Renal Failure, Acute
Renal Failure, Acute: Excerpt from The 5-Minute Pediatric Consult
Lawrence Copelovitch, MD
Renal Failure, Acute - BASICS
Renal Failure, Acute - description
- Acute renal failure (ARF) is defined as a sudden decrease of normal kidney function that compromises the normal renal regulation of fluid, electrolyte, and acid–base homeostasis.
- In practical terms, ARF is characterized by a reduction in the GFR that results in an abrupt increase in the concentrations of serum creatinine and BUN.
- Acute kidney injury (AKI) is defined as any insult to the kidney, regardless of whether or not there is a rise in serum creatinine.
- AKI often precedes ARF and goes undetected.
- In ARF the urine output is variable: Anuria, oliguria, and in some cases polyuria can all be observed at presentation.
- Oliguria: Urine output <0.5 mL/kg/h in infants or <500 mL/1.73 m2/d in older children
- Anuria: Total cessation of urinary output
- Polyuria: Urine output >2 L/m2/d in infants and children or 3 L/d in adults
Renal Failure, Acute - epidemiology
- ARF due to acute tubular necrosis is commonly seen in hospitalized patients. The combination of ischemia plus nephrotoxic agents (aminoglycosides, amphotericin B, contrast, chemotherapeutic agents) place these patients at increased risk.
- ARF secondary to dehydration, NSAID toxicity, or medication induced interstitial nephritis is common in the outpatient setting
Renal Failure, Acute - pathophysiology
ARF is commonly precipitated by an ischemic or nephrotoxic event. Initial vasodilatation is followed by intense vasoconstriction, with blood redistributed from the cortex to the juxtamedullary nephrons. Delivery of oxygen to the kidney is impaired, leading to acute tubular necrosis. Intratubular debris and cast formation develop. Tubular fluid leaks backward across the injured tubular membrane, which, in addition to tubular obstruction, causes further hemodynamic changes.
Renal Failure, Acute - etiology
ARF has many causes, which can be subcategorized into 3 groups.
- Prerenal:
- Decreased perfusion of the kidney secondary either to decreased intravascular volume (e.g., dehydration), decreased effective circulating blood volume (e.g., CHF), or from altered intrarenal hemodynamics (e.g., NSAIDs)
- Common form of ARF in children
- Postrenal:
- Obstructive process (either structural or functional)
- Obstruction can reside in the lower tract or bilaterally in the upper tracts (unless the patient has a single kidney)
- This form of renal failure more common in newborns
- Intrinsic: Disorders that directly affect the kidney. This form can be subcategorized as follows:
- Acute tubular necrosis (ATN) is the end result of either ischemic or toxin mediated damage to the tubules. Ischemic induced ATN is the result of prolonged and severe prerenal ARF which is no longer immediately reversible with the restoration of appropriate renal perfusion. Toxin mediated ATN can be caused by many medications (e.g., aminoglycosides), poisons (e.g.,mercury), or endogenous toxins (e.g., myoglobinuria)
- Glomerular disorders include the various forms of acute glomerulonephritis (e.g., postinfectious, rapidly progressive [crescentic]).
- Vascular lesions compromise glomerular blood flow. Hemolytic-uremic syndrome is the most common disorder that causes intrinsic ARF in children.
- Interstitial nephritis most often occurs as a result of exposure to a medication. It may also be associated with infections (e.g., pyelonephritis), systemic diseases, or tumor infiltrates.
