Radical cystectomy with urinary diversion including neobladder remains the standard of care for muscle-invasive bladder cancer. There has been a slow shift over the past 15 years toward a more inclusive use of bowel based neobladder reconstruction to the native urethra.  Modern forms of urinary diversion are being widely employed, necessitating an awareness by both the urologist and nephrologist of possible long term complications and appropriate follow-up to monitor oncologic, functional, and metabolic outcomes. In a large contemporary series of urinary diversion, 12.8% of patient’s experienced metabolic complications at a median of 1.9 years (range 0.1 to 25.9) following urinary diversion.1

A case study

A 65-year-old male with coronary artery disease, hypercholesterolemia, hypertension, morbid obesity (BMI 49 kg/m2), and CKD stage 2 (eGFR 70 mL/min/1.73m2) underwent radical cystoprostatectomy and creation of an ileal neobladder (Studer) for pT3aN0 (0/48)M0 7cm high grade urothelial carcinoma of the bladder.  The patient remains cancer-free at 8-years of follow-up, but developed progressive CKD 3 (eGFR 32 mL/min/1.73m2) with chronic metabolic acidosis (serum HCO3 15 mg/dl) requiring alkalinization with sodium bicarbonate.  The patient maintains close follow-up with nephrology with normalization of HCO3 (22-25 mg/dl), and receives prophylactic vitamin B12 supplementation.

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Malabsorption of calcium and fat soluble vitamins A, D, E, and K following ileal resection and incorporation of bowel segments into the urinary tract can result in hyperchloremic metabolic acidosis (Table 1). When defined as a serum bicarbonate level less than 20 mg/dl or requiring treatment with an alkalinizing agent, metabolic acidosis was present in 10.2% of patients following diversion.1

The incidence of hyperchloremic acidosis is higher in continent diversions and is most frequently encountered in diversions constructed from the sigmoid colon.  Compensatory hyperventilation may effectively counter acidosis and prevent serum electrolyte abnormalities acutely, but chronic metabolic acidosis has been shown to stimulate osteoclastic bone resorption, inhibit osteoblastic collagen synthesis, and result in hypophosphatemia due to renal phosphate wasting,2 the combined effects of which can induce metabolic bone disease with features of both osteoporosis and osteomalacia.3

Patients with pre-existing CKD or those that subsequently develop it as in this case are particularly prone to acidosis induced bone demineralization due to loss of phosphate buffer from bone and impaired activated vitamin D production secondary to tubular cell damage.4 Irrespective of its cause, even mild degrees of acidosis could be sufficient to cause appreciable bone loss over time.3 Prophylactic administration of alkalinizing agents such as potassium or sodium citrate should be readily performed.  With early correction of base excess following urinary diversion, a majority of patients demonstrate normal bone mineral density at long interval follow-up (30 years).5

Malabsorption of bile acid strongly correlates with the length of ileum resected, and urologists should strive to use the shortest feasible segment of ileum .  Vitamin B12 is exclusively absorbed in the distal ileum, and serum levels may not deplete for 5 years.  In patients with normal vitamin B12 levels at the time of cystectomy, 3.0% of patients developed deficient B12 levels at a median of 9.1 years (range 0.4 to 25.8) following ileal conduit diversion.1  Vitamin B12 levels should be checked annually and routinely  supplementedfollowing urinary diversion.3  The late occurrence of vitamin B12 deficiency underscores the need for vigorous long-term physiologic monitoring following urinary diversion. 

Long term management of bladder cancer patients with urinary diversions requires attention not only to the oncologic implications of their care but also to the potential metabolic consequences.


  1. Shimko MS, Tollefson MK, Embreit EC, et alLong-term complications of conduit urinary diversion.  J Urol 2011;185:562-567.
  2. Roosen A, Gerharz EW, Roth S, et al.  Bladder, bowel and bones—skeletal changes after intestinal urinary diversion.  World J Urol  2004;22:200-209.   
  3. Cody JD, Nabi G, Dublin N, et alUrinary diversion and bladder reconstruction/replacement using intestinal segments for intractable incontinence or following cystectomy.  Cochrane Database Syst Rev 2012;2:CD003306. 
  4. Fichtner J.  Follow-up after urinary diversion.  Urol Int  1999;63:40-45. 
  5. Stein R, Fisch M, Andreas J, et al.  Whole-body potassium and bone mineral density up to 30 years after urinary diversion.  Br J Urol  1998; 82:798-803.