Pediatric Urology Clinics: Red Urine in an 8-Year-Old Boy

Consultant for PediatriciansConsultant for Pediatricians Vol 23 No 5
Volume 23
Issue 5

An 8-year-old boy is assessed on the same day that he passed red-colored urine. The boy first noted the abnormal-colored urine when he voided on awakening.


An 8-year-old boy is assessed on the same day that he passed red-colored urine. The boy first noted the abnormal-colored urine when he voided on awakening.

The boy had been delivered vaginally at term after an uncomplicated pregnancy. He was routinely circumcised in the neonatal period. He was growing and developing normally. About 2 weeks before he passed the red urine, he had experienced an upper respiratory tract infection. There was no history of recent skin infection. His history was otherwise unremarkable.

Specific questioning revealed that the urine was passed without discomfort. The mother offered that the urine looked "tea-colored." There was no history of frequency, urgency, or incontinence. The upper respiratory tract symptoms he experienced 2 weeks before passing the abnormal-colored urine had resolved promptly. The boy did not currently have nasal congestion, sore throat, or fever. There was no history of bruising, rash, headache, abdominal pain, or joint pain or swelling. There was no family history of blood in the urine, deafness, bleeding tendency, or kidney stones.

Physical examination revealed a healthy-appearing pre-adolescent in no apparent distress. His blood pressure was 120/85 mm Hg in the right arm (taken while he was sitting). He did not have periorbital or ankle edema. His heart sounds were normal and his chest was clear to auscultation. His kidneys and bladder were normal to palpation. The urethral meatus looked elliptical, was of nor- mal caliber, and was not inflamed. Results of the phys-ical examination were otherwise unremarkable.

The boy was able to void during the clinic visit. The urine in the container looked cloudy and-- when held up to the light--had a greenish tinge. The dipstick revealed a urine pH of 6 and a specific gravity of 1.024: the urine tested 2+ for protein and was strongly positive for blood. The microscopic urinalysis revealed 50 to 100 red blood cells, 2 to 4 white blood cells, and 1 to 2 granular casts per high-power field.


A. Advise the mother to limit the child's saltand fluid intake.

B. Request a first-morning urine specimen forbright field and phase-contrast microscopy.

C. Order a complete blood cell count; anantistreptolysin O test (ASOT); and bloodlevels of complement 3 (C3), electrolytes,and total protein and albumin. Also, obtaina throat swab for group A -hemolyticstreptococci (GABHS).

D. Request a follow-up visit the next day toreassess the child.

E. All of the above.

The passage of painless, tea-colored urine and the presence of significant, albeit mild, hypertension suggest acute glomerulonephritis (AGN).


Fluid overload is a serious cause of morbidity and possible mortality in children with AGN. Limiting salt and water intake will help prevent an increase in blood pressure and possible attendant CNS and myocardial complications--including hypertensive encephalopathy and congestive heart failure with pulmonary edema. Families should be instructed to encourage small (1- to 2-oz) portions of drinks, to limit the total 24-hour fluid intake to less than 0.5 to 1 L, and to not add salt to the diet or offer exceptionally salty foods.

An active urinary sediment that includes red blood cells, white blood cells, and granular casts suggests--but does not confirm--a diagnosis of AGN. The hallmark findings in AGN are red blood cell casts and a high percentage of dysmorphic red blood cells, which are observed best by phase-contrast microscopy. A first-urine morning specimen generally contains a larger volume and is more concentrated, and therefore it offers a better opportunity to witness these diagnostic features.

Measurement of serum creatinine and urea is necessary to estimate the glomerular filtration rate (GFR), which is often reduced in AGN. These measurements also serve as a baseline for follow-up during the acute illness. Assays of serum electrolytes are necessary to determine the serum potassium level, which might be elevated if the GFR is decreased, and which might require specific therapy--such as a reduced dietary intake of potassium or diuretic therapy to increase urinary losses.

Measurement of serum total protein and albumin is also important to determine whether the urinary protein losses are sufficient to consider a nephrotic syndrome presentation. The ASOT and throat swab provide important evidence of preceding infection with GABHS, which, if present, suggests post-streptococcal glomerulonephritis (PSGN)--the most common cause of AGN in childhood.1 Determination ofC3 is important to look for evidence of hypocomplementemia, which supports a diagnosis of PSGN.

A follow-up the next day is essential to check the patient's blood pressure, to assess for other evidence of evolving fluid overload, to review the laboratory results with the family, and to plan ongoing follow-up.

At follow-up the next day, the boy states that he is voiding as often as usual, still with tea-colored urine. His blood pressure is now 130/90 mm Hg; he has no periorbital or ankle edema, but his weight has increased 0.7 kg since the day before. Heart sounds are normal, the chest is clear, and findings from the neurologic examination are normal. The laboratory tests reveal the following levels: a modestly elevated serumcreatinine and BUN; normal electrolytes, total protein, and albumin, an elevated ASOT; and a low C3. Results of the throat swab are pending.


A. Counsel the family and boy again on theimportance of fluid and salt restriction.

B. Start furosemide, 1 mg/kg q12h.

C. Continue to monitor the boy closely, at leastevery 1 to 2 days during the acute illness.

D. Repeat measurements of the serum C3level after 3 months to make sure it hasnormalized.

E. All of the above.


We recommend all of the above measures.

The increased blood pressure and weight gain suggest that the boy has not complied with the fluid and salt restriction, that the salt and water retention associated with the AGN has increased, or that both of these factors are at play. Careful salt and fluid restriction is important.

Furosemide, a loop diuretic, is usually very effective and might be all that is necessary to control the blood pressure and fluid overload. If the blood pressure does not improve at 24-hour follow-up, an antihypertensive medication--such as a calcium channel blocker or a converting enzyme inhibitor--will need to be added.

Close follow-up is necessary to continue to monitor the blood pressure and other aspects of the fluid status, to monitor the GFR and serum potassium level, and to otherwise monitor the patient's clinical status. Careful outpatient follow-up can obviate the need for hospital admission.

In patients with PSGN, the gross hematuria and reduced GFR generally resolve over several weeks. The hypertension resolves over 2 to 6 weeks. The C3 level becomes normal within 3 months, but microscopic hematuria and proteinuria can persist for up to a year. Failure of the C3 level to return to normal suggests membranoproliferative glomerulonephritis (MPGN), a distinct and chronic glomerulonephritis that can present in a fashion identical to that of PSGN. MPGN has an appreciably poorer prognosis and carries the risk of chronic renal failure.


The gross hematuria in this child lasted 10 days. Normalization of creatinine and urea levels was coincident with the clearing of gross hematuria. The hypertension required the addition of a calcium channel blocker; this therapy was maintained for several weeks. The dosage was slowly tapered and the drug discontinued over several more weeks. The furosemide dosing was reduced to once a day after the gross hematuria resolved and was discontinued a week later.

At 3-month follow-up, the child felt well. His blood pressure was normal, as were levels of creatinine, urea, and C3. His urine still showed 5 to 10 red blood cells per high-power field, but there was no protein. Microscopic hematuria was still present at 6-month follow-up but had disappeared by 12-month follow-up.



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