Renal Failure, Acute - DIAGNOSIS
Renal Failure, Acute - signs & symptoms
Fever, rash (acute interstitial nephritis, acute glomerulonephritis), bloody diarrhea, pallor (hemolytic-uremic syndrome), severe vomiting or diarrhea (prerenal), abdominal pain (obstruction), hemorrhage, shock (acute tubular necrosis), anuria (acute glomerulonephritis, obstruction), polyuria (acute tubular necrosis, acute interstitial nephritis)
Renal Failure, Acute - history
- Previous infection (acute glomerulonephritis), neurogenic bladder, single kidney (obstruction)
- Therapy with nonsteroidal anti-inflammatory agents, β-lactam antibiotics, acyclovir (acute interstitial nephritis), nephrotoxic drugs (e.g., aminoglycosides, amphotericin B, cisplatin [acute tubular necrosis])
- Toxins: Exposure to heavy metals, organic solvents (acute tubular necrosis)
- Gross hematuira: Glomerulonephritis (tea colored), renal calculi (bright red blood)
- Positive family history of hemolytic-uremic syndrome
- Trauma: Crush injury (acute tubular necrosis)
- Review of symptoms: Various systemic symptoms (acute glomerulonephritis)
Renal Failure, Acute - physical exam
- General: Weight hydration, shock (i.e., prerenal, acute tubular necrosis), edema (e.g., acute glomerulonephritis), jaundice (i.e., hemolytic-uremic syndrome, acute tubular necrosis)
- Eyes: Uveitis (i.e., acute interstitial nephritis)
- Lungs: Rales (i.e., acute glomerulonephritis)
- Heart: Gallop (i.e., acute glomerulonephritis)
- Abdomen/Pelvis: Mass (i.e., obstruction)
- Skin: Rash (i.e., acute interstitial nephritis, acute glomerulonephritis), petechia (i.e., hemolytic-uremic syndrome)
- Joints: Arthritis (i.e., acute glomerulonephritis)
Renal Failure, Acute - tests
Renal Failure, Acute - lab
- All patients with ARF should have a urinalysis with microscopic examination, serum chemistries and a CBC:
- Urinalysis: Specific gravity (>1.020 suggests prerenal ARF), proteinuria ( >3+ intrinsic, glomerular ARF), eosinophiluria (acute interstitial nephritis), pyuria (pyelonephritis), granular casts (prerenal, acute tubular necrosis), pigmenturia (i.e., acute tubular necrosis), erythrocyte casts (glomerulonephritis acute interstitial nephritis, acute tubular necrosis)
- Serum chemistries: Hyponatremia, acidosis, hyperkalemia, hyperphosphatemia, hypocalcemia, BUN /creatinine exceeding 20 (i.e., prerenal)
- CBC: Microangiopathic hemolytic anemia, thrombocytopenia (i.e., hemolytic-uremic syndrome), eosinophilia (i.e., acute interstitial nephritis)
- Selected patients require further studies including: Serologies, urine electrolytes, imaging and renal biopsy:
- Serologies: Hypocomplementemia (acute glomerulonephritis), antineutrophil cytoplasmic antibodies (acute glomerulonephritis), antinuclear antibodies (acute glomerulonephritis)
- The fractional excretion of sodium (FE
Renal Failure, Acute - imaging
- Chest radiograph: Cardiomegaly or pulmonary edema (fluid overload)
- Renal ultrasound: Hydronephrosis, trabeculated bladder (i.e., obstruction), increased echogenicity (i.e., acute tubular necrosis, acute interstitial nephritis, acute glomerulonephritis, hemolytic-uremic syndrome), abnormal doppler study (renal venous thrombosis)
Renal Failure, Acute - diag proced-surgery
Renal biopsy: Indicated in patients with prolonged, unexplained ARF or suspicion for crescentic glomerulomehritis
Renal Failure, Acute - differencial diagnosis
- Chronic renal failure: Insidious, associated with poor growth, polyuria, rickets, delayed growth and anemia
- Azotemia (elevated BUN): Hypercatabolic states including corticosteroid therapy or upper GI bleeding
- Elevated creatinine: Caused by rhabdomyolysis, drugs (trimethoprim-sulfa, cimetidine)
Renal Failure, Acute - TREATMENT
Renal Failure, Acute - initial stabilization
- If hypovolemic rapidly establish euvolemia with 0.9% NS blouses
- If urine output remains low after euvolemia is established begin fluid restrition (insensibles and urine output)
- In severe hyperkalemia (>6.5 mEq/L), consider:
- Calcium gluconate (0.5–1.0 mL/kg IV) over 5–10 minutes if severe
- Glucose (0.5 g/kg) and insulin (0.1 U/kg) IV over 30 minutes
- Sodium bicarbonate (1–2 mEq/kg) IV over 10–30 minutes if acidotic
- When administering sodium bicarbonate monitor serum calcium carefully as the hypocalcaemia may worsen.
- Kayexalate (1 g/kg) PO or PR in sorbitol
- Furosemide (1–2 mg/kg) if renal function is adequate
- Hemodialysis or peritoneal dialysis
Renal Failure, Acute - special therapy
- Supportive:
- Establish an effective circulatory volume. If the patient is in shock, administer fluids (e.g., normal saline, lactated Ringer solution) liberally, even if no urine is output.
- Maintain a normal intravascular volume. Carefully monitor urine output and provide appropriate fluids accordingly. Consider fluid restriction and diuretics if the patient suffers volume overload.
- Monitor serum potassium levels frequently. Avoid drugs, fluids, or foods containing potassium in patients with oligouria or anuria.
- Avoid nephrotoxic medications when possible.
- Hyponatremia is usually due to free water excess and should thus be managed with fluid restriction. Hypertonic saline should be used if only CNS symptoms present.
