Renal function outcomes in living kidney donors in a transplant center in Colombia.

Introduction: Living kidney donation is currently low in Colombia, and this is associated with the lack of knowledge of the risks and renal function outcomes of potential donors; there are no studies that evaluate these outcomes. The objective of this study is to evaluate the outcomes of renal function, the incidence of metabolic diseases, arterial hypertension, as well as the finding of albuminuria and/or proteinuria in living kidney donors with a 2-year follow-up post donation.

Methods: Observational study in living kidney donor patients, in which renal function outcomes were evaluated between the predonation period and up to 24 months postdonation.

Early treatment with cGMP phosphodiesterase inhibitor ameliorates progression of renal damage.

Background: Chronic renal disease is associated with oxidative stress and reduced nitric oxide availability which, in turn, promotes hypertension and further progression of renal damage. Most actions of nitric oxide are mediated by cyclic 3',5' guanosine monophosphate (cGMP) which is rapidly degraded by phosphodiesterases (PDE). Therefore, we investigated if inhibition of PDE-5 would retard the progression of chronic renal failure.

Hypertension in Page (cellophane-wrapped) kidney is due to interstitial nephritis.

Background: Cellophane wrapping of the kidneys (Page kidney) induces perinephrits and hypertension, assumed to be due to renal ischemia resulting from parenchymal compression by the fibrous hull surrounding the kidneys. We investigated if interstitial nephritis, rather than plasma angiotensin activity, played a role in the development of hypertension in the Page kidney model.

Methods: We followed for 7 weeks rats with bilateral cellophane wrapping of the kidneys that received 20 mg/kg/day of the immunosuppressive antiproliferative drug mycophenolate mofetil (MMF) (two-kidney wrap/MMF) (N = 10) or vehicle (two-kidney wrap) (N = 10), and sham-operated rats (N = 10).

Early and sustained inhibition of nuclear factor-kappaB prevents hypertension in spontaneously hypertensive rats.

Compelling evidence has emerged pointing to the interaction of oxidative stress and renal interstitial inflammation and their mutual contribution to the pathogenesis of hypertension in experimental animals. Renal interstitial inflammation in spontaneously hypertensive rats (SHR) is accompanied by and largely due to activation of redox-sensitive, proinflammatory nuclear transcription factor-kappaB (NF-kappaB). Therefore, the present study was designed to test the hypothesis that long-term inhibition of NF-kappaB, beginning early in the course of the disease, may attenuate renal interstitial inflammation and hypertension in SHR.