Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and experimental studies that discuss the different immune functions of the renin-angiotensin system (RAS) in kidney diseases were reviewed, with emphasis on studies of kidney transplantation. The RAS has been shown to affect both the innate and adaptive immune responses and has a well-established role in fibrinogenesis. Of special clinical interest is the ability of the RAS to activate the transforming growth factor beta(1) and the Smad pathways leading to fibrinogenesis. In addition to the RAS enhancing effect on the activity of T cells, several components of the RAS have also been shown to be chemotactic to macrophages, T cells, and natural killer cells. Experimental studies have found that RAS blockade decreases the histologic lesions of chronic allograft nephropathy but can enhance acute graft vasculopathy. Although the blockade of RAS has been commonly practiced to reduce posttransplantation hypertension, proteinuria, and erythrocytosis, however, its role in prolonging graft survival is not well established.
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PMID:The renin-angiotensin system: an old, newly discovered player in immunoregulation. 1953 79

Post-transplant erythrocytosis is defined as an increase in hematocrit above 55%. It occurs in 10%-15% of renal transplant recipients, most commonly from 8 to 24 months after transplantation. Twenty-five percent of patients experience spontaneous remission within 2 years, while 75% develop symptoms and signs of hyperviscosity (headache, hypertension, plethora). The etiology is multifactorial and includes erythropoietin, renin-angiotensin system (RAS) and IGF-1 as the main factors. RAS inhibition with either ACE inhibitors or angiotensin receptor blockers is efficient therapy which decreases hematocrit in 90% of patients within 2 to 6 weeks, thus decreasing the incidence of fatal complications (like pulmonary embolism and stroke).
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PMID:[Post-transplant erythrocytosis]. 2235 5

Nowadays, obstructive sleep apnea syndrome (OSAS) has been established to promote both structural and functional changes in the kidneys. The basis for these changes is pathophysiological mechanisms, such as hyperproduction of free radicals and disruption of NO-mediated vasodilator responses, activation of the sympathetic autonomic nervous system and the renin-angiotensin-aldosterone system, endothelial dysfunction, development of renal venous hypertension, and stimulation of atrial natriuretic peptide production, which in turn results in increased intraglomerular pressure and glomerular hyperfiltration. In patients with OSAS, the kidneys may be damaged by OSAS-related abnormalities, such as hypertension, diabetes mellitus, metabolic syndrome, erythrocytosis, atherosclerosis, and cor pulmonale, which may also lead to kidney injury under isolated conditions and, when concurrent OSAS is present, may even aggravate the existing kidney injury.
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PMID:[The main pathophysiological mechanisms of kidney injury in obstructive sleep apnea syndrome]. 2509 64

Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.
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PMID:Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers. 2995 63

A 29-year-old female was referred to the urology clinic because of an incidentally found left renal mass discovered during workup for secondary erythrocytosis. Since 12 years of age, she has had headaches and poorly controlled hypertension refractory to trimodal antihypertensive therapy. Laboratory workup revealed markedly elevated aldosterone and renin levels. Computed tomography demonstrated a 3 cm left renal mass. The patient was admitted for intravenous blood pressure control. After partial nephrectomy, aldosterone and renin levels normalized. The patient was weaned off of blood pressure medications. Pathology was consistent with a juxtaglomerular cell tumor secreting renin (ie, reninoma).
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PMID:A Young Female With Refractory Hypertension. 3160 68


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