The document summarizes anatomical and physiological changes during pregnancy that affect the urinary tract. The kidneys enlarge and renal function increases. The uterus compresses the bladder and displaces it superiorly. Smooth muscle tone decreases in the ureters and bladder due to progesterone. These changes cause urinary stasis and impair anti-reflux mechanisms, increasing risks of urinary tract infections. Bacteriuria prevalence is 4-6% and untreated UTIs increase risks of preterm birth and low birthweight. Screening and treatment are recommended to prevent pyelonephritis.
The document summarizes anatomical and physiological changes during pregnancy that affect the urinary tract. The kidneys enlarge and renal function increases. The uterus compresses the bladder and displaces it superiorly. Smooth muscle tone decreases in the ureters and bladder due to progesterone. These changes cause urinary stasis and impair anti-reflux mechanisms, increasing risks of urinary tract infections. Bacteriuria prevalence is 4-6% and untreated UTIs increase risks of preterm birth and low birthweight. Screening and treatment are recommended to prevent pyelonephritis.
The document summarizes anatomical and physiological changes during pregnancy that affect the urinary tract. The kidneys enlarge and renal function increases. The uterus compresses the bladder and displaces it superiorly. Smooth muscle tone decreases in the ureters and bladder due to progesterone. These changes cause urinary stasis and impair anti-reflux mechanisms, increasing risks of urinary tract infections. Bacteriuria prevalence is 4-6% and untreated UTIs increase risks of preterm birth and low birthweight. Screening and treatment are recommended to prevent pyelonephritis.
• Campbell Urology • Smith and Tanagho's General Urology • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4379362/ “Urinary tract infections in pregnancy: old and new unresolved diagnostic and therapeutic problems” • Increase in Renal Size • Renal length increases approximately 1 cm during normal pregnancy. It is thought that this does not represent true hypertrophy but is the result of increased renal vascular and interstitial volume. No histologic changes have been identified in renal biopsies ( Waltzer, 1981 ) • The glomerular filtration rate increases by 30–50%, most likely secondary to the increase in cardiac output (Waltzer, 1981). • Smooth Muscle Atony of the Collecting System and Bladder • The collecting system, especially the ureters, undergoes decreased peristalsis during pregnancy, and most women in their third trimester show significant ureteral dilatation ( Davison and Lindheimer, 1978 ; Kincaid-Smith, 1978 ; Waltzer, 1981 ). This hydroureter has been attributed both to the muscle-relaxing effects of increased progesterone during pregnancy and to mechanical obstruction of the ureters by the enlarging uterus at the pelvic brim. This will result urinary stasis during the second and third trimester of gestation. Progesterone-induced smooth muscle relaxation also may cause an increased bladder capacity ( Waltzer, 1981 ). Later in pregnancy, the dilation may be the result of the obstructive effect of the enlarging uterus ( Poole and Thorsen, 1999 ). • Bladder Changes • The enlarging uterus displaces the bladder superiorly and anteriorly. The bladder becomes hyperemic and may appear congested endoscopically ( Waltzer, 1981 ). Estrogen stimulation probably causes bladder hypertrophy, as well as squamous changes of the urethra ( Waltzer, 1981 ). Simultaneously, the enlarged uterus compresses the urinary bladder, thus increasing the intravesical pressure, which may result in vesico-ureteral reflux and urine retention in the bladder after miction, commonly observed in pregnant women • Urethral Changes • Urethral sphincter relaxation which occurs due to high levels of circulating progesterone • Augmented Renal Function • The transient increases in glomerular filtration rate and renal plasma flow during pregnancy have been well summarized by several authors and are probably secondary to the increase in cardiac output ( Zacur and Mitch, 1977 ; Davison and Lindheimer, 1978 ; Kincaid-Smith, 1978 ; Waltzer, 1981 ). Glomerular filtration increases by 30% to 50%, and urinary protein excretion increases. The significance of these physiologic changes is