Chapter 16. Nephrology

Clinical Summary

Healthy children normally have protein in their urine, at a rate of protein excretion <4 mg/m2/h or <100 mg/m2/d throughout childhood. The upper limit of normal protein excretion is up to 150 mg/d. Albumin, relatively small in molecular size, tends to be the dominant constituent, and Tamm-Horsfall protein, a mucoprotein produced in the distal tubule, makes up the remainder.

Proteinuria in children can be transient, orthostatic, or pathologic. Transient proteinuria (often associated with fever, stress, dehydration, or exercise) does not indicate underlying renal disease. Orthostatic proteinuria (elevated protein excretion when the subject is upright but normal protein excretion during recumbency) occurs most commonly in school-aged children and rarely exceeds 1 g/m/d. These patients do not have hematuria and have normal values of creatinine clearance and C3 complement. Pathologic proteinuria is likely if proteinuria is associated with hematuria and/or the first morning urine Pr/Cr ratio is >0.2 in older children. Nephrotic-range proteinuria is levels >40 mg/m/h in 24 hours.

Emergency Department Treatment and Disposition

Take a complete history and physical examination including blood pressure in a patient with proteinuria. In general, urinalysis showing mild proteinuria (trace to 1+) is not reliable during acute illness (unless there are other symptoms and signs pointing to renal disease). Discharge patients with mild proteinuria who have normal blood pressure and urine output and no evidence of kidney disease. For patients with moderate to severe proteinuria (3+ or 4+), obtain serum albumin, creatinine, cholesterol, electrolytes, serum C3/C4 complement, antinuclear antibody, serologies for hepatitis B and C, and human immunodeficiency virus as clinically indicated. Use renal ultrasound to exclude underlying renal disease. Consult pediatric nephrology for further evaluation if any of the studies are abnormal. Hospitalize patients with severe nephrosis, especially the first episode.

Pearls

1. Not all proteinuria is pathologic.

2. Exclude hematuria when evaluating patients with proteinuria in the emergency department (ED).

3. Proteinuria is not an uncommon finding in children and may indicate a completely benign condition or be the first clue to a significant renal parenchymal disease (eg, nephrotic syndrome or glomerulonephritis).

4. Heavy proteinuria (3+ or 4+ on dipstick) is typically seen in nephrotic syndrome; mild proteinuria (trace to 1+) is typically seen with fever or dehydration.

The authors acknowledge the special contributions of Binita R. Shah, MD, to prior edition.

Clinical Summary

Gross hematuria is blood in urine that can be seen with the naked eye, and major causes in children and adolescents include glomerulopathy, urinary tract infection (UTI), hypercalciuria, urolithiasis, and trauma. Less common causes include malignancy, exercise, angiomatous malformations of the collecting system, nutcracker syndrome, cystic kidney disease, and sickle hemoglobinopathies.

In patients with glomerular disease, the urine is uniformly discolored, and can be a brownish-red color or dark brown often described as being like “tea” or “Coca-Cola.” In patients with vascular bleeding or lower urinary tract bleeding, the urine appears bright red. Dysuria and urinary frequency may indicate a UTI. Viral and chemical agents can cause a hemorrhagic cystitis that may be difficult to clinically distinguish from a bacterial infection. Oliguria, edema, and hypertension suggest an acute nephritic process. The most common causes of glomerulonephritis (GN) in children are IgA nephropathy and acute poststreptococcal GN (APSGN). A history of a preceding or concurrent illness such as upper respiratory tract infections and findings such as rash (eg, impetigo) may suggest an underlying cause. Severe episodic flank or abdominal pain associated with gross hematuria strongly suggests urolithiasis.

Emergency Department Treatment and Disposition

Order complete blood count (CBC), blood urea nitrogen (BUN), serum creatinine, albumin, C3 and C4, urinalysis, and urine culture as indicated clinically. If there is high suspicion for stones, order renal and bladder ultrasound or abdominal and pelvic spiral CT scans (with thinner cuts). Send any stone collected for analysis. Order abdominal CT for patients with gross hematuria and a history of abdominal trauma to assess the injury and possible need for surgery. If blood is present at the urethral meatus, obtain retrograde urethrography before catheterization to evaluate for urethral injury.