- Hypocalcemia, if mild, may be treated by phosphate restriction. Severe hypocalcemia requires treatment with calcium gluconate (100 mg/kg) given slowly.
- Severe acidosis (pH <7.2) requires supplementation with bicarbonate. However, this may cause hypernatremia, fluid overload, and symptomatic hypocalcemia.
- The effect of aggressive nutritional support is controversial, with the exception of use in a significantly malnourished or hypercatabolic child.
- Hypertension should be treated aggressively if encephalopathy is present.
- Dialysis or hemofiltration is indicated for refractory acidosis, severe hyperkalemia, volume overload, and uremic symptoms (e.g., pericarditis, lethargy, bleeding diathesis), or for the removal of toxins (e.g., uric acid, salicylate).
- Specific:
- Each cause of renal failure may necessitate specific treatment, such as fluid resuscitation (i.e., prerenal), urologic intervention (i.e., obstruction), and corticosteroids (i.e., acute interstitial nephritis, some forms of acute glomerulonephritis).
Renal Failure, Acute - medication
- Excretion and evacuation of many medications is influenced by ARF. Careful attention to drug dosing and levels can minimize toxicity.
- Preventive: Mannitol or furosemide therapy to prevent ARF remains controversial. They may be used prophylactically (e.g., amphotericin B, cisplatin, contrast media) or in cases of hemoglobinuria or myoglobinuria to increase urine flow. Physicians consider this may convert renal failure from oliguric to nonoliguric.
Renal Failure, Acute - FOLLOW UP
- Patients usually remain hospitalized until their renal function improves. Long-term follow-up to monitor sequelae is indicated in patients with prolonged anuria.
- The likelihood of recovery from ARF depends on the amount of urine output and the underlying cause.
- Patients with nonoliguric ARF (e.g., toxin mediated ATN, interstitial nephritis, HUS) have lower complication rates than those with oliguric ARF.
Renal Failure, Acute - prognosis
- Generally, patients with nonoliguric renal failure have a lower mortality rate than patients with oliguria or anuria.
- The mortality rate increases in patients with multisystem organ failure, despite good supportive care.
Renal Failure, Acute - complications
A significant postobstructive diuresis can be seen after treatment for obstructive ARF:
- Fluid overload, resulting in congestive heart failure, hypertension, or hyponatremia
- Hyperkalemia, affecting cardiac function by causing arrhythmias
- Uremia, manifest by mental status changes, increased risk of bleeding, and infection
- Metabolic acidosis
- Hypocalcemia, causing tetany
Renal Failure, Acute - bibliography
- Andreoli SP. Acute renal failure. Curr Opin Pediatr. 2002;14:183–188.
- Flynn JT. Causes, management approaches, and outcome of acute renal failure in children. Curr Opin Pediatr. 1998;10:184–189.
Copelovitch L, Meyers K, Kaplan B. Acute renal failure. In: Docimo S, Canning D, Khoury A, ed The Kilalis-King-Belman Textbook of Clinical Pediatric Urology. Informa Healthcare; New York; 2005:357–365.- Malinoski DJ, Slater MS, Mullins RJ. Crush injury and rhabdomyolysis. Crit Care Clin. 2004;20:171–192.
- Sehic A, Chesney RW. Acute renal failure: Diagnosis. Pediatr Rev. 1995;16:101–106.
- Sehic A, Chesney RW. Acute renal failure: Therapy. Pediatr Rev. 1995;16:137–141.
- Singri N, Ahya SN, Levin ML. Acute renal failure. JAMA. 2005;289:747–751.
- Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med. 1996;334:1448–1460.
Renal Failure, Acute - CODES
Renal Failure, Acute - icd9
584.0 Acute renal failure
Renal Failure, Acute - FAQ
- Q: What is the expected recovery time in patients with ARF who present with anuria?
- A: Recovery time depends on the etiology of the ARF. Children with hemolytic-uremic syndrome may recover in days to weeks. Those with acute tubular necrosis recover days after treatment of the cause. Children whose disorder results from obstruction usually recover as soon as the obstruction is removed.
- Q: When should renal function return to normal?
- A: Renal function may never return to normal in patients with long-standing anuria. In other cases, after recovery occurs, serum creatinine levels return to normal within weeks.
- Q: Which indices should be observed after a patient recovers from ARF?
- A: Patients recovering from ARF should have BPs and urinalysis for proteinuria monitored regularly. Serum creatinine should be measured if the course of ARF was prolonged.
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Book Source Details
- Book Title: The 5-Minute Pediatric Consult
- Author(s): M. William Schwartz MD; et al.
- Year of Publication: 2008
- Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: The 5-Minute Pediatric Consult
Authors: M. William Schwartz MD; et al.
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7577-9
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