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)

Renal artery stenosis not only causes severe hypertension, but if left untreated, can progress to renal failure. A 64-year-old woman with a serum creatinine of 1.8 mg/dL and mild proteinuria developed progressively severe hypertension that was resistant to a calcium channel blocker. The patient received lisinopril, which was discontinued after 2 days because of nonspecific symptoms. One week later, an intravenous pyelogram showed a normal-sized but poorly functioning left kidney and a nonfunctional right kidney. The serum creatinine increased to 11.7 mg/dL and the patient was begun on hemodialysis. A renal arteriogram performed 6 weeks later for persistent hypertension showed bilateral renal artery occlusion; renal vein renin values from the left kidney were higher than those from the right kidney. After 11 weeks of hemodialysis, thrombolytic therapy followed by angioplasty was performed. Three weeks later, the renal function had returned to baseline (serum creatinine of 1.8 mg/dL) and hypertension was controlled with a beta-blocker. Renal artery stenosis is a potentially reversible cause of renal failure and should be considered in the evaluation of elderly patients with hypertension, even in the presence of renal failure.
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PMID:Reversible renal failure in an elderly woman with renal artery stenosis. 828 86

Renal transplantation is frequently accompanied by systemic hypertension. In the present study we evaluated the effect of 2.5 mg lisinopril in 12 hypertensive and proteinuric renal graft recipients with stable graft function over 3 months. Only patients with absence of renal artery stenosis, at least as judged by technetium-scan imaging, were included. Lisinopril was effective in lowering systemic blood pressure. Mean arterial pressure was unchanged despite reduction of concomitant antihypertensive medication. Mean serum creatinine was unchanged during the study (1.95 +/- 0.8 mg/dl in the pretreatment period vs. 1.77 +/- 0.76 mg/dl in the intervention period, n.s.). Glomerular filtration rate remained stable (62.75 +/- 21.96 vs. 60.17 +/- 18.27 ml/min/1.73 m2, n.s.) whereas renal plasma flow increased (224.75 +/- 91.66 vs. 244.92 +/- 94.13 ml/min/1.73m2, P < 0.01), leading to a drop in filtration fraction (31.4 +/- 12.4 vs. 26.8 +/- 8.6, n.s.). Renal vascular resistance was significantly reduced following angiotensin-converting enzyme (ACE) inhibitor therapy (26,447 +/- 14,574 vs. 23,425 +/- 12,430 dyne sec cm-5/1.73 m2, P < 0.01). Mean daily proteinuric decreased significantly (2.98 +/- 2.06 vs. 2.06 +/- 2.29 g, P < 0.01) whereas in a group of patients with comparable blood pressure but without ACE inhibitor therapy and similar degree of proteinuria, 24-hr proteinuria remained stable. No severe side effects were observed--in particular, mean serum potassium showed only a slight increase and no clinically significant hyperkalemic condition was observed. When lisinopril therapy was withdrawn after 3 months, blood pressure increased in all patients, requiring reinstitution of additional antihypertensive medication. Renal hemodynamic parameters and daily proteinuria returned to baseline values. We conclude that 2.5 mg lisinopril daily was safe and effective in this group of renal transplant recipients and showed a good antihypertensive as well as antiproteinuric effect.
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PMID:The effects of lisinopril on renal function in proteinuric renal transplant recipients. 839 Jul 33

