Deborah R. Liu
Renal emergencies in children represent a large and varied group of disease processes. This chapter covers common renal emergencies, including acute renal failure (ARF) in children, acute glomerulonephritis, and nephrotic syndrome.
For discussion of other renal emergencies, see the following topics and chapters: end-stage renal disease (Chapter 54, Emergencies in Renal Failure and Dialysis Patients), urolithiasis (Chapter 56, Urologic Stone Disease), hypertension (Chapter 28, Hypertension), Henoch-Schönlein Purpura (Chapter 76, Pediatric Abdominal Emergencies), hemolytic uremic syndrome (Chapter 135, Evaluation of Anemia and the Bleeding Patient), and hematuria (Chapter 55, Urinary Tract Infections and Hematuria).
ACUTE RENAL FAILURE
ARF is the abrupt loss of renal function such that body fluid homeostasis is no longer maintained.
Mortality among children with ARF ranges from 8% to 89% and varies by cause.
Common causes of ARF in children include severe dehydration, sepsis, pyelonephritis, hemolytic uremic syndrome, acute glomerulonephritis, postoperative complications, and posterior urethral valves in boys.
CLINICAL FEATURES
Patients present with symptoms of the underlying cause (eg, bloody diarrhea and abdominal pain in hemolytic uremic syndrome; or fever, hypotension, and petechiae in sepsis).
Ultimately, the patient manifests symptoms and signs of renal failure: nausea and anorexia due to uremia, headache from hypertension, edema (periorbital, scrotal or labial, dependent, or generalized), weight gain, and decreased urine output.
DIAGNOSIS AND DIFFERENTIAL
ARF may be anatomically categorized as prerenal, renal, or postrenal in etiology. Table 88-1 lists common causes of renal failure in infants and children.
Urinalysis helps distinguish among the three forms of ARF and should be obtained along with microscopic evaluation. Children who are not toilet trained or in those with significantly decreased urine output require catheterization to obtain urine.
Prerenal causes of ARF are associated with little blood or protein on urinalysis, but typically manifest high urine specific gravity (≥1.025).
Children with acute tubular necrosis typically have granular casts on urinalysis but usually have a normal specific gravity.
Glomerulonephritis and other glomerular disease are characterized by hematuria and proteinuria.
A positive urine dipstick test for blood without red blood cells on microscopy suggests hemoglobinuria or myoglobinuria.
Basic blood tests such as serum electrolytes, BUN and creatinine, as well as a complete blood count (CBC) should be obtained in all cases of ARF to help identify the cause and guide management. Additional blood tests may be indicated depending on the clinical scenario.
TABLE 88-1 Causes of Renal Failure in Infants and Children
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The goals of treatment for ARF are to identify the underlying cause of renal failure and to correct fluid and electrolyte imbalances.
Address life-threatening complications, such as severe hyperkalemia (see Chaps. 6 and 83) or hypertensive emergency (see Chapter 28) immediately.
Consult a pediatric nephrologist for most cases of ARF as many cases require inpatient admission. Treatment recommendations for prerenal ARF, intrinsic renal failure, and postrenal failure are listed in Table 88-2.
Treat hypertension with antihypertensive agents as described in Chapter 28.
For postrenal (obstructive) ARF, insert a Foley catheter to relieve the obstruction (see also Table 88-2).
When conservative measures fail, acute renal replacement therapy (dialysis) should be considered.
Indications for dialysis include severe electrolyte abnormalities, fluid overload not relieved by administration of loop diuretics, and intractable metabolic acidosis not responding to bicarbonate therapy.
Peritoneal dialysis is the preferred method of acute dialysis for children, because it is inexpensive and requires less expertise to perform than hemodialysis.
TABLE 88-2 Emergency Management of Children with Acute Renal Failure
ACUTE GLOMERULONEPHRITIS
Glomerulonephritis is an inflammatory process affecting the glomerulus.
Acute glomerulonephritis is characterized by hema-turia and proteinuria. There are many causes of acute glomerulonephritis, including postinfectious etiologies, the most common of which follows infection with group A β-hemolytic streptococcus. Other less frequent causes include Henoch-Schönlein purpura, hemolytic uremic syndrome, systemic lupus ery-thematosus, IgA nephropathy, and Goodpasture’s syndrome.
CLINICAL FEATURES
Patients typically present with sudden onset of brown, tea-colored, or grossly bloody urine. Patients may also note foamy urine due to proteinuria.