Most children with hematuria do not require hospitalization. Admit those with hematuria with hypertension, oliguria, or pulmonary edema due to APSGN, hematuria due to renal injury from trauma, hematuria due to papillary necrosis resulting from sickle cell hemoglobinopathy, or patients with urolithiasis requiring intravenous (IV) hydration (eg, vomiting and poor intake) and pain management.

If history or physical examination is not suggestive of any obvious cause of hematuria, refer to a pediatric nephrologist for evaluation for possible hypercalciuria, nephrocalcinosis, benign familial hematuria, or hereditary nephritis. If persistent bleeding seems to originate from the urinary tract and no cause is identified, refer to urology for possible cystoscopy to identify unilateral bleeding from vascular malformations.

Pearls

1. Microscopic examination of the urine is required to confirm the presence of red blood cells (RBCs). Absence of any RBCs in microscopic exam with a positive dipstick reaction suggests hemoglobinuria or myoglobinuria.

2. An occasional RBC on microscopic examination of the urine may be seen in most children. Further testing is required if examination reveals >5 RBCs/hpf.

3. Tea or cola-colored urine, RBC casts, and dysmorphic RBCs are pathognomonic for glomerular bleeding (eg, APSGN).

Clinical Summary

Nephrotic Syndrome (NS) is characterized by proteinuria severe enough to cause hypoalbuminemia (serum albumin <2.5 g/dL), hypercholesterolemia, and edema. The nephrotic range of proteinuria is >40 mg/m2/h (normal: <4 mg/m2/h). Minimal change NS (MCNS) is the most common variety of primary NS. Initially, edema is often mild and variable in distribution; being periorbital in the early morning hours. More severe degrees of edema may result in ascites, pleural effusions, scrotal or vulvar edema, and skin breakdown. Children with NS are prone to develop cellulitis and spontaneous bacterial peritonitis (usually pneumococcal). Gram-negative bacilli, such as Escherichia coli, may also cause infection in such patients. Patients with NS and primary peritonitis (especially when they present with an acute abdomen) are not uncommonly misdiagnosed as having acute appendicitis. Hypercholesterolemia can be quite severe but usually resolves when the NS has been treated successfully. Although NS is usually associated with avid sodium retention, serum sodium concentrations are low in some patients and result from water retention (secondary to high antidiuretic hormone levels). Although the total serum calcium in patients with NS is often low, resulting from the low level of protein-bound calcium, the level of free ionized calcium is usually normal. Patients with NS usually demonstrate laboratory features of a hypercoagulable state. Reduced intravascular volume predisposes to thrombotic events. Venous thrombosis may be associated with pulmonary embolism. Renal vein thrombosis (uncommon) will present with a triad of abdominal pain, palpable abdominal mass, and gross hematuria.

Emergency Department Treatment and Disposition

Order CBC, BUN, and serum values of creatinine, albumin, lipid profile, C3 and C4. Urinalysis will show a high specific gravity (intravascular volume depletion), proteinuria 3+ or 4+, and lipid droplets and broad waxy casts. Microscopic hematuria can be seen (20%-25%); gross hematuria is rare. Consult pediatric nephrology for any child with suspected NS. Admit patients with evidence of acute peritonitis, or severe anasarca. Consider admission for a first episode of nephrosis (provide education about the chronic relapsing nature of the disease, home monitoring of urine by dipstick, diet, and complications related to both the disease and therapy). Therapies include oral prednisone given daily for the first 4 to 6 weeks followed by prednisone every other day for the following 4 to 6 weeks, salt and fluid restriction, and diuretics (eg, Furosemide) during periods of symptomatic edema as indicated. Diuretics are used judiciously and avoided in patients with a history of thromboembolic events. Antiplatelet drugs and/or anticoagulants are recommended for patients with thromboembolic events.

