Response to ‘Renal microvascular and tubular injuries in type II diabetic nephropathy’

Autor: Francesca Lauria, Franco Ferrario, Barbara Villaggio, Laura Rimoldi, Mariano Mij, Giacomo Deferrari, Maria Teresa Gandolfo, M. Giannoni, Giacomo Garibotto, Daniela Verzola, Francesco Gianiorio, Maria Pia Rastaldi
Jazyk: angličtina
Předmět:
Zdroj: Kidney International. (3):390-391
ISSN: 0085-2538
DOI: 10.1038/ki.2008.178
Popis: We thank Drs Narisa and Prasit Futrakul for their interest in our paper.1 The findings observed in their studies, implying a maladaptive constriction of the efferent arteriole and downstream vascular and tubulointerstitial damage in type II diabetic patients, are appealing.2 One of the basic abnormalities in diabetic nephropathy is microalbuminuria, which eventually progresses to proteinuria. Downstream into the tubular compartment, the proteinuria induces a proinflammatory injury in tubular cells, which can ease the development of interstitial fibrosis and tubular atrophy.3 However, at variance with type I diabetic patients, a considerable number of type II diabetic patients, even with microalbuminuria or macroalbuminuria, have normal glomerular structure but show tubulointerstitial and/or arteriolar abnormalities.4 In type II diabetes, hyperglycemia5 and hypertension6 may cooperate to impair the physiologic mechanism that maintains normal glomerular capillary pressure and tubular function.6, 7
Databáze: OpenAIRE