A 28-year-old woman, gravida 1 para 0, at 16 weeks gestation comes to the office for a prenatal visit. The patient feels well and has no concerns. Medical history is significant for recurrent urinary tract infections. Her only medication is a prenatal multivitamin. Blood pressure is 116/68 mm Hg and pulse is 80/min. Physical examination shows no abnormalities and fetal heart tones are normal. Urine dipstick reveals no blood or leukocyte esterase but is positive for protein. Laboratory testing shows the following:
| Serum chemistry | |
| Sodium | 138 mEq/L |
| Potassium | 4.2 mEq/L |
| Bicarbonate | 24 mEq/L |
| Creatinine | 0.6 mg/dL |
| Glucose | 80 mg/dL |
| Liver function studies | |
| Albumin | 4.5 g/dL |
| Total bilirubin | 0.8 mg/dL |
| Alkaline phosphatase | 60 U/L |
| Aspartate aminotransferase (SGOT) | 22 U/L |
| Alanine aminotransferase (SGPT) | 24 U/L |
| Urinalysis | 1+ protein; no cells or casts |
A 24-hour urinary protein excretion is 200 mg. Which of the following processes is most likely contributing to this patient's urinary findings?
Show Explanatory Sources
In pregnancy, blood volume and cardiac output both increase physiologically due to greater metabolic demands and in preparation for expected blood loss with delivery. As a result, the maternal kidneys experience increased renal blood flow and must process greater volumes of plasma through the glomeruli, leading to increased glomerular filtration rate (GFR). During pregnancy, the release of placental hormones also increases glomerular basement membrane permeability, which allows for increased leakage of protein into the tubular lumen, and leads to decreased renal tubular protein resorption. These factors, along with increased GFR, contribute to trace proteinuria (ie, <300 mg/24 hr), which is a normal finding in pregnancy.
(Choice A) Effacement of podocyte foot processes, which occurs in minimal change disease, impairs glomerular filtration and leads to significant proteinuria (eg, 24-hour urinary protein excretion ≥300 mg) and potential nephrotic syndrome (eg, rapid-onset edema) due to selective urinary loss of albumin.
(Choice B) Generalized renal endothelial dysfunction is likely the mechanism of renal insufficiency associated with preeclampsia, which typically presents with new-onset hypertension and a 24-hour urinary protein excretion ≥300 mg. This patient is normotensive.
(Choice D) The mesangial extracellular matrix is formed by protein (eg, fibronectin, laminin) deposits from glomerular mesangial cells and provides structural support for glomerular capillary loops. Accumulation of extracellular matrix proteins occurs in diabetic nephropathy; however, this patient has no history of diabetes mellitus and has a normal serum glucose level.
(Choice E) Shedding of injured tubular epithelial cells occurs with acute tubular necrosis. Patients typically have elevated creatinine levels and muddy brown casts on urinalysis, which are not seen in this patient.
Educational objective:
Physiologic renal adaptations during pregnancy include increased glomerular filtration rate, greater basement membrane permeability, and decreased tubular resorption of filtered protein. As a result, trace urinary protein excretion (ie, <300 mg/24 hr) is a normal finding in pregnancy.