Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial hypertension develops in up to 80% of renal transplant recipients. Uncontrolled hypertension induces left ventricular hypertrophy, heart failure and death, but also promotes deterioration of allograft function. Cadaveric transplantation, delayed graft function, renal artery stenosis, presence of native kidneys, increased body weight and therapy with calcineurin inhibitors and steroids have been associated with an increased incidence of hypertension after kidney transplantation. Cyclosporine increases both systemic and renal vascular resistance, enhances sympathetic activation, endothelin production and, possibly, decreases vascular relaxation by decreasing the generation of nitric oxide. Tacrolimus has less pronounced prohypertensive role after renal transplantation. Corticosteroids contribute to the development of hypertension, since their withdrawal results in a significant decrease of blood pressure in the majority of patients. Renal artery stenosis occurs in almost 12% of hypertensive renal transplant recipients. It is a correctable cause of hypertension, and for this reason should be investigated in all suspected patients. Doppler ultrasonography is used as the screening method that is highly sensitive and specific in the hands of a well-experienced investigator. However, dependence of the method on the experience of the investigator is its major drawback. Magnetic resonance angiography and spinal computed tomography angiography are useful noninvasive methods, but arteriography remains a method for establishing the definitive diagnosis. Percutaneous balloon angioplasty, with or without placement of the stent, is successful in the majority of patients, but with a high incidence of restenoses (20%). Surgery is indicated for stenoses that cannot be treated with angioplasty or that recur. Auto-transplantation of the kidney with complex stenoses of graft arteries is useful in selected cases. Posttransplant hypertension should be aggressively treated to prevent the development of end-organ damage. Every effort should be invested in reducing immunosuppression when appropriate, together with salt restriction and weight reduction. Calcium channel blockers have good antihypertensive properties accompanied with minimization of cyclosporine-induced renal vasoconstriction. Angiotensin-converting enzyme inhibitors (ACEi) should be used in patients with proteinuria. Renal function should be carefully monitored after their introduction since they may cause transitory deterioration of glomerular filtration and/or hyperkaliemia. ACEi can induce anemia in renal transplant recipients, side effect that is often used in the treatment of posttransplant erythrocytosis. All other antihypertensive drugs could be used, with minoxidil being the most potent one. Patients with resistant hypertension should be investigated for the presence of renal artery stenosis. After exclusion of rejection, renal artery stenosis and recurrent disease, in cases of severe hypertension, native kidneys laparoscopic nephrectomy should be considered.
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PMID:[Arterial hypertension in renal transplant recipients]. 1836 9

Besides the immunological mediated damage on the graft, the intrarenal renin-angiotensin system (RAS) is viewed as an additional mechanism in the development and progression of chronic allograft injury. RAS blocking agents efficiently control post-transplant hypertension and are useful to reduce proteinuria and for treating post-transplant erythrocytosis. However, RAS blockade is associated with some potentially relevant adverse events as hyperkalemia, anemia, and even to a decline in renal function. There are consistent experimental data showing that RAS blockade has a therapeutic effect on chronic allograft injury. Some clinical studies have shown that RAS blockade reduces transforming growth factor-beta1 and other markers of fibrosis but, up to now, there is not convincing evidence supporting that RAS blockade has further benefit on the progression of chronic allograft injury in comparison with other antihypertensive interventions. Theoretically, RAS blockade may also improve cardiovascular disease, which constitutes the main cause of mortality and morbidity in renal allograft recipients. Nevertheless, to date there is lack of evidence for supporting that RAS blockade improves neither graft nor patient survival in comparison with other antihypertensive drugs. Randomized, prospective, double blind, placebo-controlled trials with enough sample size and follow-up are needed to address the potential role of RAS blockade to improve graft and patient outcome. Meanwhile, we should empirically balance case to case the pros and cons of RAS blockade in renal transplantation.
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PMID:The renin angiotensin system blockade in kidney transplantation: pros and cons. 1826 74

