Proteinuria

Proteinuriais a common finding in childhood and adolescence.

Usual pathogenesis involves increasein permeability of glomerular basement membrane. Less common isdecreased absorption or increased secretion of protein by renaltubules, which may occur with tubulointerstitial disease.

Although some uncertainty exists aboutnormal rate of protein excretion by the kidney, upper limit of normalestablished by International Study of Kidney Disease in Childrenis 4 mg/m²/hr (Hogget al., 2000).

Based on readings with semiquantitativedipstick method, which measures albumin primarily, the followingranges apply: trace (approx. 15 mg/dL); 1+ (approx.30 mg/dL); 2+ (approx. 100 mg/dL); 3+ (approx.300 mg/dL); and 4+ (>2,000 mg/dL).Normal dipstick reading is considered 0 to trace in concentratedurine specimen with specific gravity of ≥1.020.

Because 24-hr urine protein collectionis difficult to accomplish in infants and children, protein:creatinineratio (mg:mg) in a spot urine, preferably first morning specimen,has been found to accurately reflect 24-hr urine protein excretion.Normal ratio is <0.5 in infants 6–24 mos of ageand <0.2 in children >24 mos of age.

Principal Causes of Proteinuria

1. Functional/transientproteinuria
   1. Fever
   2. Strenuous exercise
   3. Extreme cold
   4. Cardiac failure
   5. Seizures
   6. Emotional stress
2. Postural proteinuria (orthostatic)
3. Nephrotic syndrome
4. Tubulointerstitial disease
   1. Refluxnephropathy
   2. Tubulointerstitial nephritis
   3. Fanconi syndrome
   4. Ischemic tubular injury
5. Benign persistent proteinuria

Clinical Features and Diagnosis

Functional/Transient Proteinuria

Fever, exercise, extreme cold, cardiac failure,seizures, and emotional stress can cause transient proteinuria.Diagnosis is usually made by history, physical exam, and clinicalcourse. Proteinuria measured on dipstick is usually <2+.

Postural Proteinuria (Orthostatic)

Occurs when patient is in upright position,not recumbent. Can be transient or persistent and is unusual before7 yrs of age. Long-term prognosis is benign.

Nephrotic Syndrome

Characterizedby proteinuria, hypoproteinemia, edema, and hyperlipidemia.

Congenital (Finnish type) form, whichis autosomal recessive, presents during first 3 mos of life. Mostcommon cause in children is minimal change disease, which most commonlyoccurs at 2–6 yrs of age. Other causes include focal glomerulosclerosis,mesangial proliferative glomerulonephritis, lupus nephritis, anddrug exposure (captopril, lithium, penicillamine, procainamide,NSAIDs).

Initial episode of nephrotic syndromeas well as relapses often follow viral URIs. First sign of generalizededema may be ankle or eyelid edema, and pleural effusions and ascitesalso may occur. UA usually reveals +3 or +4 proteinuria.Although microscopic hematuria can occur, gross hematuria is unusual.Serum albumin is usually <2 g/dL, whereas serumcholesterol and triglycerides are increased. Renal function maybe normal or impaired.

In children <6 yrs of age,in whom minimal change disease is most likely, corticosteroids canbe given as diagnostic and therapeutic trial. Lack of therapeuticresponse with persistence of proteinuria for >4–6wks is indication for renal biopsy.

Tubulointerstitial Disease

Reflux Nephropathy

Occurs asconsequence of vesicoureteral reflux, which is abnormal retrogradeflow of urine from bladder into upper urinary tract.

Proteinuria, hypertension, and chronicrenal insufficiency may occur. History of recurrent urinary tractinfection is frequent.

Combination of renal U/S,voiding cystourethrography, and renal scintigraphy is commonly usedto evaluate reflux and its effects. Reflux may be graded from Ito V, with V being most severe.

Diagnosis is usually clinical and radiologic.

Tubulointerstitial Nephritis

Syndromewith inflammation and damage of tubular and interstitial structuresand relative sparing of glomerular and vascular structures.

Common causes include infection (mostcommonly pyelonephritis and streptococcal infections), drugs (penicillins,sulfonamides, cephalosporins, phenytoin, thiazides, furosemide,allopurinol, amphotericin B, NSAIDs), and idiopathic.