apparent when the normal serum creatinine and urea nitrogen values for pregnant women are surveyed. Values considered normal in nonpregnant women may represent renal insufficiency during pregnancy. • Urinary stasis and impairment of the physiological anti-reflux mechanism create conditions favorable for bacterial growth and ascending infection. The additional predisposing factors include pregnancy-specific biochemical changes in urine, with higher amounts of glucose, amino acids and hormone degradation products, which increase urinary pH • Recent studies of E. coli adhesins and their respective specific tissue receptors have established an adhesin-based mechanism of pyelonephritis-induced preterm births and low birth weights in mice ( Kaul et al, 1999 ). There is a higher incidence of E. coli– bearing Dr adhesins during the third trimester of pregnancy in women with gestational pyelonephritis ( Nowicki et al, 1994 ) and an upregulation of Dr adhesin in the kidney, endometrium, and placenta during the third trimester of pregnancy ( Martens et al, 1993 ). When infected intravesically with E. coli– bearing Dr adhesin, nearly 90% of mice that were hyporesponsive to bacterial lipopolysaccharide and had a deficient immune response delivered preterm, compared with 10% of mice infected with E. coli without Dr adhesin. Also, there was a significant reduction in fetal birth weight in the Dr adhesin–infected group. Bacterial tissue culture showed systemic spread of the E . coli –bearing Dr adhesins to the placentae and fetuses Prevalence, Risk Factor and Mortality • It is estimated that the prevalence of bacteriuria is 4–6% (Sweet, 1977), which is not significantly different from that in nonpregnant women of comparable age. • Interestingly, approximately 30% of those who have bacteriuria on screening evaluation later have pyelonephritis, compared with only 1–2% in those who do not have bacteriuria (Sweet, 1977). • Treatment of bacteriuria decreases the incidence of pyelonephritis during pregnancy to approximately 3% (Christensen, 2000; Sweet, 1977). • A history of previous UTIs and low socioeconomic status are risk factors for bacteriuria in pregnancy (Schnarr and Smaill, 2008). • Overall, the incidence of acute bacterial pyelonephritis is 1–4% in pregnant women (Gilstrap et al, 1981; Wing, 1998). • About 60–70% of the episodes of pyelonephritis occur during the second and third trimesters of pregnancy, when urinary stasis is the greatest. • In 10–20%, recurrent episodes of pyelonephritis develop before delivery (Gilstrap et al, 1981), significant maternal risk factors include diabetes and history of UTI. • When left untreated, pyelonephritis during pregnancy is associated with a high rate of infant prematurity and its associated perinatal mortality (Locksmith and Duff, 2001; McGregor and French, 1998; Schieve et al, 1994). • It remains unclear whether treated pyelonephritis during pregnancy has any effects on the developing fetus (Gilstrap and Ramin, 2001). Screening, Diagnosis and Therapy • Consequently, it is recommended that women be screened for bacteriuria during pregnancy to prevent the development of pyelonephritis. • A voided urine specimen should be obtained at the first prenatal visit and at 16 weeks of gestation (Stenqvist et al, 1989). • For asymptomatic individuals, significant bacteriuria is defined as two voided urine cultures with >105 CFU/mL of a single organism. • For symptomatic pregnant women, >103 CFU/mL is considered to be significant (Rubin et al, 1992). • Pregnant women who are found to have bacteriuria should be treated with penicillins, oral cephalosporins (Christensen, 2000; Wing et al, 1999), or fosfomycin trometamol (Minassian et al, 1998). • However, amoxicillin is not recommended because of the rate of bacterial resistance (Hart et al, 2001). • A 3-day course is suggested, although single-dose therapy may be effective in some patients (Tincello and Richmond, 1998). • Repeat urine culture to document eradication of bacteriuria is necessary in all patients. • Patients with acute bacterial pyelonephritis should be treated with parenteral cephalosporins, penicillins with beta-lactamase inhibitors, or monobactams (Rubin et al, 1992). • Periodic surveillance urine culture is recommended because many of these women will have recurrent episodes of pyelonephritis.