Resistanceassociated 23S rRNA Mutation in Mycoplasma genitalium, Japan To the Editor: Mycoplasma genitalium is now recognized as a serious pathogen in sexually transmitted infections (1, 2) . Azithromycin regimens have been commonly used for treatment of M. genitalium infections (3). However, failure of azithromycin treatment has been reported in cases of M. genitalium-positive nongonococcal urethritis (NGU) (4, 5) , and macrolideresistant strains of M. genitalium have been isolated from case-patients in Australia, Sweden, and Norway for whom azithromycin treatment has failed (4, 5) . In these strains, mutations in the 23S rRNA gene were associated with macrolide resistance, and mutations in ribosomal protein genes L4 and L22 were also found (5) . Surveillance for antimicrobial resistance of M. genitalium is essential to identify antimicrobial resistant strains and to then determine appropriate treatment. Coculture of patient specimens with Vero cells has improved the primary isolation rate of M. genitalium from clinical specimens and offered some current clinical strains for antimicrobial drug susceptibility testing (6) . To determine their antimicrobial susceptibilities, a molecular real-time PCR method has been developed (7, 8) . However, isolating M. genitalium from clinical specimens and antimicrobial drug susceptibility testing of clinical isolates remain labor-intensive, time-consuming tasks. In addition, no methods are available to directly determine antimicrobial drug susceptibilities of M. genitalium in clinical specimens. To monitor macrolide susceptibilities in clinical Increased Urinary Angiotensin-Converting Enzyme 2 in Renal Transplant Patients with Diabetes Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be a renoprotective enzyme, since it converts angiotensin (Ang) II to Ang-(1-7). ACE2 has been detected in urine from patients with chronic kidney disease. We measured urinary ACE2 activity and protein levels in renal transplant patients (age 54 yrs, 65% male, 38% diabetes, n = 100) and healthy controls (age 45 yrs, 26% male, n = 50), and determined factors associated with elevated urinary ACE2 in the patients. Urine from transplant subjects was also assayed for ACE mRNA and protein. No subjects were taking inhibitors of the renin-angiotensin system. Urinary ACE2 levels were significantly higher in transplant patients compared to controls (p = 0.003 for ACE2 activity, and p≤0.001 for ACE2 protein by ELISA or western analysis). Transplant patients with diabetes mellitus had significantly increased urinary ACE2 activity and protein levels compared to non-diabetics (p<0.001), while ACE2 mRNA levels did not differ. Urinary ACE activity and protein were significantly increased in diabetic transplant subjects, while ACE mRNA levels did not differ from non-diabetic subjects. After adjusting for confounding variables, diabetes was significantly associated with urinary ACE2 activity (p = 0.003) and protein levels (p<0.001), while female gender was associated with urinary mRNA levels for both ACE2 and ACE. These data indicate that urinary ACE2 is increased in renal transplant recipients with diabetes, possibly due to increased shedding from tubular cells. Urinary ACE2 could be a marker of renal renin-angiotensin system activation in these patients. Angiotensin-converting enzyme 2 (ACE2) is a recently identified member of the renin-angiotensin system (RAS) that degrades angiotensin (Ang) II to the seven amino acid peptide fragment Ang-(1-7) [1, 2] . ACE2 is a homologue of angiotensin-converting enzyme (ACE), but is not blocked by ACE inhibitors. Although ACE2 is found in many tissues, expression is especially high in the kidney, particularly within cells of the proximal tubule [3] [4] [5] . In mice deletion of the ACE2 gene is associated with development of late-stage glomerulosclerosis, and acceleration of diabetic nephropathy, in the absence of hypertension [6, 7] . In spontaneously hypertensive rats, administration of human recombinant ACE2 reduces blood pressure [8] , and in diabetic mice, exogenous human ACE2 diminishes blood pressure and glomerular injury [9] . Thus, ACE2 may be an endogenous protector against the progression of chronic kidney disease (CKD).