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ObjectiveThe prevalence of fecal incontinence (FI) is 8% in the United States. Many patients will not seek treatment and the condition is underdiagnosed. Sacral neuromodulation (SNM) is effective in treating FI, and so urologists can play a key role in its treatment. We examine the practice patterns and treatment of FI with SNM in our institution.Material and methodsThe electronic medical record was queried for the proportion of patients seen for FI in the institution, the urology department, and among the female pelvic medicine and reconstructive surgery (FPMRS) urologists. The patients who underwent SNM for FI were evaluated for progression to second stage procedure.ResultsThe proportion of patients seen for FI is 0.96% in the institution as a whole, 7.9% in the urology department, and 17.9% among FPMRS urologists. Fourteen patients underwent first stage SNM for FI or dual urinary/fecal incontinence, and they all progressed to a second stage procedure. Thirteen of these were performed by FPMRS urologists.ConclusionIn our institution, the proportion of patients seen for FI was lower than the prevalence of this condition. Because patients with urinary incontinence are more likely to have FI, urologists are in a unique position to identify these patients and offer treatment that can improve their quality of life. We acknowledge a gap in care of the patients with FI and an opportunity for urologists to help patients with this devastating yet treatable condition.

Aldosterone-induced intestinal [Na.sup.+] absorption is mediated by increased activities of apical membrane [Na.sup.+]/[H.sup.+] exchange (aNHE3) and basolateral membrane [Na.sup.+]-[K.sup.-]ATPase (BLM-[Na.sup.+]-[K.sup.-]-ATPase) activities. Because the processes coordinating these events were not well understood, we investigated human intestinal Caco-2BBE cells where aldosterone increases within 2-4 h of aNHE3 and [alpha]-subunit of BLM-[Na.sup.+]-[K.sup.-]-ATPase, but not total abundance of these proteins. Although aldosterone activated Akt2 and serum glucorticoid kinase-1 (SGK-1), the latter through stimulation of phosphatidylinositol 3-kinase (PI3K), only the SGK-1 pathway mediated its effects on [Na.sup.+]-[K.sup.-]-ATPase. Ouabain inhibition of the early increase in aldosterone-induced [Na.sup.+]-[K.sup.-]-ATPase activation blocked most of the apical NHE3 insertion, possibly by inhibiting [Na.sup.+]-[K.sup.-]-ATPase-induced changes in intracellular sodium concentration ([[Na].sub.i]). Over the next 6-48 h, further increases in aNHE3 and BLM-[Na.sup.+]-[K.sup.-]-ATPase activity and total protein expression were observed to be largely mediated by aldosterone-activated SGK-1 pathway. Aldosterone-induced increases in NHE3 mRNA, for instance, could be inhibited by RNA silencing of SGK-1, but not Akt2. Additionally, aldosterone-induced increases in NHE3 promoter activity were blocked by silencing SGK-1 as well as pharmacological inhibition of PI3K. In conclusion, aldosterone-stimulated intestinal [Na.sup.+] absorption involves two phases. The first phase involves stimulation of PI3K, which increases SGK-dependent insertion and function of BLM-[Na.sup.+]-[K.sup.-]-ATPase and subsequent increased membrane insertion of aNHE3. The latter may be caused by [Na.sup.+]-[K.sup.-]-ATPaseinduced changes in [Na] or transcellular Na flux. The second phase involves SGK-dependent increases in total NHE3 and [Na.sup.+]-[K.sup.-]ATPase protein expression and activities. The coordination of apical and BLM transporters after aldosterone stimulation is therefore a complex process that requires multiple time- and interdependent cellular processes. [Na.sup.+] transport; intestine; intracellular [Na.sup.+], intestinal adaptation; fluid and electrolyte transport; diarrhea; malabsorption; [Na.sup.+]-[H.sup.+] exchange