Why do some patients with cirrhosis show spontaneous improvement in features of portal hypertension? The answer is the development of increasing numbers of collateral channels that decompress the portal system and lower portal pressures. Common sites for these collaterals include the gastric cardia, rectum, retroperitoneum and umbilicus. Less commonly, collaterals may involve the left renal vein and, if large, can function as significant portosystemic shunts. Two patients with spontaneous splenorenal shunts are illustrated below. The patient whose image is shown in Fig. 1 was a woman, aged 31 years, who was diagnosed with autoimmune hepatitis at the age of 4 years. She had been taking prednisolone, 5 mg per day, for at least 10 years. On examination, she had a large spleen. Blood tests revealed a low white cell count and platelet count, abnormal coagulation studies and a low plasma albumin (19 g/L). Upper gastrointestinal endoscopy was normal. An abdominal ultrasound study showed splenomegaly and numerous dilated vessels in the splenic hilum but no ascites. She had antegrade portal blood flow (velocity 2.3 cm/s) and a hepatic venous pressure gradient of 8 mmHg. Selective catheterization of the superior mesenteric artery showed the mesenteric vein, a small portal vein, back flow to the splenic vein (black arrow) and a large shunt between the splenic and left renal vein (red arrow). The patient illustrated in Fig. 2 was a male, aged 31, who had portal hypertension because of portal vein thrombosis associated with factor V Leiden mutation. Over a period of 5 years, esophageal varices were treated by endoscopic ligation on several occasions. Subsequently, however, varices appeared to regress spontaneously. Abdominal gray-scale and color-Doppler sonography showed a large splenorenal shunt and this was confirmed by magnetic resonance imaging (arrows). Spontaneous splenorenal shunts appear to be uncommon in adults but may be more common when portal hypertension occurs in children.