Pearls

1. Heavy proteinuria is an essential element of NS. Proteinuria from other causes (eg, transient proteinuria associated with fever, dehydration or exercise) or orthostatic proteinuria rarely exceeds 1 g/24 h and is not associated with edema.

2. Children with periorbital edema due to NS are often misdiagnosed as having angioedema (allergic reaction) on initial presentation. Absence of itching and a positive urine dipstick for proteinuria should alert to the possibility of NS in such children.

Clinical Summary

Acute poststreptococcal glomerulonephritis (APSGN) is characterized by abrupt onset of one or more features of acute nephritic syndrome: hematuria, proteinuria, volume overload, hypertension, and azotemia. Pyoderma (impetigo) and pharyngitis are the most common antecedent infections. Streptococcal pharyngitis occurs more commonly in children between 5 and 15 years old during the winter and spring; impetigo occurs most commonly in summer and fall. There is a latent period between onset of primary infection and nephritis. With pharyngitis, the latent period is 7 to 14 days; with impetigo the latent period is up to 6 weeks. Some children present with the disease without any identifiable prodrome, due to the high incidence of streptococcal carriage (20%) in schoolchildren. Children with APSGN typically present with sudden onset of painless gross hematuria often described as “coke or tea-colored.” Some edema is usually present. Patients may also present with features of congestive failure (CHF) or pulmonary edema. Hypertension is common and can lead to hypertensive encephalopathy. Patients may also be oliguric or even anuric.

Differential diagnosis includes IgA nephropathy in which patients present with sudden onset of gross hematuria during an episode of pharyngitis. This is in contrast to APSGN in which hematuria comes after an episode of pharyngitis. IgA nephropathy also presents with hypertension and edema. APSGN is also mimicked by other glomerulonephritides including membranoproliferative glomerulonephritis (MPGN), lupus nephritis, and rapidly progressive glomerulonephritis. The prognosis of APSGN is excellent, with about 95% of patients recovering spontaneously and the gross hematuria disappearing in a few days. Microscopic hematuria may persist for 1 to 2 years. Serum C3 value usually returns to normal in 6 to 8 weeks in APSGN while prolonged depression of C3 is seen in other disorders.

Emergency Department Treatment and Disposition

Obtain urinalysis, which usually shows proteinuria, hematuria, and active sediment including dysmorphic RBC, WBC, cellular and granular cast including RBC cast. Obtain basic metabolic panel. Blood urea nitrogen and serum creatinine are generally elevated. Serum total hemolytic complement (CH50) and C3 are low in almost all patients in the first week of illness but C4 is generally normal. As indicated, obtain throat culture, serum antistreptolysin titers, or streptozyme test for evidence of recent streptococcal infection.

Treatment is primarily supportive. Admit patients with obvious edema, hypertension, azotemia, or signs of CHF. Consult pediatric nephrology. Restrict fluid intake to insensible water loss plus urine output and salt intake to one-third to one-half of the usual intake. Treat hypertension by using peripheral vasodilators like hydralazine or nifedipine. Use furosemide to induce diuresis and decreasing volume expansion. Treat mild to moderate hyperkalemia with potassium restriction and exchange resin. Manage severe hyperkalemia with bicarbonate administration, insulin and glucose infusion, and finally with hemodialysis.

Treatment with antimicrobials does not alter the course of APSGN in patients with established glomerulonephritis. Family members of patients with APSGN should be cultured for GABHS and treated if culture is positive. Discharged patients should be referred to their primary care physician for a close follow-up.

Pearls

1. APSGN is a delayed nonsuppurative sequelae of pharyngeal or skin infection by nephritogenic Streptococcus pyogenes strains.

2. APSGN is the most common type of acute nephritis and one of the most common glomerular causes of gross hematuria in children.

3. Acute nephritic syndrome associated with hypocomplementemia and antecedent streptococcal infection strongly suggests the diagnosis of APSGN.

4. The hallmark of APSGN is hematuria and urinary RBC casts, with minimal to moderate proteinuria. Multiple microscopic examinations may be needed to confirm RBC casts.

