Effect of Prostaglandins on Renal Function in Uninephrectomized Humans

Mizuiri, Sonoo; Takano, Masaaki; Hayashi, Ikuko; Aikawa, Atsushi; Ohara, Takahiro; Hasegawa, Akira

doi:10.1159/000187247

Cited by 8 publications

(2 citation statements)

References 17 publications

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“…A severely diminished renal mass can cause a decline in renal prostaglandin production because renal tissue produces the renal prostanoids. Renal parenchymal diseases can give rise to various changes in renal prostaglandin production including an increase or decrease of the excretion depending on the offending condition [29][30][31][32]. However, between the two groups the endogenous creatinine clearance was not statistically different, indicating a comparable renal functional mass, and also the eicosanoid excretion indexed to creatinine excretion showed a lower 6-ketoprostaglandin FI~ excretion in the patients with a RAS, which makes a diminished functional renal mass unlikely as the cause of the different findings.…”

Section: Discussionmentioning

confidence: 99%

Urinary prostaglandin and prostaglandin metabolite excretion in patients with essential hypertension or hypertension with renal artery stenosis

Postma

Boo²,

Thomas

et al. 1995

The Netherlands Journal of Medicine

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Background: Recent studies have reported elevated prostaglandin levels in patients with renal artery stenosis and hypertension. To investigate whether a distinction between essential hypertension and hypertension with renal artery stenosis is possible by measuring eicosanoid excretion, we studied the excretion of these compounds in patients with essential hypertension and in hypertensives with concomitant renal artery stenosis.Methods: The 24-h urinary excretion of metabolites of prostaglandin I2, prostaglandin E 2 and metabolites of thromboxane A 2 was sampled under standardised conditions, in 15 patients with essential hypertension and in 15 patients with unilateral renal artery stenosis with hypertension. Also clinical and biochemical characteristics of the subjects were analysed.Results: The patients with renal artery stenosis had significantly lower excretion of prostaglandin I 2 than did the essential hypertensive patients. However, the overlap in the values was large, thus not allowing a diagnostic differentiation according to urinary prostaglandin I z levels. The excretion of prostaglandin E 2 and of metabolites of thromboxane A 2 showed no significant differences among the groups.Conclusions: Measurement of urinary prostaglandin or prostaglandin metabolite excretion did not contribute to the non-invasive detection of the presence of a renal artery stenosis in the patients in this study.

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Section: Discussionmentioning

confidence: 99%

Urinary prostaglandin and prostaglandin metabolite excretion in patients with essential hypertension or hypertension with renal artery stenosis

Postma

Boo²,

Thomas

et al. 1995

The Netherlands Journal of Medicine

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“…Indomethacin administered at 75 mg/day for 3 days abolished the increase in GFR, ERPF and sodium excretion with reduced urinary excretion rate of PGE 2 and 6-keto PGF1 alpha but not the increase in urine flow and potassium excretion. These findings suggest that renal prostaglandins may play a role in renal functional adaptation following unilateral nephrectomy [125]. …”

Section: Hyperfiltration and Eicosanoids In Kidney Diseasementioning

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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Inherited factor H deficiency and collagen type III glomerulopathy

et al. 1995

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A non-immune complex-mediated glomerulonephritis associated with persistent hypocomplementemia occurred in a young boy. Measurement of complement components revealed complete factor H deficiency, inherited as an autosomal recessive trait. Evaluation of the renal lesion revealed extensive deposition of type III collagen suggestive of collagen type III glomerulopathy, a recently identified cause of chronic renal insufficiency in children and adults. This report represents the first association of inherited factor H deficiency with collagen type III glomerulopathy.

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Effect of Prostaglandins on Renal Function in Uninephrectomized Humans

Cited by 8 publications

References 17 publications

Urinary prostaglandin and prostaglandin metabolite excretion in patients with essential hypertension or hypertension with renal artery stenosis

Urinary prostaglandin and prostaglandin metabolite excretion in patients with essential hypertension or hypertension with renal artery stenosis

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

Inherited factor H deficiency and collagen type III glomerulopathy

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