期刊
CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 11, 期 12, 页码 2288-2294出版社
AMER SOC NEPHROLOGY
DOI: 10.2215/CJN.02560316
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资金
- Office of Research and Development, Medical Research Service, Department of Veterans Affairs [1 IP1 BX001595]
- National Institutes of Health George M. O'Brien Kidney and Urological Research Centers Program [P30 DK079337]
Disorders of plasma and B cells leading to paraproteinemias are associated with a variety of renal diseases. Understanding the mechanisms of injury and associated nephropathies provides a framework that aids clinicians in prompt diagnosis and appropriate adjunctive treatment of these disorders. Glomerular diseases that may be associated with paraproteinemias include amyloid deposition, monoclonal Ig deposition disease, proliferative GN with monoclonal Ig deposits, C3 glomerulopathy caused by alterations in the complement pathway, immunotactoid glomerulopathy, fibrillary GN, and cryoglobulinemia. Tubular lesions include the classic Fanconi syndrome, light chain proximal tubulopathy, interstitial fibrosis, and cast nephropathy. These paraproteinemic renal diseases are distinct in their pathogenesis as well as their urinary and kidney biopsy findings. Renal pathology is usually initiated by deposition and direct involvement of the intact monoclonal Ig or Ig fragments with resident cells of the nephron. Our review summarizes current insights into the underlying molecular pathogenesis of these interesting kidney lesions.
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