reactions, hyperadrenocorticism (HAC) and less frequently percutaneous penetration of calcium-rich products. The aim of this report is to describe a presentation of calcinosis cutis affecting the skin of the back, internal face of hind limbs and anal region of a 9-years-old bitch. Case: A 9-year-old, non-defined breed, bitch, ovariohysterectomized, weighing 9.45 kg, was attended at the Dermatological Service of companion animals at the Veterinary Hospital of the Federal University of Jataí (UFJ). The animal came in with the complaint of extensive dorsal alopecia, covered by firm lesions, with a 3-month evolution, additionally to polyuria and polydipsia. After physical examination, alopecic areas of great extension were confirmed on the dorsum, on the internal surface of the hind limbs and in the anal region. Also, an exudative and painful lesion located on the back was detected, plus loss of elasticity of the ventral abdomen skin and visible abdominal vessels. The screening tests showed a marked increase in the alanine aminotransferase enzyme (ALT), alkaline phosphatase (ALP) and total cholesterol. The specific urinary density was decreased. On the ultrasound examination, hepatomegaly and an increase in the caudal pole of the left adrenal were detected. Based on these findings, calcinosis cutis secondary to spontaneous hyperadrenocorticism (HAC) was suspected. For confirmation, skin biopsy and low dose dexamethasone suppression test (LDDS) were performed. LDDS test showed no reduction of serum cortisol after 8 h of dexamethasone dose administration and histopathological evaluation revealed multiple foci of calcinosis characterized by the deposition of basophilic material on the pre-existing collagen fibers, plus areas with pyogranulomatous inflammatory reaction and peripheral fibrosis with transepidermal elimination of minerals. Thus, trilostane and intense hydration of skin plaques were applied as treatment. Discussion: The dermatological alterations were compatible with those described in the consulted literature, with remarkable yellow-brown, firm, sandy-looking plaques, located on the back, internal face of hind limbs and anal region, possibly related to HAC later confirmed by LDDS test and biopsy. The management of the underlying disease and possible secondary bacterial infections are the basis of the treatment. Therefore, the patient was treated with trilostane, antibiotic therapy and intensive hydration of the mineralized plaques resulting in a satisfactory involution of the clinical signs. Even though there are reports of calcinosis cutis on the dorsum, in the consulted literature there was no evidence of dorsum large extension lesion due to HAC as in this case report, but secondary to exogenous corticosteroid treatment, systemic blastomycosis and leptospirosis. In this case report, the affected thorax portion was the dorsum, differently from a study that pointed the ventral thorax as the affected portion. Similarly, anus and ventral part of the tail were hardly affected together with secondary inflammation and ulceration. Thus, the existent literature shows areas of calcinosis cutis in dogs in different parts of the body, but neither extensive as in the back of this reported female dog, nor widely affected as in the anal area, additionally to the internal face of hind limbs as already reported in the literature. [ABSTRACT FROM AUTHOR]