Anatomy
Genitourinary system: Composed of internal and external organs of the urinary and genital/reproductive systems. Both systems are contained in the abdominal and pelvic regions.
Urinary system: Comprises kidneys, ureters, bladder, and urethra
Reproductive system: Male (penis and testicles) and female (ovaries, fallopian tubes, uterus, vagina, and vulva)
Female genitourinary system: Situated within the pelvis, except for the vulva, which is external ( Fig. 32.1A )
Figure 32.1
Genitourinary system.
Male genitourinary system : The prostate and internal portion of the male urethra located within the pelvis; the penis, scrotum, and testes are located externally and are most vulnerable in men (see Fig. 32.1B )
Kidneys: Located in the retroperitoneal region from T12 through L3 vertebral level ( Fig. 32.2 ); the right kidney lies slightly lower than the left owing to the position of the liver
Figure 32.2
Kidneys in situ.
The kidneys are contained in the cushion of pericapsular fat and protected by the posterior abdominal wall musculature (erector spinae muscles and latissimus dorsi).
Ureters: Run along the posterior peritoneal wall from the kidneys to the urinary bladder; also protected by muscles of the posterior abdominal wall; most vulnerable where they cross the brim of the pelvis
Bladder: When empty, lies completely within the pelvis and is protected anteriorly by pubic rami; therefore, is most vulnerable when full
Physiology
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The major function of the kidney is to maintain the stable composition of the blood via regulation of fluid and electrolytes.
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Renal blood flow at rest is approximately 1100 mL/min and is approximately 20% of the cardiac output.
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Oxygen consumption of the kidneys at rest is 26 mL/min and is approximately 10% of the resting metabolism.
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Daily urine volume may vary from 500 mL to 15 L.
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Urine volume determined primarily by antidiuretic hormone (ADH)
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ADH regulates water reabsorption by increasing permeability of distal tubules of the nephron and collecting duct.
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ADH is released from the posterior pituitary in response to signals from the hypothalamus.
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Primary stimuli for ADH release:
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Increased plasma osmolality
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Decreased blood volume
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Decreased blood pressure
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ADH release may increase three-fold during heavy exercise in order to prevent free water loss and dehydration.
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At rest, 15%–20% of renal plasma flow is continuously filtered by the glomeruli.
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Results in 170 L of filtrate per day
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99% is reabsorbed in the tubular system
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Exercise results in a reduction of renal blood flow proportional to the intensity of activity owing to shunting of blood to the exercising muscles.
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Mechanism is via constriction of afferent and efferent arterioles owing to increased circulating levels of epinephrine and norepinephrine.
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Moderate exercise (50% V̇O 2 max) results in a 30% reduction; strenuous exercise leads to a 40%–50% decrease in both renal blood flow and glomerular filtration rate (GFR).
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During maximal exercise (65% V̇O 2 max), there is a 75% reduction in renal blood blow, which is approximately 1% of the cardiac exercise output.
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Decreases even more if an individual is dehydrated or uses NSAIDs
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Usually returns to pre-exercise levels within 60 minutes
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Hematuria
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Can be gross or microscopic ( Fig. 32.3 )
Figure 32.3
Hematuria.
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Microscopically defined as >3 red blood cells (RBCs) per high-power field.
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In athletes, rates of hematuria can be as high as 75%–80% and can occur in both contact and noncontact sports.
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Although hematuria typically resolves within 48–72 hours after exercise or athletic events, resolution may take up to 7 days in ultraendurance athletes.
Etiology
Etiological factors can be categorized by location (kidney vs. bladder):
Nontraumatic renal: Decreased renal blood flow (RBF) (up to 50% reduction, with the decrease proportional to the intensity) leads to ischemia in the nephron, increased permeability, and subsequent passage of RBCs.
Also increased glomerular filtration pressure, secondary to efferent vasoconstriction, leads to passage of RBCs at the glomerulus.
Clots are usually not renal in etiology; dysmorphic cells are suggestive.
Traumatic renal: Direct contact (e.g., helmet, ski pole, or balance beam) vs. indirect trauma (e.g., jarring during running or jumping)
Bladder: Sports hematuria of bladder origin is almost always traumatic.
Can be due to a single, large blunt trauma or multiple lesser forces; repetitive contact of flaccid posterior bladder wall against anterior wall (trigone) is known as a “bladder slap”; it can occur in athletes participating in intense physical activities such as long-distance running, track, swimming, lacrosse, and football. Cystoscopy shows damage of the superficial urothelium or contusion. Incidence can be decreased if the bladder is partially filled and adequate hydration is maintained.