Clinical Summary

Urinary tract infection (UTI) may involve upper urinary tract and kidneys (acute pyelonephritis) or lower tract and bladder (acute cystitis). Most UTIs in children result from ascending infections, although hematogenous spread may be more common in the first 3 months of life. Most UTIs in children are monomicrobic with E coli (60%–80%), Proteus (more common in boys and those with renal stones), Klebsiella, Enterococcus, and coagulase-negative staphylococci. Older children may present with dysuria, frequency, urgency, hesitancy, small-volume voids, or lower abdominal pain. Infants more commonly present with nonspecific symptoms such as fever, irritability, jaundice, vomiting, or failure to thrive. Infants with UTI may have vomiting and diarrhea, similar to gastroenteritis. Differential diagnosis of UTI includes meningitis (infants with irritability), vulvovaginitis and retained vaginal foreign bodies (girls with dysuria; erythema and inflammation of introitus and labia, presence of vaginal discharge, poor hygiene, or history of bubble baths may provide clues), sexual abuse (children may present with urinary complaints) or appendicitis (abdominal pain, vomiting and pyuria on urine analysis). If urinary frequency is present, consider impaired bladder distention from constipation, abdominal mass, or pregnancy.

Emergency Department Treatment and Disposition

Take a thorough history and a physical examination and obtain dipstick urinalysis and urine culture. Obtain CBC, serum electrolytes including creatinine and BUN, if clinically indicated. Urethral catheterization and suprapubic aspiration provide the best urine specimens for the diagnosis. Urine from bagged and voided specimens has significant false-positive rates because of contamination with skin flora (up to 63% for the bag method). However negative urine culture from bag specimen rules out bacterial UTI in the majority of cases. Pyuria with negative urine culture suggests viral infection, infection with fastidious organisms such as mycobacterium, or noninfectious cystitis. A positive urine culture without pyuria may indicate contamination or an immunosuppressed host.

Management is dependent on the patient’s age and whether pyelonephritis or cystitis is present. Admit patients who are <2 months of age, appear ill or toxic, are vomiting, or have underlying conditions or raised creatinine. Initiate treatment of acute pyelonephritis with broad antibiotic coverage until culture results are available, at which time an appropriate antibiotic for the organism(s) found can be substituted. Common IV antibiotics used for treatment of UTI include ceftriaxone, cefotaxime or cefazolin or gentamicin. Ampicillin should not be used as a first-line medication (resistance of E coli to ampicillin is as high as 30%–40% in some centers). Common oral medications for treatment of UTI (treat for 7–10 days) include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, cefixime, or cefpodoxime proxetil. Patients generally show clinical improvement in 24 to 48 hours. When improvement does not occur in 24 to 48 hours, consider urinary tract abnormalities like obstruction, infection of renal cyst, or perinephric abscess.

Treat children with cystitis with oral antibiotics and discharge with instructions to follow up with their primary care physician. Urinary tract imaging (typically a renal and bladder ultrasound is recommended in a febrile infant or young child between the ages of 2 months and 2 years with a first documented UTI. A voiding cystourethrogram (VCUG) is indicated with recurrent infections, poor urinary stream or palpable kidneys, unusual organism, bacteremia or septicemia, failure to respond to antibiotic treatment within 48 to 72 hours, or unusual clinical presentation.

Pearls

1. In the ED, UTI is prevalent in febrile infants without a definitive source for fever, and the highest prevalence of UTI is in girls and uncircumcised males.