The blockade of the renin-angiotensin-aldosterone system may limit the progression of graft dysfunction in patients receiving kidney transplantations. We retrospectively evaluated the safety and efficacy of angiotensin-converting enzyme inhibitors (ACEI) in renal allograft recipients. Fifty-seven cadaveric kidney recipients (58% of recipients), were prescribed an ACEI (lisinopril). The indications for ACEI were isolated proteinuria (1 patient), erythrocytosis (6 patients), and arterial hypertension (50 patients). The choice of an ACEI for blood pressure control was due to presence of left ventricular hypertrophy (2 patients), mild proteinuria (4 patients), and high hemoglobin (4 patients). There was a significant reduction in the mean arterial pressure after 1 month (P = .0004) and 1 year (P = .0002) of therapy. Overall, the estimated glomerular filtrate rate (eGFR), calculated using the Cockcroft-Gault equation, remained unchanged. Among patients who had serum creatinine values above 2.0 mg/dL at the beginning of ACEI therapy, there was a significant rise in eGFR from 39.3 +/- 13.2 to 44.1 +/- 16.8 mL/min after 6 months (P = .01), and 43.3 +/- 17.3 mL/min after 1 year (P = .04). In patients with erythrocytosis, the hemoglobin showed a significant and sustained reduction after 1 month (P = .004) and 1 year (P = .001). Six patients suspended ACEI owing to adverse events: cough (n = 4), worsening of graft function (n = 1), and hypotension (n = 1). Six patients required erythropoiesis-stimulating agents. No patient suspended treatment owing to hyperkalemia. In conclusion, ACEI were well tolerated, safe, and effective antihypertensive agents in kidney graft recipients. They seemed to have some beneficial effect in preserving GFR in patients with worse graft function.
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PMID:Angiotensin-converting enzyme inhibitors after renal transplantation. 1845 3

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

Amyloidosis is the most common and devastating complication of familial Mediterranean fever (FMF). Renal transplantation is the choice of treatment of in most end-stage renal disease (ESRD). We report our experience on the outcomes in eight patients who underwent renal transplantation for ESRD due to FMF secondary to amyloidosis, and we provide a discussion on the current evidence on this topic of study. The clinical charts of eight renal transplant patients (seven male, one female) who underwent ESRD due to FMF-related amyloidosis were investigated. Five patients underwent living-donor renal transplantation and three patients underwent deceased-donor renal transplant. The mean follow-up period was 35 months (range 3-72). All patients were on triple immunosuppressive treatment and received colchicine. All allografts are currently functioning well with a mean serum creatinine level of 1.4 (range 0.7-2.6) mg/dL. Posttransplantation complications included acute rejection (n = 4), chronic rejection (n = 1), severe gastroenteritis (n = 2), and erythrocytosis (n = 5). None of the patients had proteinuria. During follow-up, we did not observe clinically severe FMF attack, septicemia, rhabdomylosis, symptoms related to vasculitis, and clinical neuropathy. The clinical outcome of the patients in this cohort was similar to that of other renal transplant patients with ESRD due to other causes. This study shows favorable prognosis of eight ESRD patients due to amyloidosis caused by FMF after renal transplantation. Renal transplantation is a safe procedure for ESRD patients having amyloidosis due to FMF. Regular use of colchicine after transplantation should be mentioned.
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PMID:Renal transplantation in patients with familial Mediterranean fever. 2256 68

We report a case of idiopathic erythrocytosis in a 31-year-old male who was incidentally detected to have hypertension during his preemployment checkup. Urine routine showed proteinuria and hematuria. Biochemical parameters revealed raised serum creatinine, and histological findings of the renal biopsy showed IgAN.
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PMID:Idiopathic erythrocytosis in IgA nephropathy. 2818 57

Myeloproliferative neoplasms (MPNs) with Janus kinase 2 (JAK2) mutation are associated with a high risk for occlusive vascular diseases. We report 2 cases of renovascular hypertension associated with JAK2 V617F mutation-positive MPNs and provide a literature review. In Case 1, a 63-year-old woman had resistant hypertension, massive proteinuria, and erythrocytosis. Evaluations revealed right renal artery stenosis causing renovascular hypertension and polycythemia vera with JAK2 V617F mutation. Renin-angiotensin system inhibitors and subsequent angioplasty controlled the blood pressure and the proteinuria resolved. In Case 2, a 74-year-old woman had resistant hypertension and thrombocytosis. Evaluations confirmed left renal artery stenosis and essential thrombocythemia with JAK2 V617F. Angioplasty cured the hypertension. A literature review of 18 cases revealed the following as the most common characteristics of MPN-associated renovascular hypertension: manifests primarily in women; is associated with untreated polycythemia vera and essential thrombocythemia, concomitant leukocytosis, and JAK2 mutation positivity; and is responsive to angioplasty. This report demonstrates that JAK2 mutation-positive MPNs are a less common but important underlying cause of adult renovascular hypertension.
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PMID:Renovascular hypertension associated with JAK2 V617F positive myeloproliferative neoplasms treated with angioplasty: 2 cases and literature review. 2965 57


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