This chapter reviews relevant aspects of renal disease that have implications for sport participation by adolescents, including solitary kidney, hypertension, hyponatremia, proteinuria, hematuria, exercise-related acute renal failure, and chronic/end-stage renal disease (ESRD).1 The effects of creatine and protein supplementation, including renal effects, are reviewed in Chapter 6.2,3
Solitary kidney refers to the occurrence of one kidney instead of the normal situation with two kidneys. Approximately 1 in 1500 children and adolescents have a solitary kidney.4 The concern is whether sports activity should be avoided or limited for fear of injuring the one kidney the child or teen has and then having no kidney at all.
Solitary kidney may result from congenital or acquired causes (Table 13-1). Congenital causes include renal fusion anomalies. Acquired causes include the removal of a kidney because of malignancy or trauma.
Congenital |
Unilateral renal agenesis |
Multicystic dysplastic kidney |
Hypoplastic kidney |
Nephrectomy |
Renal trauma |
Hydronephrosis |
Vesicoureteral reflux |
Renal artery thrombosis |
Renal vein thrombosis |
Kidney donation |
Maligancy |
Wilms tumor |
Neuroblastoma |
Renal trauma from sports is fortunately an unusual condition and most of these are seen as a result of blunt trauma in contact/collision sports.4 Recreational bicycle riding is the most common cause of sports-related kidney injury in children, sometimes leading to major renal injury; team contact sport activity is an unusual cause of major renal injury.5 Also, the incidence of renal trauma from motor vehicle accidents is significantly higher in adolescents than renal trauma from sports activities.6
Solitary kidney is typically asymptomatic and often is not known. Renal anomalies may be suspected in infants, if there is only one umbilical artery or other anomalies are present, such as congenital heart disease or multiple anomalies (such as imperforate anus, scoliosis, external ear defects, and others). Clinically, there are no specific manifestations of a solitary functioning kidney including renal agenesis. However, because of the generalized use of prenatal ultrasound, the diagnosis is commonly made prenatally and confirmed after delivery by repeated ultrasonography or nuclear renal scan. Unilateral renal agenesis in otherwise healthy individuals is compatible with normal longevity. Hypertension, proteinuria, hyperuricemia, focal segmental sclerosis, and decreased glomerular filteration rate (GFR) developing in individuals with a solitary functioning kidney are well documented in the literature. Renal hyperfiltration has been implicated as the cause of these abnormalities.
A renal sonogram may be done in cases of suspected renal anomalies or if an enlarged kidney is palpated.
More advance studies are undertaken in consultation with nephrologists as indicated based on initial clinical evaluation Box 13-1.
There is no consensus among nephrology consultants regarding whether or not children or adolescents with one normal kidney should be involved in contact/collision sports.4,7–10 In a survey of pediatric urologists published in 2002, 68% recommended the avoidance of contact sports in this situation, though 88% (182 out of 231) of those who answered the survey noted that the risk of loss the single kidney from sports trauma was less than 1%.4 Another survey of sports medicine clinicians noted that 54% agreed with contact sports activity in these patients after reviewing potential risks of kidney damage with the athlete and family, though only 41.6% would allow such participation if this patient was their child.11
Other than the motor-vehicle-related injuries, the most frequent causes of severe renal injuries were associated with bicycle riding, being struck by the handlebars seems to be the mechanism of injury and may occur even when the speed of the riding is low. Renal injuries occur in team sports at much lower rate and severity than with other external causes of injury, and seldom are associated with loss of a kidney. Because of these observations, some pediatric urologists allow these children to participate in contact sports.
Besides the solitary functioning kidney, other renal disorders may predispose to renal trauma. We have seen a 12-year-old girl who after a mild trauma, when playing at school presented with gross hematuria. Family history and renal ultrasound revealed autosomal dominant polycystic kidney disease. Renal abnormalities such as hydronephrosis and horseshoe kidney as well as cross ectopia with fusion may predispose to blunt trauma resulting in renal injury.