2. Infants <1 year with fever without an apparent source should be considered at risk for UTI.

3. Female infants between 1 and 2 years old with fever without an apparent source should be considered at risk for UTI.

Clinical Summary

Hemolytic uremic syndrome (HUS) is characterized by the triad of microangiopathic anemia, thrombocytopenia, and renal failure and is generally classified as diarrhea associated (D+HUS) and atypical or sporadic (D–HUS). The typical form is most commonly caused by E coli O157:H7 and is one of the most common causes of renal failure in children younger than age 2 to 3 years. Boys and girls are affected equally. Typically, there is a prodromal illness, usually gastroenteritis, although sometimes following upper respiratory infections. Gastrointestinal symptoms include abdominal pain, vomiting, and diarrhea, which may be bloody. Patients may have hepatitis, pancreatitis with endocrine and exocrine dysfunction. The abdomen is often tender. Central nervous symptoms include drowsiness, lethargy, irritability, and seizures. Oligoanuria with renal failure is common at presentation. There may be evidence of fluid overload, including hypertension and congestive heart failure. Most patients look pale, and petechiae and ecchymoses may be present. All patients have microangiopathic hemolytic anemia with negative direct and indirect Coombs. Peripheral smear shows fragmented and helmet-shaped red cells. Haptoglobin is low, and indirect bilirubin and plasma lactic dehydrogenase (LDH) are usually elevated. Platelets are usually diminished to <100,000. These patients have normal prothrombin and partial thromboplastin time. Urinalysis shows hematuria, proteinuria, and cellular casts. Acute renal failure is manifested with oligoanuria, raised BUN and creatinine, and other features of renal failure, including hyperkalemia, hypocalcemia, and metabolic acidosis. Gastrointestinal manifestation may be confused with intussusception, ulcerative colitis, and rectal prolapse or acute bacterial enterocolitis.

Emergency Department Treatment and Disposition

Consult pediatric nephrology as soon as the diagnosis is suspected and admit patient to ICU. Management is essentially supportive, including strict adherence to fluid and electrolyte balance. Begin aggressive fluid resuscitation if patients are dehydrated or hypotensive unless there is oliguria with hypertension and edema, in which case fluids must be limited to insensible losses plus the urine output. Additional therapies may include dialysis (if unable to control medically electrolyte imbalance such as hyperkalemia, hyponatremia, or severe metabolic acidosis), packed red blood cells (with ongoing hemolytic process and hemoglobin concentration <6 g/dL) and avoiding platelet transfusions except for an invasive procedure (with active bleeding or profound thrombocytopenia).

Pearls

1. Agents that retard peristalsis may potentially be harmful by delaying the elimination of toxin.

2. Antibiotics for diarrhea may increase the release of toxin produced by E coli O157:H7.

3. The onset of atypical D–HUS is insidious and the course is often progressive.

Clinical Summary

Postrenal failure results from obstruction of the urinary tract anywhere from the tip of the urethra to the pelvicalyceal system. Causes of obstruction include posterior urethral valves (PUV), ureteropelvic junction (UPJ) obstruction, ureteroceles, bladder outlet obstruction, neurogenic bladder, phimosis, renal calculi, blood clot, and retroperitoneal or intraabdominal tumor. Although not very common beyond the neonatal period, obstructive uropathy is potentially reversible if diagnosed and treated promptly when found in later childhood. A history of prenatal ultrasound (US) demonstrating bilateral hydronephrosis and hydroureters suggests the presence of PUV. Neonates may have a distended bladder, palpably large kidneys, or may present with urosepsis. A history of poor urinary stream may suggest PUV. Older boys may have urinary infection or urinary frequency and diurnal incontinence. Patients with renal stones may reveal signs or symptoms of an obstruction (eg, gross hematuria, colicky pain).

Emergency Department Treatment and Disposition

Obtain CBC and basic metabolic panel. Look for evidence of renal failure suggested by elevated BUN and serum creatinine, hyperkalemia and metabolic acidosis. Urine output and urinary sediment findings may be variable. Obtain renal US which may show evidence of ureteropelvic junction obstruction (dilated renal pelvis with normal ureter) or ureterovesical junction obstruction (dilated renal pelvis and dilated ureter), presence of urinary tract duplication or ureterocele, as well as renal parenchymal findings (eg, thinning, dysplasia, cysts, impaired perfusion). In patients with PUV, the bladder has thick wall musculature, which may be trabeculated. In obstruction, a radioisotope scan shows isotope collection within the kidney or bladder, with delayed or absent excretion of the isotope.