Clinical manifestations vary from mildazotemia to oliguric renal failure. Proteinuria may occur aloneor with hematuria (usually microscopic).

Renal biopsy is necessary for definitivediagnosis, unless serum creatinine begins to decrease followingwithholding of suspected offending agents.

Fanconi Syndrome

This autosomal-dominantdisorder whose gene locus has been mapped to chromosome 15q15.3is characterized by

Generalized dysfunction of proximal tubuletransport causing excessive urinary excretion of amino acids, glucose,phosphate, bicarbonate, and other solutes

Vitamin D–resistant metabolicbone disease (rickets in children)

Clinical features include aminoaciduria,proteinuria, glycosuria, hypokalemia, hypophosphatemia, metabolicacidosis, rickets, and impaired growth.

This syndrome also may be associatedwith cystinosis (most common), galactosemia, hereditary fructoseintolerance, tyrosinemia, Wilson disease, Lowe syndrome, lead poisoning,and drugs (aminoglycosides, cisplatin, valproic acid).

Ischemic Tubular Injury

Acute tubularnecrosis usually occurs as result of prerenal failure or after severehypoxic insult.

UA may be unremarkable or show low-gradeproteinuria and granular casts. There is inability to conserve sodiumand water.

Renal U/S shows normal-sizedkidneys with loss of corticomedullary differentiation, and renalscintigraphy demonstrates decreased renal function.

Benign Persistent Proteinuria

Persistentproteinuria without evidence for postural proteinuria or renal disease.

Renal biopsy is normal or shows minimalnonspecific changes.

This is a diagnosis of exclusion.

Even though this is a benign disorder,follow-up is important because focal glomerulosclerosis may presentsimilarly.

Diagnostic Approach

First stepin evaluation of a child with proteinuria is to determine if thereare any predisposing factors for transient or functional proteinuria(e.g., fever or strenuous exercise).

If history is negative for these factorsand dipstick protein is persistently ≥1+, next step isto do complete UA and determine protein:creatinine ratio in a firstmorning spot urine specimen.

If results of UA are normal and protein:creatinineratio is in normal range, diagnosis is postural proteinuria andno further studies are necessary.

If results of UA are otherwise abnormalor first morning protein:creatinine ratio is above normal, furtherstudies are necessary. Serum electrolytes, creatinine, albumin,and cholesterol as well as blood urea nitrogen should be measured,and renal U/S should be performed. C3 and antinuclear antibody shouldbe considered.

If diagnosis remains uncertain andno chemical or radiographic evidence of renal disease exists, renalbiopsy may be performed or child may tentatively be considered tohave benign persistent proteinuria. If renal biopsy is not performedor is normal, child should be monitored at 6-mo intervals for urinaryand chemical changes indicative of renal disease.

References

1. Barratt TM, et al. Pediatric nephrology,4th ed. Baltimore: Lippincott Williams & Wilkins, 1999.
2. Behrman RE, et al., eds. Nelson textbook of pediatrics,16th ed, Philadelphia: WB Saunders, 2000.
3. Ettenger RB. The evaluation of the child with proteinuria.Pediatr Ann 1994;23:486–494.
4. Feld LG, et al. Evaluation of the child with asymptomaticproteinuria. Pediatr Rev 1984;5:248–254.
5. Hogg RJ, et al. Evaluation and management of proteinuriaand nephrotic syndrome in children: recommendations from a pediatricnephrology panel established at the National Kidney Foundation Conferenceon proteinuria, albuminuria, assessment, detection, and elimination.Pediatrics 2000;105:1242–1249.
6. Norman ME. An office approach to hematuria and proteinuria.Pediatr Clin North Am 1987;34:545–560.
7. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
8. Vehaskari VM, Robson AM. Proteinuria. In: Edelman CMJr, ed. Pediatric kidney disease. Boston: Little, Brown, 1992:531–551.
9. Welch TR. Current management of selected childhoodrenal diseases. Curr Prob Pediatr 1992;22:432–451.
10. West CD. Asymptomatic hematuria and proteinuria inchildren: causes and appropriate diagnostic studies. J Pediatr 1976;89:173–182.
11. Yoshikawa N, et al. Asymptomatic constant isolatedproteinuria in children. J Pediatr 1991;110:375–379.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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