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PRACTICE: Josip Car Urinary tract infections in women: diagnosis and management in primary care BMJ 2006; 332: 94-97 [Full text]

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Urinary Tract Infections

Vinod H. Nargund   (15 January 2006)

Screening for UTI in pregnancy

Michael R Lewis   (16 January 2006)

Risk of calcium nephrolithiasis associated with intake of cranberry juice

Ngiaw Khoon Saw   (16 January 2006)

Treatment of urinary tract infections: implications of chronic kidney disease

Mark S. MacGregor, Aileen Currie, Renal Pharmacist   (16 January 2006)

UTI management in practice

Joe A Moran   (19 January 2006)

Urea-splitting organisms in urinary infection were not mentioned

Chandra Shekhar Biyani, Doddametikurke Ramegowda Basavaraj   (28 March 2006)

Urinary Tract Infections 15 January 2006
Vinod H. Nargund, Consultant Urological Surgeon St Bartholomew's Hospital, EC1A 7BE Send response to journal: Re: Urinary Tract Infections	Urinary tract infections in women… This paper includes details of symptomatic treatment of UTIs with antimicrobials in women at times misguiding the reader. Cystitis is a vague term used by most patients for their lower urinary tract symptoms (LUTS). The paper starts with a wrong definition of cystitis. Cystitis can be both bacterial and nonbacterial (e.g. interstitial cystitis). There are number of ways women get cystitis and these should be explored in the history once the diagnosis of cystitis has been confirmed and treated. The source of bacteria in healthy women comes from the perineum mainly in peri -anal region. It is amazing that doctors do not ask any questions about bowel habits, constipation, presence of fissure in ano or piles as bacterial colonization is likely to occur in these areas. This paper is no exception to this general trend. The treatment obviously in these cases is completely different and patients need a proper explanation about the mechanism and management. Car mentions vaginal douching in the non-drug management which itself particularly combined with chemical agents can lead to mucosal damage and decolonization of helpful bacteria. Other common causes are pelvic inflammatory disease, tight underclothing (eg tight panties) and incomplete bladder emptying. It is also important to make sure that there is no latex allergy. When symptoms are of low grade, a differential diagnosis of carcinoma in situ of the bladder should be considered. Bladder cancer similarly can produce cystitis like symptoms and this need to be remembered in older women and in those who have history of chronic smoking. Urological referral may be needed in such cases. The antimicrobial treatment is only a part of the management of UTI in women and not the treatment as depicted in this paper. Competing interests: None declared
Screening for UTI in pregnancy 16 January 2006
Michael R Lewis, GP Welshpool Medical Centre SY21 7ER Send response to journal: Re: Screening for UTI in pregnancy	Josip Car advises that 'all pregnant women should be screened for bacteriuria', implicitly because this will reduce the risk of pyelonephritis and subsequent complications (1). Unfortunately this statement is not corroborated, nor are there details of when, with what frequency and by what method women should be screened. It is important that statements about good practice are evidence- based as the uncritical application of 'rules' can be counter-productive both for the health service and patients. Michael Lewis 1.Urinary tract infections in women: diagnosis and management in primary care. Car J. BMJ 2006;332:94-97 Competing interests: None declared
Risk of calcium nephrolithiasis associated with intake of cranberry juice 16 January 2006
Ngiaw Khoon Saw, Clinical research fellow South Manchester University Hospital Trusts, Wythenshawe, Manchester M23 9LT Send response to journal: Re: Risk of calcium nephrolithiasis associated with intake of cranberry juice	Josip Car highlighted that consumption of cranberry juice (CBJ) and cranberry concentrate tablets can prevent recurrent urinary tract infection. However, it is worth noting that intake of CBJ is associated with an increased risk of renal calcium stone formation due to increased urinary excretion of calcium and oxalate 1. Daily intake of 1L of CBJ has been associated with elevated urinary excretion of calcium and oxalate culminating in a raise in urinary calcium oxalate supersaturation in healthy subjects and stone formers. In particular, consumption of cranberry concentrate tablets can increase urinary oxalate excretion markedly, as high as 40% 2. It is therefore important that patients are advised to consume CBJ in moderation. Patients who are known to have recurrent calcium stone disease should be monitored closely for increased excretion of calcium and oxalate while taking CBJ or cranberry concentrate tablets. 1. Gettman MT, Ogan K, Brinkley LJ, et al. Effect of cranberry juice consumption on urinary stone risk factors. J Urol 2005;174:590-4; 2. Terris MK, Issa MM, Tacker JR. Dietary supplementation with cranberry concentrate tablets may increase the risk of nephrolithiasis. Urology 2001;57:26-9 Competing interests: None declared
