ASN Clinicopathologic Conference

Singh, Ajay K.; Racusen, Lorraine C.

doi:10.2215/cjn.05300611

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…These illustrations suggest that both these staining methods may complement each other and will aid in better interpretation of the staining characteristics. Our conclusion is further supported by studies that showed usefulness of the IHC method in differentiating MFLC from PFLC in AL amyloidosis [31,32], monoclonal interstitial nephritis [5], and monoclonal proximal tubulopathy [33]. …”

Section: Discussionsupporting

confidence: 82%

Contribution of Polyclonal Free Light Chain Deposition to Tubular Injury

Parasuraman

Wolforth²,

Wiesend³

et al. 2013

Am J Nephrol

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Introduction: Excretion of monoclonal free light chains (MFLC) beyond the renal threshold can cause kidney injury, but evidence for polyclonal free light chains (PFLC)-mediated injury is limited. We aimed to study the degree of PFLC deposition in the proximal tubules of chronic kidney disease (CKD) and hypothesized that excess deposition may contribute to tubular injury. Methods: In this retrospective study, immunohistochemical staining to assess the degree of FLC deposition, periodic acid-Schiff staining for the degree of tubular brush border injury and trichrome staining for interstitial fibrosis were evaluated. Normal renal parenchyma from tumor nephrectomy specimens (control group I, n = 39), minimal change disease controls (group II, n = 13), renal biopsies from CKD and proteinuria (polyclonal study group III, n = 33) and monoclonal light chain nephropathy (group IV, n = 37) were studied. The results of the study including serum creatinine were compared between groups. Results: Both polyclonal and monoclonal groups (groups III and IV) had significantly higher light chain deposition and brush border injury by periodic acid-Schiff scores compared to control groups (groups I and II). When the first three polyclonal groups (groups I-III) were analyzed together, polyclonal light chain deposition was significantly correlated with serum creatinine levels, brush border injury and interstitial fibrosis. Conclusion: The results of our study suggest that in CKD patients with proteinuria, excess PFLC deposition in the proximal tubules may cause acute tubular injury akin to monoclonal gammopathy and lead to renal chronicity.

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Section: Discussionsupporting

confidence: 82%