Prostate/urethra: Usually traumatic, most often observed in cyclists because of repetitive jarring or direct trauma from bicycle top tube; inappropriate seat height, tilt, and fore/aft adjustments may contribute
Other causes of hematuria:
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Nephrolithiasis
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Urinary tract infections
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Sickle cell anemia or other blood disorders
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Malignancy
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Drug or medication use (including penicillin, cephalexin, thiazides, allopurinol, nonsteroidal anti-inflammatory drugs [NSAIDs], aspirin, furosemide, and oral contraceptives)
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Rhabdomyolysis (hematuria on urinalysis [UA] with absent RBCs on microscopy)
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Red urine w/o RBCs attributed to beets, berries, food coloring, phenazopyridine, phenytoin, ibuprofen, nitrofurantoin, sulfamethoxazole, and rifampin
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Diagnostic Considerations
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Assess using urine dipstick and confirm with microscopy
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Timing of hematuria during urination is important to consider:
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Initial hematuria (beginning of urination) often urethral in origin
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Terminal hematuria (end of urination) may originate in the bladder or prostate (men)
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Mean corpuscular volume (MCV) and RBC morphology may help establish the origin of hematuria:
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MCV <72 fL considered to be of glomerular origin
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MCV >72 fL considered to be of nonglomerular origin
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Casts or dysmorphic appearance of cells consistent with glomerular origin
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Treatment
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If no concerning history, physical examination or diagnosis, stop exercise and/or suspected medications and repeat UA after 24–72 hours
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If urine clears after 24–72 hours and patient is <40 years old, is likely exercise-induced hematuria
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If gross or microscopic hematuria persists or patient is >40 years old, further evaluation indicated:
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Urine: culture, cytology
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Blood: blood urea nitrogen (BUN), creatinine, PT/PTT, CBC, sickle cell screen (in African Americans)
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Cystoscopy to exclude bladder lesions
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If testing remains normal and hematuria persists, must consider intrinsic renal disease:
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Creatinine clearance and protein excretion should be measured.
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Upper urinary tract may be imaged using CT urography, renal ultrasound, and intravenous urography.
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Nuclear renal scans, arteriography, retrograde pyelography, and voiding cystourethrography are less common, used when clinically indicated.
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Renal biopsy occasionally needed to establish medical cause and subsequent treatment of hematuria
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Return to Play
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Athletes with benign hematuria secondary to exercise may return to activity once hematuria resolves.
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Return to play for other causes of hematuria is diagnosis dependent.
Prevention
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Athletes, particularly those with previous episodes of hematuria, should be encouraged to drink fluids before and during exercise to avoid dehydration.
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Keeping a slightly distended bladder during exercise can help prevent “bladder slap.”
Proteinuria
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May be present in up to 70% of athletes after exertion
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Exercise-induced proteinuria is a function of the intensity of exercise.
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Strenuous exercise can cause protein excretion to reach 1.5 mg/minute but usually does not increase beyond 1–2 g/day (normal 150–200 mg/day).
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Usually occurs within 30 minutes of exercise and clears in 24–48 hours
Etiology
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Cause unknown, but the renin–angiotensin system (RAS) and prostaglandins (PGs) play a major role:
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Plasma concentration of angiotensin II increases during exercise, resulting in increased protein filtration through glomerular membrane.
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Moreover, strenuous exercise activates the sympathetic nervous system, which releases catecholamines, thereby increasing glomerular membrane permeability.
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In patients with underlying chronic kidney disease (CKD), low-intensity exercise does not increase proteinuria or lead to progression of CKD.
Diagnostic Considerations
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Urine dipstick is a good screening tool but poorly quantifies the degree of proteinuria.
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Screening for proteinuria is not recommended during prepreparticipation evaluation because the diagnostic utility is low.
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If routine UA shows protein and was collected within 24 hours of intense exercise, repeat testing in the absence of prior exercise to determine transient vs. persistent proteinuria
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Other causes of false-positive proteinuria on UA:
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Highly concentrated urine (specific gravity >1.030)
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Contamination with antiseptics
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Pyridium (phenazopyridine HCl) use
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Highly alkaline urine (pH > 8)
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Thorough history should be taken, including personal and family history of:
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Renal disease
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Anemia
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Hypertension
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Diabetes
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Medication use (e.g., NSAIDs or antibiotics)
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Further workup may include:
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First step is to quantify degree of proteinuria or microalbuminuria by using spot urine for protein, microalbumin, and creatinine (protein/creatinine, microalbumin/creatinine ratios)
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Serum tests for renal function (BUN, creatinine)
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24-hour urine for total protein, creatinine, and creatinine clearance (sometimes indicated)
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Fasting blood glucose or hemoglobin A1c
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CBC or other tests, as medically indicated
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Imaging: renal ultrasound and CT
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Renal biopsy
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Treatment
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If proteinuria is transient or exercise-induced, no treatment is indicated.
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Otherwise, treatment depends on underlying cause.
Return to Play
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If proteinuria clears after 24 hours, can return to activity or exercise
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If significant proteinuria persists, further evaluation as indicated before clearance
Prevention
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No known prevention strategies needed because it is a normal physiologic process
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Exercise-induced proteinuria does not decrease with regular physical training, even in high-level athletes.
Acute Kidney Injury
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Acute kidney injury (AKI) is uncommon in sports, but occurrence is well documented.
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Becoming more prevalent in athletes with rise of ultraendurance events
Etiology
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Combined effects of exercise-to-exhaustion, dehydration, hyperpyrexia, and rhabdomyolysis culminate in renal dysfunction by release of muscle enzymes and myoglobin that precipitates in renal tubules ( Fig. 32.4 ).
