Diabetic nephropathy with marked extra-capillary cell proliferation: a case report

Abstract

Background Extra-capillary hypercellularity is a common finding in crescentic glomerulonephritis (GN) and focal segmental glomerulosclerosis (FSGS). In diabetic nephropathy (DN), extra-capillary hypercellularity is often observed as a finding of complications such as IgA nephropathy or microscopic polyangiitis superimposed on DN. However, in rare cases, epithelial cell proliferation may accompany DN. We experienced a case of nodular diabetic glomerulosclerosis with marked extra-capillary hypercellularity and revealed the origin of this atypical lesion using immunostainings. Case presentation A man in his 50 s was admitted to the hospital with nephrotic syndrome, and a renal biopsy was performed. Diffuse nodular lesions and extra-capillary hypercellularity were observed, but the results of serological examination or immunofluorescent assays did not implicate any other crescentic GN. Immunostaining for claudin-1 and nephrin was performed to identify the origin of the extra-capillary lesions. Given the clinical course and pathological findings, a diagnosis of DN-associated extra-capillary cell proliferation was made. Conclusions Extra-capillary hypercellularity, which resembles FSGS or crescentic GN, is a rare finding in DN and should therefore be treated with caution. In such cases, co-staining for claudin-1 and nephrin may facilitate the diagnosis of DN.

Ability of NAD and Sirt1 to epigenetically suppress albuminuria

“…Because of our findings regarding the role of the Sirt1/Claudin-1 axis on podocyte function, many other reports have shown that depressed Sirt1 and amplified Claudin-1 were detectable in damaged podocytes in DN [ 10 , 11 ] and in other kidney diseases such as focal segmental glomerulosclerosis [ 12 , 13 ] and hypertension-induced glomerular sclerosis [ 14 ]. In this regard, the regulatory mechanism by which repressed Sirt1 augmented Claudin-1 is considered significant for establishing the potential of diagnostic markers and/or therapeutic targets of the Sirt1/Claudin-1 axis in kidney diseases [ 15 , 16 ]. This is explained in more detail in the following section.…”

Evaluating the State of Glomerular Disease by Analyzing Urinary Sediments: mRNA Levels and Immunofluorescence Staining for Various Markers

“…When this barrier is disturbed by PEC injury, its permeability increases, possibly resulting in interstitial inflammation subsequent to periglomerular leakage of filtered protein. PECs are also involved in the formation of crescents [17][18][19], so claudin1-positive cells are expected to be excreted in the urine of patients with glomerular crescents.…”

Glomerular crescents are associated with the risk of type 2 diabetic kidney disease progression: a retrospective cohort study

“…The presence of glomerular crescents is a characteristic feature of rapidly progressive glomerulonephritis and can be observed in the severe forms of various types of glomerulonephritis, including postinfectious glomerulonephritis, membranoproliferative glomerulonephritis, lupus nephritis, and immunoglobulin A nephropathy [14][15][16]. While glomerular crescents have primarily been identified in the acute form of glomerulonephritis, there have been reports of their occurrence in isolated cases of DKD [17][18][19][20][21]. Some single-center cohort studies have examined the relationship between glomerular crescents and a poorer kidney prognosis in patients with type 2 DKD [22][23][24][25].…”