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Patterns of Proteinuria: Urinary Sodium Dodecyl Sulfate Electrophoresis Versus Immunonephelometric Protein Marker Measurement Followed by Interpretation with the Knowledge-Based System MDI-LabLink

¹ INSERM Research Unit 402, Faculty of Medicine Saint-Antoine, University Pierre & Marie Curie, Paris, France;
² Department of Biochemistry, Tenon Hospital, Paris, France;
³ Department of Laboratory Medicine, Kantonsspital Basel, University Hospital, Basel, Switzerland;
⁴ Department of Nephrology, Tenon Hospital, Paris, France;

^aaddress correspondence to this author at: Service de Biochimie et Hormonologie, Hôpital Tenon, 4 rue de la Chine, 75970 Paris Cedex 20, France; fax 33-1-5601-7840, e-mail mustapha.maachi@tnn.ap-hop-paris.fr

The first 300 words of the full text of this article appear below.

Increased urinary total protein is a nonspecific and unreliable marker of renal function. Analysis of the pattern of proteinuria, however, can provide information regarding the pathophysiologic changes in the affected nephrons. In physiologic proteinuria, the range of daily urinary protein excretion is typically 40–80 mg/24 h with an upper limit of 150 mg/24 h. Albumin represents the main component (30–40%), whereas IgG, light chains, and IgA represent 5–10%, 5%, and 3%, respectively, of urinary proteins. The remainder consists mostly of Tamm–Horsfall protein.

Patterns of pathologic proteinuria may be classified as glomerular, tubular, prerenal, mixed, or postrenal, with glomerular patterns the most frequent. Total urine protein excretion can exceed 2 g/day, with albumin representing the main component (70%) and other large-molecular-weight proteins, such as transferrin and IgG, accounting for the remaining 30%. Tubular proteinuria is characterized by the dominant excretion of low-molecular-weight proteins such as ₁-microglobulin (A1M) or retinol-binding protein (RBP), which correlate better with the extent of tubulo-interstitial damage than does determination of total 24-h protein concentrations (1).

Urinary total protein is frequently undetectable in predominantly tubular kidney disease, and common chemical methods also often fail to detect urinary total protein in predominantly tubular kidney disease, in which albumin usually represents <30% of the total protein content (2)(3)(4)(5)(6)(7)(8). However, some renal tubular disorders or interstitial nephritis (e.g., when caused by antibiotics and other tubulo-toxic substances) are easily treatable. Prerenal proteinuria (Bence Jones proteinuria), attributable to overproduction of light chains in monoclonal diseases, or lysozymuria in patients with leukemia and the resulting overload of tubulo-interstitial reabsorption in the kidney often lead to secondary kidney damage. Mixed proteinuria presents with glomerular and tubular protein fractions in urine, i.e., high- and low-molecular-weight proteins. Postrenal proteinuria closely . . . [Full Text of this Article]

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				Y. Luo, M. Chen, Q. Wen, M. Zhao, B. Zhang, X. Li, F. Wang, Q. Huang, C. Yao, T. Jiang, et al. Rapid and Simultaneous Quantification of 4 Urinary Proteins by Piezoelectric Quartz Crystal Microbalance Immunosensor Array Clin. Chem., December 1, 2006; 52(12): 2273 - 2280. [Abstract] [Full Text] [PDF]