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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://dk.um.si/IzpisGradiva.php?id=91276"><dc:title>The role of vascular lesions in diabetes across a spectrum of clinical kidney disease</dc:title><dc:creator>Rodriguez-Rodriguez,	Rosa	(Avtor)
	</dc:creator><dc:creator>Hojs,	Radovan	(Avtor)
	</dc:creator><dc:creator>Trevisani,	Francesco	(Avtor)
	</dc:creator><dc:creator>Morales,	Enrique	(Avtor)
	</dc:creator><dc:creator>Fernández,	Gema	(Avtor)
	</dc:creator><dc:creator>Bevc,	Sebastjan	(Avtor)
	</dc:creator><dc:creator>Cases Corona,	Clara Maria	(Avtor)
	</dc:creator><dc:creator>Cruzado,	Josep Maria	(Avtor)
	</dc:creator><dc:creator>Quaro,	María	(Avtor)
	</dc:creator><dc:creator>Navarro Díaz,	Maruja	(Avtor)
	</dc:creator><dc:creator>Hornum,	Mads	(Avtor)
	</dc:creator><dc:creator>Fernandez-Fernandez,	Beatriz	(Avtor)
	</dc:creator><dc:creator>Bettiga,	Arianna	(Avtor)
	</dc:creator><dc:creator>Di Marco,	Federico	(Avtor)
	</dc:creator><dc:creator>López Martínez,	Marina	(Avtor)
	</dc:creator><dc:creator>Moreso,	Francisco J.	(Avtor)
	</dc:creator><dc:creator>García Garro,	Clara	(Avtor)
	</dc:creator><dc:creator>Khazim,	Khaled	(Avtor)
	</dc:creator><dc:creator>Ghanem,	Fedaa	(Avtor)
	</dc:creator><dc:creator>Praga,	Manuel	(Avtor)
	</dc:creator><dc:creator>Ibernón,	Meritxell	(Avtor)
	</dc:creator><dc:creator>Laranjinha,	Ivo	(Avtor)
	</dc:creator><dc:creator>Mendonça,	Luís	(Avtor)
	</dc:creator><dc:creator>Bigotte Vieira,	Miguel	(Avtor)
	</dc:creator><dc:creator>Feldt-Rasmussen,	Bo	(Avtor)
	</dc:creator><dc:creator>Fox Concepción,	Patricia	(Avtor)
	</dc:creator><dc:creator>Negrín Mena,	Natalia	(Avtor)
	</dc:creator><dc:creator>Ortiz,	Alberto	(Avtor)
	</dc:creator><dc:creator>Porrini,	Esteban L.	(Avtor)
	</dc:creator><dc:subject>albuminuria</dc:subject><dc:subject>chronic kidney disease</dc:subject><dc:subject>diabetes</dc:subject><dc:subject>diabetic nephropathy</dc:subject><dc:subject>histology</dc:subject><dc:subject>normoalbuminuria</dc:subject><dc:description>Introduction: The clinical-histologic correlation in diabetic nephropathy is not completely known.
Methods: We analyzed nephrectomy specimens from 90 patients with diabetes and diverse degrees of proteinuria and glomerular filtration rate (GFR).
Results: Thirty-six (40%) subjects had normoalbuminuria, 33 (37%) microalbuminuria, and 21 (23%) non-nephrotic proteinuria. Mean estimated GFR (eGFR) was 65±23 (40% &lt;60 ml/min per 1.73 m2). About 170 glomeruli per patient were analyzed, and all samples included vascular tissue. Six subjects (7%) were classified in diabetic nephropathy class I, 61 (68%) in class II-a, 13 (14%) in class II-b, 9 (10%) class III, and 1 (1%) in class IV. Eighty percent to 90% of those with normoalbuminuria or microalbuminuria were classified in class II-a or II-b and &lt;10% in class III; 52% of those with proteinuria were in class II-a, 15% in class II-b, and 19% in class III. Nodular sclerosis (57%) and mesangial expansion (15%) were more frequent in cases with proteinuria than in normoalbuminuria (28% and 8%; P = 0.028 and 0.017). About 20% to 30% of all cases, regardless the level of albuminuria or proteinuria or the histologic class had tubular atrophy, interstitial fibrosis, or inflammation in &gt;10% to 20% of the sample. Moderate hyalinosis and arteriolar sclerosis were observed in 80% to 100% of cases with normoalbuminuria, microalbuminuria, proteinuria, as well as in class I, II, or III.
Conclusions: Weak correspondence between analytical parameters and kidney histology was found. Thus, disease may progress undetected from the early clinical stages of the disease. Finally, vascular damage was a very common finding, which highlights the role of ischemic intrarenal disease in diabetes.</dc:description><dc:publisher>Elsevier</dc:publisher><dc:date>2021</dc:date><dc:date>2024-12-06 10:39:02</dc:date><dc:type>Znanstveno delo</dc:type><dc:identifier>91276</dc:identifier><dc:language>sl</dc:language></rdf:Description></rdf:RDF>
