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Oliguria Clinical Presentation

  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
 
Updated: Jun 10, 2014
 

History

Careful evaluation of the patient's history and physical examination often reveals the cause of oliguria. This is especially important in prerenal and postrenal processes because early diagnosis and treatment frequently results in complete recovery.

Fluid losses

A recent history of diarrhea or vomiting should be sought because this is the most common cause in children.

Less commonly, fluid loss may result from traumatic hemorrhage or burns or following polyuric states, such as diabetes insipidus and diabetes mellitus.

The loss of intravascular fluid volume into the interstitial space accompanies surgery, shock syndromes, and nephrotic syndrome. Children with fluid losses may report thirst, dizziness, palpitations, and fatigue, and a history of weight loss may be present.

Drugs

A detailed history of all recent medications should be obtained. In the presence of mild prerenal insufficiency, the administration of medications that impair renal autoregulation can precipitate oliguric acute kidney injury.

Cyclosporine, tacrolimus, and contrast agents are direct afferent arteriolar constrictors that interfere with the myogenic response.

NSAIDs inhibit the renal synthesis of vasodilatory prostaglandins. They are an important cause of oliguric acute kidney injury when administered to febrile children with intercurrent dehydration.

Drugs that induce direct tubular necrosis include aminoglycosides, amphotericin B, cyclosporine, tacrolimus, antineoplastic agents (eg, methotrexate, cisplatin), and contrast agents. Acyclovir and sulfonamides can precipitate within the tubular lumen and result in obstruction.

In addition, a large number of medications, especially penicillins, cephalosporins, sulfonamides, ciprofloxacin, NSAIDs, and diuretics, can cause interstitial nephritis.

Endogenous tubular toxins

These include the following:

  • Myoglobin - Released following crush injuries, myositis, and prolonged grand mal seizures
  • Hemoglobin - Hemolysis
  • Uric acid - Tumor lysis syndrome

Diet

A history of ingesting undercooked meat may suggest the presence of hemolytic-uremic syndrome in a child with bloody diarrhea.

Symptoms of glomerular disease

Many children have a history of gross hematuria and edema. An antecedent streptococcal infection may suggest a postinfectious glomerulonephritis, and a history of bloody diarrhea often precedes the hemolytic-uremic syndrome.

Suspect systemic lupus erythematosus or allergic interstitial nephritis in children with fever, joint symptoms, and skin rashes who present with oliguria.

A history of recurrent sinusitis or lower respiratory tract infections may suggest Wegener granulomatosis, and hemoptysis may suggest Goodpasture disease.

Symptoms of urinary tract obstruction

These symptoms include the following:

  • Complete absence of urine output
  • Alternating periods of polyuria and oligoanuria
  • Poor urinary stream or dribbling

Symptoms of chronic renal failure

Although oliguria is usually acute at initial presentation, it may also be a presenting symptom of chronic renal failure. Children may have additional symptoms suggestive of previous renal disease, including the following:

  • Frequent urinary tract infections
  • Hematuria
  • Proteinuria
  • Hypertension
  • Edema
  • Fatigue
  • Pallor
  • Anorexia
  • Bone pain
Next

Physical Examination

Signs of intravascular volume depletion

The following may be noted:

  • Tachycardia
  • Orthostatic hypotension
  • Decreased skin turgor
  • Dry mucous membranes

Signs of acute kidney injury

Children may present with edema, anemia, and signs of congestive heart failure, such as hepatomegaly, gallop rhythm, and pulmonary edema.

Hypertension is common, especially in acute glomerulonephritis, and may be secondary to volume overload and alterations in vascular tone.

Although many children with hypertension are asymptomatic, encountering patients with signs of congestive heart failure, visual disturbances, or encephalopathy is not uncommon.

Signs specific to the underlying renal disease

A butterfly rash on the face and joint swelling are highly suggestive of systemic lupus erythematosus.

Patients with Henoch-Schönlein purpura present with a characteristic purpuric rash over the buttocks and the extensor surface of the lower extremity.

Acute interstitial nephritis may be accompanied by fever, arthralgias, and fleeting, maculopapular or urticarial rashes. Various skin rashes may be detected in vasculitides.

Oliguria with palpable kidneys during infancy suggests renal vein thrombosis, polycystic kidneys, multicystic dysplasia, or hydronephrosis. In older children, enlarged kidneys should also raise the suspicion of tumors. A transplanted kidney that is tender to palpation is indicative of rejection.

Signs of postrenal failure

Poor urinary stream, urinary dribbling, and a palpably enlarged urinary bladder are indicative of obstruction. The external genitalia may reveal meatal stenosis or urethral trauma.

The diagnosis of obstruction may be strengthened by the reestablishment of urine output after the gentle passage of a catheter. Patients with indwelling urinary catheters who develop oliguria should undergo flushing of the catheter to rule out blockage.

Signs of chronic renal failure

The following may be noted:

  • Poor growth
  • Hypertension
  • Edema
  • Anemia
  • Renal osteodystrophy
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Contributor Information and Disclosures
Author

Prasad Devarajan, MD, FAAP Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of the Nephrology Fellowship Program, Medical Director of the Kidney Stone Center, Co-Director of the Institutional Office of Pediatric Clinical Fellowships, Director of Clinical Nephrology Laboratory, CEO of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

Prasad Devarajan, MD, FAAP is a member of the following medical societies: American Heart Association, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, Society for Pediatric Research

Disclosure: Received none from Coinventor on patents submitted for the use of NGAL as a biomarker of kidney injury for none.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Acknowledgements

Laurence Finberg, MD Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Luther Travis, MD Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine

Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Pathogenesis of prerenal failure
Compensatory mechanisms for preventing a fall in glomerular filtration rate (GFR) in the presence of prerenal failure
Mechanisms of intrinsic acute renal failure.
 
 
 
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