The AAP Committee on Sports Medicine and Fitness recommendation for contact/collision sports is a “qualified yes” and based on “clinical judgment.” Most pediatric urologists differ from these recommendations. The reasons are not clear. Contact sports are often not related to high-grade renal injury, at least in individuals with two normally functioning kidneys. A few cases of solitary functioning kidney being injured during physical activities have been reported. The solitary functioning kidney is usually hypertrophic and it is not known, if this characteristic makes it more susceptible to blunt trauma.
In general, children or adolescents with one healthy kidney can be allowed participation in contact/collision sports if they wish such after careful explanation is provided to the athletes and their family of the low, but potential risks.12–14 The importance of proper protection with recommended sports equipment and an appropriate supervision should be emphasized in these discussions. Some might say that one has only one brain and it needs proper protection as well in any sports activity. However, contact/collision sports activity should not be allowed, if there is a multicystic kidney, if hydronephrosis is present, if a pelvic or iliac location is present, or if there are uteropelvic junction abnormalities.12
Hypertension is defined as an average systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) ≥95th percentile for gender, age, and height on ≥3 occasions.15 Prehypertenion in children is defined as average levels of SBP or DBP that are ≥90th percentile but <95th percentile. Teenagers with blood pressure readings ≥120/80 are considered to be prehypertensive. The prevalence of hypertension is adolescents is approximately 5%.
Blood pressure results from the interaction between cardiac output and peripheral resistance, and it is increased if either of these factors increase. If no overt cause for the hypertension is found, the term primary or essential hypertension is used. If another disease is found to cause the rise in blood pressure, it is called secondary hypertension. White-coat hypertension refers to elevated blood pressure in the office setting (or other anxiety-provoking situations) but normal blood pressure readings otherwise. Table 13-2 lists causes for hypertension in adolescents.
Primary (essential) hypertension |
White coat hypertension |
Secondary causes of hypertension
|
Most adolescents with hypertension are asymptomatic and the finding of an increased blood pressure is typically noted during a sports preparticipation or other preventive examination. The physical examination is typically normal except for the elevated blood pressure. Those with severe, sustained hypertension eventually develop retinopathy, left ventricular hypertrophy, and other hypertensive complications.
In general, patients younger than 10 years with hypertension have secondary hypertension and adolescents typically have essential or primary hypertension. An adolescent with mild to moderate hypertension and a positive family history for primary hypertension usually has primary or essential hypertension.
The patient should have at least three elevated blood pressure measurements before using the term hypertension. Those with presumed primary hypertension can have a work-up including a complete blood count, electrolytes, blood urea nitrogen, creatinine, and urinalysis. Other tests include serum uric acid (often increased in primary hypertension), fasting lipid profile, electrocardiogram, and echocardiographic examination. Table 13-3 lists tests used for evaluation of adolescents with secondary hypertension.
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Children or adolescents who have severe, symptomatic hypertension should be immediately and rapidly treated to bring their blood pressure down to safer levels even before diagnostic tests are ordered. Those with mild to moderate hypertension should receive nonpharmacologic intervention that consists of lifestyle modifications to improve exercise patterns, diet, and overweight or obesity, if present. The patient should be counseled to avoid cigarette smoking if using this substance. Adolescents who are in a prehypertensive state, should receive instruction in lifestyle modifications as well.
