Abnormal Renal Development
David A. Hatch, M.D.

Abnormalities of Renal Induction


If two ureteric buds arise from the mesonephric (Wolfian) duct, or if a single bud divides into two branches before it invades into the metanephrogenic blastema, a duplication occurs. Complete duplication results when two entirely separate ureters drain separate parts of the kidney. Partial duplication occurs when the two ureters join before reaching the bladder.

See more about duplication.


When the ureteric bud does not meet the nephrogenic blastema, normal nephrogenesis does not occur. If the bud originates from the mesonephric duct either caudal to or cranial to the normal position, dysplasia may occur. When the ureteric bud arises from an abnormal position on the mesonephric duct, the drainage of the resulting ureter may also be abnormal (reflux or ureteric ectopy). This may explain why some kidneys with reflux or ectopic ureters have diminished function and capacity.

Multicystic Kidney

Early in development, the ureter goes through a period during which it has no lumen (six weeks). As the metanephros is induced to develop functioning glomeruli and tubules the ureter opens to become a conduit. Occasionally, this canalization fails to occur resulting in complete obstruction of the developing metanephros. Functioning nephrons fill with fluid and become cystic because there is no outlet for the fetal urine. This collection of cysts of varying sizes in the renal fossa, called a multicystic kidney has no function at birth.

Abnormalities of Ascent and Rotation

If the kidney fails to ascend, it remains unrotated (pelvic kidney, also called an ectopic kidney or a pancake kidney because of its flattened shape). Such kidneys often maintain their fetal blood supply from the iliac vessels or the distal aorta. See a picture of a pelvic kidney.

If the two developing kidneys make contact in their ascent, fusion may occur, resulting in a horseshoe kidney. This most often occurs with the lower poles of each kidney fusing. The bridge of parenchyma by which they are fused is called the isthmus. When the isthmus of a horseshoe kidney reaches the inferior mesenteric artery the kidneys can rise no further. Like pelvic kidneys, horseshoe kidneys have multiple renal arteries and veins. Horseshoe kidneys are at increased risk for development of hydronephrosis, kidney stones and renal cell carcinoma.

Occasionally, fusion of the two developing kidneys may occur with one kidney moving to the opposite side, following ascent of the other kidney. This condition is called crossed fused ectopia. See a picture of crossed fused ectopia.

Abnormalities of Renal Vasculature

As the kidney ascends, new blood vessels arise from the iliac artery, the distal aorta and, finally, the upper abdominal aorta. Occasionally, caudal branches of the kidney persist as the kidney ascends. Accessory renal arteries may arise from the aorta adjacent to the main renal artery, distal to the ostium of the main renal artery, or even from the iliac artery. When multiple arteries occur, each artery supplies a distinct segment of the kidney; there is no collateral perfusion. Occlusion of one artery will result in infarction of its associated segment. Why is this important? See pictures.

Multiple renal veins may drain to the vena cava. Unlike the arteries, however, the renal veins interconnect within the kidney. If one renal vein is occluded, the remaining renal vein(s) will continue to drain the entire kidney.


During development, the ureteropelvic junction (the point at which the ureter and renal pelvis meet) may be narrow or kinked or it may have abnormal peristalsis so that urine flow is obstructed. This results in a pooling of fetal urine within the pelvis. Hydronephrosis [literally, water within the kidney] is the term used to describe this enlargement. Hydronephrosis is usually caused by a ureteropelvic junction obstruction although it can result from abnormalities of the ureter or bladder. Why is hydronephrosis important?

Return to Normal Renal Development.

Return to G/U Development Home Page.

©David A. Hatch, M.D., 1996