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38: Renal & Genitourinary Emergencies

Scott A. McAninch; Scott A. Letbetter

IMMEDIATE MANAGEMENT OF LIFE-THREATENING CONDITIONS

OLIGURIA/ANURIA & ACUTE KIDNEY INJURY

Anuria or oliguria is characterized as decreased urine output (< 1 mL/kg/hr in infants, < 0.5 mL/kg/hr in children) due to a decrease in glomerular filtration rate (GFR), resulting in varying degrees of acute kidney injury (AKI), also known as acute renal failure. AKI may be nonoliguric, where urine output is normal or increased. Decreased GFR in AKI results in changes in body fluid composition, blood pressure, and regulation of electrolytes and nitrogenous waste. Complications include hyperkalemia, uremia with neurologic sequelae, severe hypertension with fluid overload, pulmonary edema, and hypertensive encephalopathy.

AKI is categorized by the underlying etiology: prerenal, renal (intrinsic), postrenal in origin. Prerenal causes are conditions that result in inadequate renal perfusion. Renal causes are due to many etiologies that result in intrinsic injury to the components of the nephron. Insult to the glomerulus, renal tubules, interstitium, and renal vasculature may be due to prolonged hypoperfusion from a prerenal cause, sepsis, or nephrotoxins. Postrenal causes are typically due to a urinary tract obstruction distal to the kidneys, which may be congenital or acquired. AKI due to postrenal causes generally requires bilateral urinary tract obstruction, or obstruction to a known or undiagnosed solitary kidney. Neurogenic bladder and medications may cause urinary retention and AKI. Table 38–1 lists causes of AKI.

Table 38–1.Causes of acute kidney injury in children.
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Table 38–1. Causes of acute kidney injury in children.

Prerenal causes

Hypovolemia

  • Gastrointestinal losses, urinary losses (diabetes mellitus), skin losses (burns), traumatic hemorrhage, gastrointestinal bleed

  • Decreased effective circulation from congestive heart failure (CHF), nephrotic syndrome, cirrhosis, sepsis

  • Decreased arterial pressure due to low cardiac output

Intrarenal (intrinsic) causes

Glomerular disease

  • Glomerulonephritis (GN) (poststreptococcal, Henoch-Schönlein purpura nephritis, immunoglobulin A nephropathy, systemic lupus erythematosus nephritis)

  • Nephrotic syndrome

Acute tubular necrosis (ATN)

  • Due to prolonged hypoperfusion from prerenal AKI

  • Nephrotoxins: aminoglycosides, acyclovir, IV contrast, hemoglobinuria, myoglobinuria, ethylene glycol, uric acid from tumor lysis syndrome

  • Interstitial nephritis due to medications (NSAIDs, beta-lactam ­antibiotics, sulfonadmides, thiazide diuretics) and pyelonephritis

Renal vasculature

  • Hemolytic uremic syndrome (HUS)

  • Thrombosis of the renal artery or vein

Postrenal causes

  • Congenital obstructions (posterior urethral valves)

  • Acquired obstructions from renal stones, urinary blood clots, extrinsic compression (abdominal lymphoma, rhabdomyosarcoma, renal tumor)

  • Neurogenic bladder, medication causing bladder spasm

Clinical Findings

The clinician should attempt to identify the cause of the AKI, and uncover and treat life-threatening complications. A meticulous history of chronic medical conditions, recent illnesses, medications, intravenous (IV) contrast exposure should be obtained to elicit specific etiologies of AKI. Patients may present with decreased or no urine output, or be referred for evaluation of abnormal creatinine or urinalysis (UA) results.

Patients with prerenal causes of AKI often appear dehydrated with signs of intravascular depletion and poor perfusion. History of streptococcal pharyngitis or skin ...

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