Prostaglandin E1 for preventing the progression of diabetic kidney disease

Wang, Han; Deng, Jue Lin; Yue, Jirong; Li, Jun; Hou, Yan

doi:10.1002/14651858.cd006872

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Urinary PGI 2 showed no relationship with the development of hemolytic uremic syndrome and was not protective [141]. PGE 1 infusion reduced albuminuria and proteinuria in diabetic nephropathy in six studies included in Cochrane Review [142]. PGE 1 infusion was not helpful in 8 adults with CKD [143] or in 9 adults with GN [144] but PGE1 with ACEI was helpful in 52 adults with CKD [145].…”

Section: Amelioration Of Hyperfiltration-induced Glomerular Dysfunmentioning

confidence: 99%

Hyperfiltration-associated biomechanical forces in glomerular injury and response: Potential role for eicosanoids

Sharma

McCarthy

et al. 2017

Prostaglandins & Other Lipid Mediators

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Hyperfiltration is a well-known risk factor in progressive loss of renal function in chronic kidney disease (CKD) secondary to various diseases. A reduced number of functional nephrons due to congenital or acquired cause(s) results in hyperfiltration in the remnant kidney. Hyperfiltration-associated increase in biomechanical forces namely pressure-induced tensile stress and fluid flow-induced shear stress (FFSS) determine cellular injury and response. We believe the current treatment of CKD yields limited success because it largely attenuates pressure-induced tensile stress changes but not the effect of FFSS on podocytes. Studies on glomerular podocytes, tubular epithelial cells and bone osteocytes provide evidence for a significant role of COX-2 generated PGE2 and its receptors in response to tensile stress and FFSS. Preliminary observations show increased urinary PGE2 in children born with a solitary kidney. FFSS-induced COX2-PGE2-EP2 signaling provides an opportunity to identify targets and, for developing novel agents to complement currently available treatment.

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Section: Amelioration Of Hyperfiltration-induced Glomerular Dysfunmentioning

confidence: 99%

Hyperfiltration-associated biomechanical forces in glomerular injury and response: Potential role for eicosanoids

Sharma

McCarthy

et al. 2017

Prostaglandins & Other Lipid Mediators

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“…However, the precise mechanism of action remains to be established. It has been suggested that PPAR α agonists may inhibit prostaglandin production, a key regulator of renal blood flow and diabetic renal pathology, may also be responsible [76]. …”

Section: The Renoprotective Actions Of Pparα Agonistsmentioning

confidence: 99%

The Renoprotective Actions of Peroxisome Proliferator-Activated Receptors Agonists in Diabetes

2012

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Pharmaceutical agonists of peroxisome proliferator-activated receptors (PPARs) are widely used in the management of type 2 diabetes, chiefly as lipid-lowering agents and oral hypoglycaemic agents. Although most of the focus has been placed on their cardiovascular effects, both positive and negative, these agents also have significant renoprotective actions in the diabetic kidney. Over and above action on metabolic control and effects on blood pressure, PPAR agonists also appear to have independent effects on a number of critical pathways that are implicated in the development and progression of diabetic kidney disease, including oxidative stress, inflammation, hypertrophy, and podocyte function. This review will examine these direct and indirect actions of PPAR agonists in the diabetic kidney and explore recent findings of clinical trials of PPAR agonists in patients with diabetes.

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