In recent years, the ability of the various antihypertensive drugs to provide renal protection has been the subject of increased attention. Whether calcium antagonists prevent or reduce the rate of progression of renal damage is still a matter of controversy. This paper reviews the findings of recent animal and human studies on the haemodynamic and renal protective effects of calcium antagonists. These agents preferentially vasodilate afferent arterioles, leading to an increase in renal blood flow and glomerular filtration rate. These effects are more pronounced in hypertensive patients than in normotensive subjects and persist even when renal function is impaired. In animal models of chronic renal failure, calcium antagonists can reduce glomerulosclerosis. However, the mechanisms involved in their renal protective effect appear to be different from those of angiotensin converting enzyme (ACE) inhibitors as they do not reduce intraglomerular pressure. Renal failure caused by vasoconstriction related to radiocontrast agents or cyclosporine can be partly prevented by the administration of a calcium antagonist. Furthermore, in patients with renal artery stenosis, calcium antagonists reduce blood pressure with less renal blood flow impairment than ACE inhibitors. Preliminary clinical studies suggest that verapamil or diltiazem may reduce proteinuria in hypertensive diabetic patients. Whether these compounds can also retard the progression of renal failure in these patients remains to be established with larger trials.
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PMID:Renal haemodynamic and protective effects of calcium antagonists in hypertension. 886 98

In many reports, the prevalence of target organ damage in renovascular hypertension (RVH) appears to be higher than in essential hypertension (EH). Since in most studies the renal artery stenosis is part of a diffuse atherosclerotic disease, it is not known whether these complications are due to RVH itself or to the vascular disease. We have undertaken a case control study of 92 patients divided into two groups (46 in each), one with RVH and the other with EH and abdominal aortic aneurysm, with a comparable degree of diffuse atherosclerotic vascular disease. The vascular state of the extracranial carotid arteries and abdominal and inferior limb districts was investigated with angiography and sonography. The prevalence of left ventricular hypertrophy (LVH) and ischemic heart disease (IHD) were assessed by electrocardiography. Serum creatinine and urinary protein excretion were employed in the renal evaluation. While the analysis of the results confirmed an even diffusion of atherosclerotic vascular disease between the two groups, a significant difference was found in the prevalence of heart and renal damage. LVH was present in 32.6% of RVH patients versus 10.8% in EH (P = .02). Serum creatinine > 1.4 mg/dL was found in 50% of RVH and in 23.9% of EH, (P = .01). The prevalence of proteinuria in RVH was also higher although not reaching the statistical significance. The results suggest that, in patients with comparable degrees of atherosclerotic vascular disease, RVH is responsible for the higher prevalence of target organ damage in this condition compared to those with EH.
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PMID:Comparison of target organ damage in renovascular and essential hypertension. 893 30

Treatment with ACE inhibitors results in kidney protection due to reduction of systemic blood pressure, intraglomerular pressure, an antiproliferative effect, reduction of proteinuria and a lipid-lowering effect in proteinuric patients (secondary due to reduction of protein excretion). Elderly patients with diabetes melitus, coronary heart disease or peripheral vascular occlusion are at risk for deterioration of kidney function due to a high frequency of renal artery stenosis in these patients. In patients with renal insufficiency dose reduction of ACE inhibitors is necessary (exception: fosinopril) but more important is the risk for development of hyperkalemia. Patients at risk for renal artery stenosis and patients pretreated with diuretics should receive a low ACE inhibitor dosage initially ("start low - go slow"). For compliance reasons once daily ACE inhibitor dosage is recommended.
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PMID:[ACE inhibitors and the kidney]. 903 82

In recent years, the importance of renovascular disease as a cause of end-stage renal disease has been emphasized. Among 1,788 cases autopsied during the 12-year period between 1981 and 1992 at the National Cardiovascular Center Hospital, we examined cases over 40 years of age with autopsy evidence of myocardial infarction to determine the prevalence and predictors of atherosclerotic renal artery stenosis in the atherosclerotic population. Two hundred ninety-seven patients remained for analysis. In this population, atherosclerotic renal artery stenosis was found in 35 patients (12%), and 10 of them had bilateral renal artery stenosis. In patients with hypertension, proteinuria, and renal insufficiency, renal artery stenosis was found in 19%, 39%, and 39%, respectively. As the number of coronary vessels with significant stenosis increased, the prevalence of renal artery stenosis increased. The severity of stenotic lesions of coronary artery was also correlated with the presence of renal artery stenosis. Multiple logistic regression analysis identified age, hypertension, proteinuria, and renal insufficiency as independent predictors of renal artery stenosis. Patients with hypertension, proteinuria, and renal insufficiency had 3.4-, 13.5-, and 4.8-fold increased risk of renal artery stenosis in the population with myocardial infarction. The number of coronary arteries with severe stenosis was also an independent predictor of renal artery stenosis, and had a relative risk of 2.1. These results indicated that atherosclerotic renal artery stenosis is common in patients with myocardial infarction, particularly when hypertension, proteinuria, or renal insufficiency is present. The presence of severe multivessel coronary artery disease suggests a higher incidence of renal artery stenosis.
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PMID:Prevalence and predictors of renal artery stenosis in patients with myocardial infarction. 915 8

