Is endothelial dysfunction more deleterious than podocyte injury in diabetic nephropathy

Kidney International

Volumn 83, Issue 6, 2013, Pages 1202-1203

  Nakagawa, Takahiko ^a  

^a KYOTO UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

ALBUMIN; ENDOTHELIAL NITRIC OXIDE SYNTHASE; NITRIC OXIDE; VASCULOTROPIN;

CELL DAMAGE; CELL SURVIVAL; DIABETIC NEPHROPATHY; ENDOTHELIAL DYSFUNCTION; ENDOTHELIUM CELL; ENDOTHELIUM INJURY; GLOMERULUS; HUMAN; LETTER; MICROALBUMINURIA; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PATHOPHYSIOLOGY; PODOCYTE; PRIORITY JOURNAL; URINARY EXCRETION;

EID: 84882245955     PISSN: 00852538     EISSN: 15231755     Source Type: Journal    
DOI: 10.1038/ki.2013.36     Document Type: Letter

References (4)

1. Weil EJ, Lemley KV, Mason CC et al. Podocyte detachment and reduced glomerular capillary endothelial fenestration promote kidney disease in type 2 diabetic nephropathy. Kidney Int 2012; 82: 1010-1017.
2. Eremina V, Jefferson JA, Kowalewska J et al. VEGF inhibition and renal thrombotic microangiopathy. N Engl J Med 2008; 358: 1129-1136.
3. Nakayama T, Sato W, Kosugi T et al. Endothelial injury due to eNOS deficiency accelerates the progression of chronic renal disease in the mouse. Am J Physiol Renal Physiol 2009; 296: 317-327.
4. Nakagawa T, Sato W, Glushakova O et al. Diabetic eNOS knockout mice develop advanced diabetic nephropathy. J Am Soc Nephrol 2007; 18: 539-550.