Treatment of urinary tract infections: implications of chronic kidney disease 16 January 2006
Mark S. MacGregor, Consultant Nephrologist John Stevenson Lynch Renal Unit, Crosshouse Hospital, Kilmarnock, KA2 0BE, SCOTLAND, Aileen Currie, Renal Pharmacist Send response to journal: Re: Treatment of urinary tract infections: implications of chronic kidney disease	In his review of urinary tract infection, Car recommends reducing the dose of amoxicillin in renal failure, and avoiding the use of tetracyclines and nitrofurantoin.1 Unfortunately, “renal failure” has no accepted definition in terms of glomerular filtration rate (GFR). In the USA, the Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation has established a classification of chronic kidney disease (CKD; Table 1),2 which has been accepted internationally. The K/DOQI classification has been adopted by the UK guidelines on CKD3 and by the National Service Framework for renal services in England.4 As of 1st April 2006, most UK laboratories should report estimated GFR (eGFR)4,5 whenever a serum creatinine is requested, allowing easy use of the K/DOQI classification.   The British National Formulary (BNF) recommends reduction of the dose of amoxicillin in “severe renal failure”.6 It is important to note that the BNF has yet to implement the K/DOQI classification and uses the severe label for a GFR <10 ml/min (cf Table 1: stage 5 CKD or established renal failure). Similarly, the BNF advises avoiding tetracycline and nitrofurantoin in what they call “mild renal failure”, that is a GFR <50 ml/min (cf Table 1: CKD stages 3 to 5).   Finally, Car recommends trimethoprim as the first choice for empirical treatment of urinary tract infections. Trimethoprim increases serum creatinine by competitively inhibiting tubular secretion of creatinine, though without a change in the GFR.7 This effect is exaggerated in patients with a reduced GFR.8 More importantly, trimethoprim also causes hyperkalaemia by an amiloride-like action on epithelial sodium channels and basolateral sodium-potassium adenosine triphosphatase in the distal nephron.9 Patients who are predisposed to hyperkalaemia (e.g. those with CKD or diabetes mellitus, the elderly, those receiving angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, non-steroidal anti-inflammatory drugs, or potassium sparing diuretics) are at increased risk. The incidence of severe hyperkalaemia due to trimethoprim remains to be established. Although it is likely to be infrequent with standard dose courses of 3 to 5 days, we feel that trimethoprim is not a good choice in these patients, given this potentially life-threatening complication, when safer alternatives such as amoxicillin and cephalosporins are available. If its use is essential in these high risk patient groups, trimethoprim should be used for as short a course as possible, and in an appropriately reduced dose depending on the eGFR. Monitoring of serum potassium may also be a sensible precaution.   References 1.      Car J. Urinary tract infections in women: diagnosis and management in primary care. Brit Med J 2006;332:94-7. 2.      K/DOQI. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39 (Suppl 1): S1-S266. http://www.kidney.org/professionals/kdoqi/guidelines_ckd/toc.htm (accessed 14th January, 2006). 3.      Renal Association. Chronic kidney disease in adults: UK guidelines for identification, management and referral. http://www.renal.org/CKDguide/ckd.html  (accessed 14th January 2006). 4.      Department of Health. National service framework for renal services – part two: chronic kidney disease, acute renal failure and end of life care. London: Department of Health, Feb. 2005. 5.      Levey AS, Greene T, Kusek JW, Beck GJ. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephrol 2000;11:A0828. 6.      Joint Formulary Committee. British National Formulary. 50th ed. London: BMJ Publishing Group Ltd and Royal Pharmaceutical Society of Great Britain, Sept. 2005. 