Admit patients with acute renal failure (ARF). Management includes maintaining renal perfusion and fluid and electrolyte balance, controlling blood pressure, adjusting medications for the degree of renal impairment, and initiating dialysis as indicated. Specific therapy for postrenal failure includes removal of obstruction by decompression or diversion of the urinary tract. The site of the obstruction will determine the approach: placement of a Foley catheter, vesicostomy, ureteral catheters (stents), or nephrostomy tubes. Obtain pediatric nephrology and urology consultations in all these cases.

Pearls

1. Consider urinary tract obstruction whenever the cause of ARF is not evident.

2. Sudden development of anuria should strongly suggest the possibility of total urinary obstruction.

3. Initial management of patient with suspected PUV involves insertion of a fine urethral catheter into the bladder; do not use a balloon type of catheter (Foleys) as the catheter may become lodged in posterior urethra and not drain freely.

Clinical Summary

Hypertensive emergency is defined by the presence of acute end-organ injury, and the gravity of manifestations often depends on chronicity and magnitude of BP elevation. The most common symptoms of severe hypertension (HTN) in older children are hypertensive encephalopathy manifested by headache, nausea, vomiting, mental confusion, blurred vision, agitation, or frank seizures. These features along with radiologic findings of edema in the white matter of the brain areas perfused by the posterior brain circulation (best demonstrated by magnetic resonance imaging [MRI]) constitute posterior reversible encephalopathy syndrome (PRES).

Hypertensive emergencies may also present with cerebral infarction, intercerebral or retinal hemorrhage, congestive heart failure (CHF), acute pulmonary edema, acute renal insufficiency, or microangiopathic hemolytic anemia. Uncommon sequelae of hypertensive emergencies in children include myocardial infarction or aortic dissection. Newborns and infants with severe HTN may present with CHF, respiratory distress, apnea or cyanosis, extreme irritability, convulsions, or coma. Hypertensive urgency is a term used to denote severe elevations of BP in children without any signs or symptoms of end-organ involvement.

Emergency Department Treatment and Disposition

Patients with severe symptoms need to be treated rapidly. However, it may be risky to lower the BP too rapidly, especially in those whose HTN has been longstanding. Cerebrovascular and myocardial ischemia can occur in patients whose BP is normalized too rapidly. Reduce BP by 25% of the planned BP reduction over the first 8 to 12 hours, a further 25% over the next 8 to 12 hours, and the final 50% over the 24 hours after that.

Obtain a chest radiograph and an electrocardiograph. Obtain a head CT scan in patients with abnormal neurologic findings. Obtain BUN, creatinine, electrolytes, plasma renin activity, plasma cortisol, and aldosterone. An MRI can be obtained once the BP is better controlled. Consult pediatric nephrology and admit patient to ICU.

Choose antihypertensive medication based on etiology, side-effect profile, and physician familiarity with the drug. Sodium nitroprusside has a rapid onset and short duration of action. Prolonged administration (>24–48 hours) may cause nausea, vomiting, neurologic symptoms, dyspnea, and lactic acidosis due to accumulation of its metabolic end products composed of cyanide and thiocyanate.

Nicardipine also has rapid onset, short duration, and is given by continuous IV infusion. It may be more suitable for children with renal insufficiency and also be given as mini-boluses. Labetalol can be used as a bolus or as continuous infusion. The hypotensive effects of a single dose of IV labetalol administration appear within 2 to 5 minutes, peak at 5 to 15 minutes, and last up to 2 to 4 hours. Adverse reactions include β-adrenergic blockage including bradycardia and bronchospasm. It is contraindicated in patients with acute left ventricular failure. Fenoldopam, a vascular dopamine receptor agonist, is also effective and suitable for hypertensive emergencies with renal insufficiency. Fifty percent of the maximal effect is seen within 15 minutes after commencing an IV infusion with maximal BP reduction occurring at about 1 hour. Esmolol is an ultra-short-acting (cardioselective β1-adrenergic blocker) that may be given by constant infusion (onset of action ˜60 seconds and short duration of action of 10–20 minutes). Its rapid metabolism by an intracytoplasmic red blood cell esterase makes it well suited for critically ill patients with multiorgan failure.