Regular exercise is a key part of systemic hypertension management in adolescents. The benefits of exercise on hypertension are supported by research and these youth should be instructed in being physically active and given full guidance in exercise and sports participation.16–19 The 36th Bethesda Conference20 and the American Academy of Pediatrics16 have published their recommendations for sports participation by athletes with systemic hypertension. Full athletic participation is allowed for those with hypertension in the 95th to 98th percentile for age and gender (significant hypertension) who have no evidence of target organ damage or other cardiovascular disease. Adolescent athletes with hypertension in the 99th percentile for age and gender (severe hypertension) are recommended to avoid competitive sports and activities with high-static loads until the blood pressure is controlled and there is no evidence for target organ damage. Table 13-4 reviews medications used to treat hypertension in adolescents.15
Class | Drug | Dose† | Dosing Interval |
|---|---|---|---|
Angiotensin-converting enzyme (ACE) inhibitor | Benazepril | Initial: 0.2 mg/kg/d up to 10 mg/d | qd |
Maximum: 0.6 mg/kg/d up to 40 mg/d | |||
Captopril | Initial: 0.3–0.5 mg/kg/dose | tid | |
Maximum: 6 mg/kg/d | |||
Enalapril | Initial: 0.08 mg/kg/d up to 5 mg/d | qd bid | |
Maximum: 0.6 mg/kg/d up to 40 mg/d | |||
Fosinopril | Children >50 kg: | qd | |
Initial: 5–10 mg/d | |||
Maximum: 40 mg/d | |||
Lisinopril | Initial: 0.07 mg/kg/d up to 5 mg/d | qd | |
Maximum: 0.6 mg/dg/d up to 40 mg/d | |||
Quinapril | Initial: 5–10 mg/d | qd | |
Maximum: 80 mg/d | |||
Angiotensin-receptor blocker | Irbesartan | 6–12 y: 75–150 mg/d | qd |
≥13 years: 150–300 mg/d | |||
Losartan | Initial: 0.7 mg/kg/d up to 50 mg/d | qd | |
Maximum: 1.4 mg/kg/d up to 100 mg/d | |||
α- and β-blocker | Labetalol | Initial: 1–3 mg/kg/d | bid |
Maximum: 10–12 mg/kg/d up to 1200 mg/d | |||
β-blocker | Atenolol | Initial: 0.5–1 mg/kg/d | qd bid |
Maximum: 2 mg/kg/d up to 100 mg/d | |||
Bisoprolol/HCTZ | Initial: 2.5/6.25 mg/d | qd | |
Maximum: 10/6.25 mg/d | |||
Metoprolol | Initial: 1–2 mg/kg/d | bid | |
Maximum: 6 mg/kg/d up to 200 mg/d | |||
Propranolol | Initial: 1–2 mg/kg/d | bid tid | |
Maximum: 4 mg/kg/d up to 640 mg/d | |||
Calcium channel blocker | Amlodipine | Children 6–17 y: | qd |
2.5–5 mg once daily | |||
Felodipine | Initial: 2.5 mg/d | qd | |
Maximum: 10 mg/d | |||
Isradipine | Initial: 0.15–0.2 mg/kg/d | tid qid | |
Maximum: 0.8 mg/kg/d up to 20 mg/d | |||
Extended-release nifedipine | Initial: 0.25–0.5 mg/kg/d | qd bid | |
Maximum: 3 mg/kg/d up to 120 mg/d | |||
Central α-agonist | Clonidine | Children ≥12 y: | bid |
Initial: 0.2 mg/d | |||
Maximum: 2.4 mg/d | |||
Diuretic | HCTZ | Initial: 1 mg/kg/d | qd |
Maximum: 3 mg/kg/d up to 50 mg/d | |||
Chlorthalidone | Initial: 0.3 mg/kg/d | qd | |
Maximum: 2 mg/kg/d up to 50 mg/d | |||
Furosemide | Initial: 0.5–2.0 mg/kg/dose | qd bid | |
Maximum: 6 mg/kg/d | |||
Spironolactone | Initial: 1 mg/kg/d | qd bid | |
Maximum: 3.3 mg/kg/d up to 100 mg/d | |||
Triamterene | Initial: 1–2 mg/kg/d | bid | |
Maximum: 3–4 mg/kg/d up to 300 mg/d | |||
Amiloride | Initial: 0.4–0.625 mg/kg/d | qd | |
Maximum: 20 mg/d | |||
Peripheral α-antagonist | Doxazosin | Initial: 1 mg/d | qd |
Maximum: 4 mg/d | |||
Prazosin | Initial: 0.05–0.1 mg/kg/d | tid | |
Maximum: 0.5 mg/kg/d | |||
Terazosin | Initial: 1 mg/d | qd | |
Maximum: 20 mg/d | |||
Vasodilator | Hydralazine | Initial: 0.75 mg/kg/d | |
Maximum: 7.5 mg/kg/d up to 200 mg/d | qid | ||
Minoxidil | Children <12 y: | qd tid | |
Initial: 0.2 mg/kg/d | |||
Maximum: 50 mg/d | |||
Children ≥12 y: | |||
Initial: 5 mg/d | |||
Maximum: 100 mg/d |
The normal serum sodium concentrations or [Na+] is between 138 and 142 mmol/L and is maintained within these narrow limits despite large variations in water intake. Hyponatremia is defined by a serum sodium level that is below 135 mEq/L. Hyponatremia develops when there is an increased ratio of water to sodium that involves the total body water and total body sodium.
