++
Proteinuria can be divided into four basic etiologies: glomerular (increased glomerular permeability), tubular (decreased tubular reabsorption), overflow (excess production exceeding normal kidney capabilities), and postrenal (inflammation in the urinary tract).
++
Examine patient to gauge severity of protein loss and to look for underlying causes.
Because most cases are functional, examination is often normal.
Significant proteinuria leads to edema, ranging from dependent peripheral edema to anasarca (protein wasting in urine → decreased plasma oncotic pressure → increased interstitial fluid).
Ask about history of recent viral or systemic illness, change in medications, hypertension, diabetes, cardiac, or renal disease, and any signs of systemic illness (weight loss, fatigue, etc).
++
Blood urea nitrogen (BUN)/creatinine (Cr) should be obtained to gauge underlying renal function.
Proteinuria in combination with other urinalysis findings may be markers of disease:
Red blood cell (RBC) casts and hematuria → glomerulonephritis (GN)
Fatty casts or oval fat bodies → nephrotic syndrome
White blood cells (WBCs), WBC casts without bacteria → interstitial nephritis
Hyaline casts → benign causes
Frequent false-positive proteinuria within 24 hours of iodinated radiocontrast agents, in setting of highly alkaline urine, in presence of gross hematuria, or in presence of specific antiseptics (eg, chlorhexidine, benzalkonium).
++
Patients may be referred for primary care provider follow-up in the absence of edema, azotemia, hypertension, or evidence of systemic illness affecting the kidneys.
Persistent proteinuria may require referral to a nephrologist, possibly for renal biopsy.
++
KEY FACT
Nephrotic syndrome: proteinuria, hypoalbuminemia, edema, hyperlipidemia, hypercoagulability.
++
A form of glomerular proteinuria in which protein losses exceed the liver’s capacity to synthesize albumin, resulting in hypoalbuminemia and subsequent systemic effects. It may be caused by a primary glomerular disease process or secondary to diabetes, lupus, etc.
++
++
Based on characteristic clinical and laboratory findings
Fatty casts or oval fat bodies on UA: possibly related to associated hyperlipidemia.
Hypoproteinemia and hypoalbuminemia.
BUN and Cr are often normal.
++
Symptomatic: Fluid restriction, intravenous (IV) diuretics, BP control with angiotension-converting enzyme (ACE) inhibitors.
Corticosteroids may reverse or delay disease progression.
++
Increased risk of thrombosis—deep vein thrombosis and renal vein thrombosis (hematuria, flank pain, and worsening renal function)
++
Q
A 5-year-old boy presents to the emergency department (ED) with 3 days of “brown urine” and facial swelling. One week earlier he had experienced a fever ...