Use oral agents in children with mild manifestations and no evidence of active organ injury.

Clonidine, an oral agent with a rapid onset of effect (about 15–30 minutes), is useful in the acute setting, particularly in hemodialysis patients. Clonidine is minimally removed by hemodialysis and does not require dose adjustment in renal failure. Somnolence and dry mouth are the most common adverse effects. Short-acting nifedipine may cause severe hypotension, palpitations, and headaches and its use has become controversial. Isradipine (dihydropyridine calcium channel blocker) is a useful oral antihypertensive with a rapid onset of action. It reduces BP within 1 hour of administration with a peak effect in 2 to 3 hours. Isradipine has limited effects on myocardial contractility, thus a suitable agent for patients with myocardial dysfunction.

Pearls

1. Infants with severe hypertension will present with poor feeding and respiratory distress.

2. Essential hypertension rarely causes hypertensive emergencies. Look for a renal or renovascular cause.

3. Always take blood pressure readings in all 4 extremities during the initial evaluation to check for vascular diseases (eg, coarctation of the aorta, Takayasu arteritis).

Clinical Summary

The classic presentation of sudden, debilitating flank pain due to urinary tract stones seen in adults is uncommon in children. Nonetheless, some form of abdominal, flank, or pelvic pain is present in about 50% of children, usually those who are older. Gross or microscopic hematuria is found in 33% to 90% of children with urolithiasis and occurs equally across age groups. Frequently, UTI is the presenting sign of urolithiasis in preschoolers. Approximately 78% of pediatric stones are located in the kidney, and the most common types, in order of frequency, are calcium oxalate, calcium phosphate, and struvite. The differential includes acute appendicitis, pyelonephritis, ectopic pregnancy, ovarian torsion, ovarian cyst, diverticulitis, musculoskeletal pain, peritonitis, bowel obstruction, Henoch-Schönlein purpura, renal papillary necrosis, and biliary colic.

Emergency Department Treatment and Disposition

Obtain urinalysis, CBC with differential, electrolytes, BUN, creatinine, and in postmenarchal girls, a urine pregnancy test. Presence of leukocyte esterase and nitrites in the urine suggests infection. Review the microscopic findings for white blood cells, bacteria, and number of epithelial cells. If UTI is suspected by history or urinalysis, take a urine culture. Send any “passed” stones for analysis and instruct the patients to keep any stones they pass at home (use urine strainers or paper coffee filters to strain urine). Order abdominal radiograph, which will reveal all large stones except pure uric acid stones. Renal ultrasound is a valuable imaging technique for detecting renal stones and usually allows visualization of calculi ≥3 mm and acute obstruction. Noncontrast CT is the imaging modality of choice for the diagnosis of urolithiasis; advantages include rapid examination, lack of IV contrast, ability to determine size accurately, and detect other conditions that may mimic nephrolithiasis.

Consult pediatric nephrologists and urologist as indicated. Admit patients with an obstructing stone and evidence of infection for decompression and IV antibiotics, patients with intractable vomiting and/or pain, single functional kidney, or history of transplantation with obstruction. Provide IV fluids to patients with clinical dehydration secondary to vomiting and decreased oral intake. Make a priority of rapid and adequate pain control.

Up to 50% of children will spontaneously pass stones within 2 weeks of diagnosis. Otherwise, removal of obstructing calculi can be performed through shock wave lithotripsy, percutaneous nephrolithotomy, or cystoscopy and ureteroscopy for bladder and ureteral stones, respectively. Long-term prevention of stones depends on the exact metabolic abnormality and often includes increasing water intake and decreasing salt intake.

Pearls

1. In the United States, urinary calculi in children occur more often from metabolic disorders; in Europe, they occur more frequently in children with UTI.

2. Calcium oxalate stones are the most common.

3. Uric acid stones are radiolucent stones.

4. Calcium oxalate crystals associated with an anion gap metabolic acidosis may indicate possible ethylene glycol ingestion.

5. Calcium phosphate stones occur with distal renal tubular acidosis, type I.