Other symptoms include decreased urine output, headaches due to hypertension, or peripheral edema.
In post-streptococcal glomerulonephritis, there may be a history of sore throat 1 to 2 weeks preceding urinary symptoms.
The physical examination can be completely normal, or may demonstrate hypertension, edema, or signs of congestive heart failure.
DIAGNOSIS AND DIFFERENTIAL
The diagnosis of glomerulonephritis is made by examination of the urine. The urinalysis shows hema-turia and proteinuria (usually at least 2+ protein [100 milligrams/dL] on the urine dipstick). Red blood cell casts are seen on microscopy.
Additional laboratory testing should include a CBC, electrolytes, BUN and creatinine, and urine culture (infection may present as hematuria with proteinuria).
Further evaluation for post-streptococcal glomerulonephritis includes antistreptolysin O titers and C3 and C4 complement levels.
Serum albumin, triglycerides, and cholesterol should be obtained to help differentiate acute glomerulonephritis from nephrotic syndrome.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The treatment of glomerulonephritis is determined by the underlying cause.
Address hypertensive emergencies first.
Patients with new-onset glomerulonephritis and olig-uria or hypertension usually require admission.
Patients with mild disease may be discharged home on a low-sodium diet with monitoring of fluid intake and with close follow-up with a pediatric nephrologist.
NEPHROTIC SYNDROME
Nephrotic syndrome is a chronic disease in children characterized by increased permeability of the glomerular capillary wall, with resulting urinary loss of protein.
Nephrotic syndrome is characterized by significant proteinuria, hypoproteinemia, edema, and hyperlipidemia.
Nephrotic syndrome can be divided into primary (only affecting the kidney) or secondary (multisystem disease with kidney involvement) nephrotic syndrome.
The most common form of primary nephrotic syndrome is minimal change disease.
Other causes include focal glomerulosclerosis, mesangial proliferative glomerulonephritis, and mem-branoproliferative glomerulonephritis.
Secondary forms of nephrotic syndrome include lupus, Henoch-Schönlein purpura, sickle-cell disease, and drug or toxin exposure (eg, heavy metals).
CLINICAL FEATURES
Patients typically present with edema, which may involve the face, abdomen, scrotum or labia, or extremities.
Because facial swelling or puffy eyes are not specific symptoms, patients are easily misdiagnosed as having an allergic reaction.
The patient or parent may note foamy urine (proteinuria) or dark urine (hematuria).
Extreme hypoproteinemia can cause pleural effusions with associated shortness of breath or orthopnea; abdominal ascites can cause pain, nausea, vomiting, or anorexia.
DIAGNOSIS AND DIFFERENTIAL
Diagnostic criteria include edema, heavy proteinuria (usually 3+ [300 milligrams/dL] or 4+ [2000 milligrams/dL] on urine dipstick testing), and hypoproteinemia (serum albumin <3.0 grams/dL). Hypercholesterolemia (>200 milligrams/dL) is classically seen with nephrotic syndrome, although an inconsistent finding.
Further testing is useful to distinguish primary from secondary nephrotic syndrome, and may include serum antinuclear antibody, serum immunoglobulins, screening for sickle-cell disease, or serum complement levels.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Fluid management in the nephrotic patient can be challenging. Patients may be intravascularly depleted but have signs of fluid overload (edema).
Mild cases of nephrotic syndrome do not require fluid resuscitation. Treatment of most cases of nephrotic syndrome should be performed in consultation with a pediatric nephrologist.
Treat hypovolemic shock with 20 mL/kg normal saline, even in the setting of severe edema.
Treat mild to moderate dehydration with small but frequent amounts of a low-sodium oral solution.
Treat volume overload and edema with furosemide 1 milligram/kg/dose. If the serum albumin is extremely low, administer 25% albumin (0.5–1 g/kg) over 4 hours followed by furosemide 1 to 2 milligrams/kg IV (higher dose of furosemide may be needed in this setting).
Definitive treatment of nephrotic syndrome often includes oral corticosteroids; however, this should be initiated only after consultation with a pediatric nephrologist.
Many patients with nephrotic syndrome can safely be discharged home on a low-salt diet with close follow-up.
Indications for admission include severe edema (eg, pulmonary effusion or ascites causing respiratory symptoms), symptomatic hypertension, suspected bacterial infection (eg, spontaneous bacterial peritonitis with ascites), significant intravascular dehydration, and renal insufficiency.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 128, “Renal Emergencies in Infants and Children,” by Christine E. Koerner.