Causes of hyponatremia in athletes are listed in Table 13-5.21,22 Mildly symptomatic or asymptomatic hyponatremia is a common phenomenon in athletes and an incidence as high as 30% has been reported in long-distance runners.21 However, rare deaths caused by hyponatremia have been reported in long-distance runners.21,22
Excessive water intake |
Prolonged exercise in heat |
Syndrome of inappropriate antidiuretic hormone |
Increased rate of sweat and sodium loss |
Inadequate sodium intake in replacement fluid |
Inadequate sodium in diet |
Poor aerobic conditioning and acclimatization |
CFTR gene in patients with cystic fibrosis |
Non-steroidal anti-inflammatory drugs |
Hypotonic or dilutional hyponatremia is the main situation seen in athletes and is owing to excessive water intake before and during the sporting event or physical activity, particularly when occurring in hot and humid conditions.9 Most cases of exercise-associated hyponatremia (EAH) are owing to a combination of increased fluid intake with modest increases of plasma arginine vasopressin (AVP) levels from various stimuli during prolonged exercise.23 Those at increased risk for hyponatremia are athletes with smaller total body surface area and who sweat excessively. The potentially fatal outcome of hyponatremia should be understood by athletes who seek to keep themselves properly hydrated during sports events and other physical activities.
Numerous factors acting in the concentrating and diluting mechanisms in the kidney contribute to the regulation of the normal serum [Na+]. Most of the changes in serum sodium concentration that occur acutely are the result of changes in the total body water content, rather than rapid changes in total body sodium content. Significant amount of water loss relative to sodium loss will result in an increase in serum sodium concentration, whereas a decrease in water excretion, because of disorders of renal diluting capacity without a significant change in solute (Na2+ K+) will result in dilutional hyponatremia.
There are a few conditions in which the serum sodium does not reflect serum osmolality, when osmotically active substances (i.e., glucose, mannitol, glycine) are present in the extracellular fluid. Increased serum osmolality without changes in sodium concentration is seen when osmolytes (i.e., urea, ethanol, methanol, ethylene glycol) are distributed in the total body water. Pseudohyponatremia is present when the solid content of plasma is increased (hyperlipidemia, dysproteinemias), and the sodium is measured by flame photometer rather than specific sodium electrode.
Most athletes remain asymptomatic with sodium levels between 125 mEq/L and 135 mEq/L. Mild cases of hyponatremia may result in nausea, emesis, headaches, lethargy, confusion, irritability, edema of hands, as well as feet. However, rapid decreases in sodium levels, especially if rapid drop off are noted, can result in significant osmotic fluid shifts with resultant cerebral edema, seizure activity, coma, and rarely, death.
Hypotonic hyponatremia causes increase in water content in all body cells. However, the central nervous system swelling causes most relevant clinical manifestations. The severity of the neurologic manifestations correlates with the rapidity with which the hyponatremia develops. The more rapid the hyponatremia develops, the more severe the clinical manifestations occur. Rapidly developing cerebral edema causes increased intracranial pressure and the risk of brain herniation, death, or severe neurologic sequelae. Although the brain has the ability to adapt to hyponatremia by extruding electrolytes and organic osmolytes out of the brain cells, this adaptative response requires time, an average of 48 hours.
The development of moderate, asymptomatic hypernatremia correlates with body weight loss, whereas hyponatremia correlates with weight gain. Acute symptomatic hyponatremia results from both excessive fluid intake and decreased urine formation contributing to its rapid onset. Life-threatening complications secondary to pulmonary edema and cerebral edema may result. Susceptibility for the development of exercise associated hyponatremia includes female gender, medications that interfere with hemodynamic renal compensatory mechanism such as the use of NSAIDs, lower prerace body weight, and weight loss of <0.75 kg. Patients with exercise associated hyponatremia fulfill the criteria of SIADH (Table 13-6).
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