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  • Proteinuria with bland urine sediment (few if any cells or cellular casts).

  • Nephrotic syndrome (if present) manifestations:

    • –Nephrotic-range proteinuria (urine protein excretion > 3 g per 24 hours).

    • –Hypoalbuminemia (albumin < 3 g/dL).

    • –Peripheral edema.

    • –Hyperlipidemia.

    • –Oval fat bodies may be seen in the urine.


In American adults, the most common cause of nephrotic spectrum glomerular disease is diabetes mellitus. Other causes include minimal change disease, FSGS, membranous nephropathy, and amyloidosis. Clinical presentations along the nephrotic spectrum vary based on etiology, with diabetic nephropathy and secondary FSGS typically on the less severe end (bland UA and proteinuria), and minimal change disease, membranous nephropathy and amyloidosis presenting with the full nephrotic syndrome. Serum creatinine may be abnormal at the time of presentation, depending on the severity and chronicity of the disease.


A. Symptoms and Signs

Patients with simple proteinuria do not manifest symptoms of kidney disease. In those with the nephrotic syndrome, peripheral edema is present—most likely due both to sodium retention and hypoalbuminemia-induced low plasma oncotic pressure. Edema may develop solely in dependent regions, such as the lower extremities, or it may become generalized and include periorbital edema. Dyspnea due to pulmonary edema, pleural effusions, and diaphragmatic compromise due to ascites can occur.

B. Laboratory Findings

1. UA

Proteinuria occurs as a result of podocytopathy and variable alterations of the GBM. The urine dipstick is a good screening test for albuminuria; if positive, urinary protein excretion should be quantified (see earlier Proteinuria section). A spot urine protein to urine creatinine ratio gives a reasonable approximation of grams of protein excreted per day; a 24-hour urine sample for protein excretion is rarely needed.

Microscopically, the urinary sediment has relatively few cellular elements or casts. However, if marked hyperlipidemia is present, urinary oval fat bodies may be seen. They appear as “grape clusters” under light microscopy and “Maltese crosses” under polarized light.

2. Blood chemistries

The nephrotic syndrome results in hypoalbuminemia (less than 3 g/dL [30 g/L]). Hyperlipidemia occurs in over 50% of patients with early nephrotic syndrome, due to falling oncotic pressure that triggers increased hepatic lipid production and to decreased clearance of very LDLs with resultant hypertriglyceridemia. Hyperlipidemia becomes more frequent and worsens as the severity of the nephrotic syndrome increases. An elevated erythrocyte sedimentation rate may be seen as a result of increased levels of fibrinogen. Heavy urinary excretion of binding proteins may result in deficiencies of vitamin D, zinc, and copper.

Laboratory testing to help elucidate the underlying cause of the glomerular disease includes complement levels, serum and urine protein electrophoresis, serum free light chains, antinuclear antibodies, PLA2R antibody titers, ...

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