A RARE CASE OF URINARY PROTEIN LEAKAGE CAUSED BY RECTAL CANCER WITH BLADDER INVASION

Proteinuria and hypoalbuminemia are typically regarded as hallmarks of glomerular disease and usually prompt renal biopsy in nephrology practice. However, extrarenal protein loss, though rare, must also be considered. Malignancy-related protein leakage is particularly uncommon and may mimic nephrotic syndrome, leading to significant diagnostic challenges. Misdiagnosis as intrinsic renal disease can result in unnecessary therapy or interruption of anticancer treatment. We present a rare case of rectal cancer with bladder invasion causing urinary protein leakage and hypoalbuminemia, which provides important diagnostic insights for the nephrotic syndrome.

A 53-year-old woman with rectal cancer invading the bladder, right ovary, and right ureter, complicated by right hydronephrosis, underwent colostomy and chemotherapy with FOLFOX plus panitumumab. She subsequently required right nephrostomy. Approximately one year later, she developed generalized edema, marked proteinuria, and hypoalbuminemia (serum albumin 1.6 g/dL, urinary protein-to-creatinine ratio 2.05 g/gCr). She was referred to our department with suspected nephrotic syndrome. Although proteinuria did not strictly meet the diagnostic threshold for nephrotic syndrome, renal biopsy was performed after discussion with the patient, as clarifying the cause of edema was essential before continuing anticancer therapy. Renal biopsy showed no significant abnormalities on light microscopy, immunofluorescence, or electron microscopy. Given the presence of two urinary drainage routes, protein levels were compared: nephrostomy urine contained 0.56 g/gCr, while bladder urine contained 11.19 g/gCr. This striking discrepancy suggested that protein was added after urine entered the bladder. To confirm the suspected extrarenal origin, a protein-losing scintigraphy was performed.

Scintigraphy demonstrated tracer accumulation in the descending colon, rectal tumor, and bladder, strongly indicating protein leakage from rectal cancer invading the bladder. In combination with the negative renal biopsy and the supportive findings from route-specific urine analysis, these results established extrarenal protein loss as the cause of hypoalbuminemia and edema. The diagnostic key was protein-losing scintigraphy, while nephrostomy urine comparison provided valuable supportive evidence.

This case highlights several important lessons for nephrology practice. Not all cases of proteinuria and hypoalbuminemia originate from glomerular disease, and extrarenal causes must be considered, particularly in patients with malignancy. Nephrostomy urine analysis proved to be a practical and clinically useful approach to differentiate renal from extrarenal protein loss. Furthermore, a stepwise diagnostic process—beginning with renal biopsy, followed by urine route comparison, and culminating in scintigraphy—was essential to establishing the final diagnosis. By carefully integrating renal and extrarenal perspectives, this case broadened our differential diagnosis in nephrology and emphasized the need for vigilance in complex clinical scenarios, especially those involving oncologic backgrounds.