7.      Berglund F, Killander J, Pompeius R. Effect of trimethoprim-sulfamethoxazole on the renal excretion of creatinine in man. J Urol 1975;114:802-8 8.      Myre SA, McCann J, First MR, Cluxton RJ Jr. Effect of trimethoprim on serum creatinine in healthy and chronic renal failure volunteers. Ther Drug Monit 1987;9:161-5. 9.      Perazella MA. Trimethoprim-induced hyperkalaemia: clinical data, mechanism, prevention and management. Drug Saf 2000;22:227-36.   Stage Description GFR (ml/min/1.73m2) Prevalence Focus of care* 1 Kidney damage with normal or increased GFR >90 3.3% Diagnosis and disease-specific therapies 2 Kidney damage with mildly impaired GFR 60-89 3.0% Slowing of progression and reduction of cardiovascular risk   3   Moderately impaired GFR     30-59   4.3%   Addressing complications of CKD 4 Severely impaired GFR   15-29 0.2% Preparation for dialysis 5 Established renal failure <15 or on dialysis 0.2% Dialysis, transplantation or conservative care Table 1. K/DOQI classification of CKD (with minor adaptations).2 Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. Note that even with a mildly reduced GFR, kidney damage must be present to diagnose CKD, whereas stages 3 to 5 require only a reduced GFR. Reduced GFR and/or kidney damage must be present for >3 months to make the diagnosis of CKD. *Each stage also incorporates the areas of care of the stages above it.     Competing interests: AC is the co-editor of the second edition of "The Renal Drug Handbook". MMcG is a member of the Executive Committee of the Renal Association and of the Scottish Intercollegiate Guidelines Network group on chronic kidney disease. The views expressed are the authors' own.
UTI management in practice 19 January 2006
Joe A Moran, GP Medical Clinic, McCurtain St, Fermoy, Co Cork, Ireland Send response to journal: Re: UTI management in practice	Sir I have previously reported a case of recurrent UTI affecting a female patient which was related to tampon use (1). Is tampon use as a risk factor for recurrent UTIs? Should GPs routinely enquire about tampon use when they encounter women with recurrent cystitis? (1) Recurrent UTI associated with tampon use. IMJ 1998 Volume 91 Competing interests: None declared
Urea-splitting organisms in urinary infection were not mentioned 28 March 2006
Chandra Shekhar Biyani, Consultant Urologist Pinderfileds General Hospital, Wakefield, WF1 4DG, Doddametikurke Ramegowda Basavaraj Send response to journal: Re: Urea-splitting organisms in urinary infection were not mentioned	Urea-splitting organisms in urinary infection were not mentioned To the Editor We read with great interest the article on urinary tract infection in women: diagnosis, treatment, and evaluation in primary care.1 However, infection with urea-splitting organisms was not mentioned. Proteus mirabilis may be present in the faecal flora in 25% of women and Klebsiella may account for up to 20% of community-acquired urinary infection.2 P. mirabilis causes intense alkalinisation of the urine with precipitation of calcium, magnesium, ammonium, and phosphate salts and subsequent formation of struvite stones. Supravesical urine may be colonised in up to 50% of bacteriuic women without fever or flank pain and this may explain the fact that large struvite stones may be asymptomatic.3 Patients with first infection or recurrent infection with urea-splitting organisms require meticulous bacteriological surveillance. In addition, patients with recurrent P. mirabilis infection should have a plain film of the abdomen or ultrasound scan of the kidneys.4 Chandra Shekhar Biyani Consultant Urologist Pinderfields General Hospital, Wakefield, WF1 4DG shekharbiyani@hotmail.com Doddametikurke Ramegowda Basavaraj Specialist Registrar Urology Pinderfields General Hospital, Wakefield, WF1 4DG References 1. Car J. Urinary tract infection in women: diagnosis and management in primary care. BMJ 2006;332:94-97. 2. Michaels EK. Surgical management of struvite stones. In Kidney Stones:Medical and Surgical Management. Edited by F L Coe, M J Favus, C Y C Pak, J H Parks and G M Preminger. Lippincott-Raven Publishers, Philadelphia, 1996, chapter 43, page 951-970. 3. Stamey TA. Pathogenesis and Treatment of Urinary Tract infections. Baltimore, Williams & Wilkins, 1980. 4. Schaefffer AJ. Infection of the urinary tract. In Campbell’s Urology, Editors P C Walsh, A B Retik, E Darracott Vaughan Jr., A J Wein, Seventh edition, W B Saunders Company, Philadelphia, 1998, chapter 15, page 533- 614. Competing interests: None declared