Hydatid disease is a worldwide zoonosis produced by the larval stage of the echinococcus tapeworm; the two main types involved are e. granulosus and e. multilocularis. ^[1]

Dogs or other carnivores are definitive hosts, whereas sheep or other ruminants are intermediate hosts ^[2]. The adult worm lives in the proximal small bowel of the definitive host and is attached by hooklets to the mucosa. Eggs are released into the host’s intestine and excreted in the feces. Humans may become intermediate hosts through contact with a definitive host or ingestion of contaminated water or vegetables. The ovum loses its protective layer as it is digested in the duodenum. Once the parasitic embryo passes through the intestinal wall to reach the portal venous system or lymphatic system, the liver acts as the first line of defense and is therefore the most frequently involved organ (approximately 75% of cases). Kidney involvement is extremely rare (2%–3% of cases), even in areas where hydatid disease is endemic.

Renal hydatid cysts usually remain asymptomatic for many years; but they may present with a flank mass, renal colic, persistent fever, hematuria, dysuria, pyuria, renal stones, or hypertension-symptoms that are by no means specific to reliably establish the diagnosis. There are no pathognomonic clinical signs except when the cyst ruptures into the collecting system, which leads to acute renal colic and hydatiduria ^{[3, 4].} Our patient presented with only flank pain.

Ultrasound findings depend on the stage of cyst growth and are described as of four types based on their appearance.
Type I (simple cyst with no internal architecture): appears as a well-defined anechoic mass with or without hydatid sand and septa.
Type II (cyst with daughter cyst(s) and matrix): daughter cysts are seen inside the mother cyst. Floating membranes or vesicles can also be seen in the cyst. Sometimes multiple cysts and echogenic areas that are enclosed together within a single capsule give rise to a “racemose” or “wheel spoke” appearance. Consolidation of the daughter cysts may produce echogenic solid lesions.
Type III (calcified cyst): these are dead cysts with total calcification, which produce strong posterior shadowing.
Type IV (complicated hydatid cyst): these include rupture and superinfection of the cyst and may be seen in both Type I and Type II hydatid cysts. 

Rupture occurs in 50%–90% of cases. Cyst rupture is mainly due to the degeneration of parasitic membranes as a result of age, chemical reactions, or a host defense mechanism. Hydatid cyst rupture may be contained, communicating, or direct. In contained rupture, undulating membrane resulting from separation of the endocyst from the pericyst is seen by ultrasound and shows changes with movement. A “snowstorm” pattern has been described on ultrasound. The infected hydatid cyst may exhibit mixed echogenicity. Communicating rupture appears more echogenic than contained rupture by ultrasound.
Bacterial superinfection of hydatid cyst is always secondary to rupture. Up to 25% of ruptured cysts may become infected. Numerous signs of cyst infection have been described, including poor delineation, mixed internal echoes, and air-fluid or fluid-fluid levels. However, these signs can also be seen in both intact hydatid cyst and in ruptured, uninfected hydatid cyst. The presence of air within the cyst establishes the diagnosis of a direct or communicating rupture but does not necessarily imply infection ^[2,3]. 

Surgery is the treatment of choice in renal hydatid cyst. Kidney-sparing surgery (cystectomy with pericystectomy) is possible in most cases (75%). Nephrectomy (25% of cases) must be reserved for destroyed kidneys.