Proteinuria
Asymptomatic Proteinuria
Always verify true proteinuria with quantification by urine protein/creatinine ratio. This value is determined by obtaining urine protein mg/dl and creatinine mg/dl on any urine specimen. The urine protein divided by the urine creatinine (protein/creatinine ratio) is normal at 0.2 or less. If elevated on 2 samples, 2 weeks apart, proceed with work-up.
Please note: If the first sample has a ratio greater than 1, repeat in 2-3 days since rapid increase may herald nephrotic syndrome.
First rule out benign postural or orthostatic proteinuria by obtaining the second urine sample in the following way: Have the child empty the bladder immediately before getting into bed (not one or two hours before), and collect the urine specimen immediately on waking up (not after being up and around). If the protein/creatinine ratio on this specimen is normal, no further work up is needed.
Non-postural proteinuria work up includes serum creatinine, BUN and renal/urinary tract ultrasound.
If hydronephosis is found, a VCUG should be done with referral to urology.
Mild elevations in urine protein/creatinine (less than 0.5) with an otherwise negative work-up may be followed by the PCP with repeat of urine protein/creatinine and clinical assessment in 6 months as spontaneous improvement could occur.
Referral to nephrology is needed at any time for increasing proteinuria, associated hypertension or elevation in serum creatinine. Of course referral may be made at any time for parental or clinician preference.
Nephrotic Syndrome
Proteinuria (3+ or greater on dipstick) associated with hypoalbuminemia, edema due to low serum oncotic pressure and hyperlipidemia constitutes the nephrotic syndrome. Hyperlipidemia is an expected part of the “syndrome” but does not play a physiologic role in the clinical symptoms of edema, pre-renal azotemia (variable) and hypertension (variable).
Usually the protein/creatinine ratio is 3 or more, but it is not absolutely necessary to diagnose the nephrotic syndrome, if accompanied by hypoalbuminemia.
Mild increase in serum creatinine suggests the pre-renal effect of third spacing intravascular volume. Pulmonary edema is usually not present, as excess intravascular volume is generally not present, but small pleural effusions may be seen. Hypertension may be present and should be treated.
In children, treatment of the nephrotic syndrome is immediately begun with prednisone, with the presumption of “minimal change disease” as the underlying histologic diagnosis. Mild presentations (depends on the degree of hypoalbuminemia and /or edema and the degree of hypertension) are often managed as outpatients, and by PCPs with nephrologic guidance.
A child who is not tolerating severe edema may be helped by the infusion of 25% albumin and subsequent, physiologic diuresis (may be aided by diuretics like furosemide). Restoration, even partially, of oncotic pressure should at least temporarily – since the protein will be again lost by the kidneys until remission occurs – improve clinical symptoms related to third spaced fluids and intravascular volume contraction.
This therapy is frequently administered in an Emergency Department setting, and can be provided PRN until there is a response to the prednisone (1-3 weeks). A serum albumin of at least 2.5g/dl is generally well tolerated. Complicated or difficult cases (and of course when there is parental need) should be referred to nephrology in a timely fashion.