Focal and segmental sclerosed lesions in the glomeruli are found in several pathological entities and more often are found in the corticomedullary junction where renal blood flow and filtration pressure is maximal. Experimental data suggest that hyperfiltration injury results in focal and segmental glomerulosclerosis (FSGS). In keeping with this concept, malignant hypertension is a known cause of nephrotic-range proteinuria and nephrotic syndrome pathalobically represented by FSGS. We report a case of unilateral renal artery stenosis associated with nephrotic syndrome and FSGS in the contralateral kidney only. The kidney with the stenosed renal artery showed normal glomeruli with juxtaglomerular hyperplasia, suggesting that protection from hyperfiltration injury was provided by the presence of high-grade stenosis. Serum creatinine concentration, blood pressure, and proteinuria normalized after aorto-renal bypass surgery. This case shows the importance of hemodynamic factors on the pathogenesis of secondary FSGS and the progression of renal disease.
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PMID:Renal artery stenosis and unilateral focal and segmental glomerulosclerosis. 1070 47

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.
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PMID:[Antihypertensive therapy in diabetes mellitus]. 1006 31

Hypertension in renal allograft recipients is a common problem arising from multiple factors, including peripheral vascular damage caused by pretransplant hypertension, side effects of immunosuppressive medications, allograft dysfunction, renal artery stenosis, recurrent glomerulonephritis, synthesis of vasoconstrictive hormones by the native kidneys, and excessive dietary salt intake. Identification of modifiable factors causing hypertension and concurrent medical conditions, and measurement of glomerular filtration rate, cyclosporine/tacrolimus blood levels, and magnitude of proteinuria are essential to tailor treatment for an individual patient. Lifestyles that exacerbate hypertension should be modified. For pharmacological therapy, diuretics and calcium channel blockers are first-line agents in patients on cyclosporine shortly after transplant. Angiotensin-converting enzyme inhibitors are good choices for patients with significant proteinuria. Reduction of immunosuppression will improve hypertension in some patients, but entails a potential risk of rejection or graft loss. Angioplasty is necessary in patients with a functionally significant stenosis of the allograft renal artery. Other patients on maximal medical therapy may benefit from native nephrectomy.
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PMID:The best way to manage hypertension after renal transplantation. 1067 27

Hypertension is highly prevalent after renal transplantation and has been associated with lower graft survival. Optimum management of post-transplant hypertension remains to be defined. Losartan, a potent, orally active and selective non-peptide blocker of the angiotensin subtype 1 receptor, could represent a useful drug for treating post-transplant hypertension. Recently, a prospective study of 12 weeks treatment with losartan has showed a satisfactory control of arterial hypertension associated with a decrease in proteinuria in this high-risk group of renal transplant patients. A retrospective study was performed to review the role of losartan as a renoprotective agent (evaluating blood pressure and proteinuria) in renal transplant recipients in a long-term follow-up. A total of 150 transplant recipients were included in the study. None of the patients had a serum creatinine >3 mg/dl, or suspected renal artery stenosis, or other severe concomitant diseases. The indication for losartan therapy was hypertension, proteinuria and/or post-transplant erythrocytosis. The values of blood pressure, results of fasting haematology, blood chemistry and total proteinuria in 24-h urine samples were recorded at the time of initiation of losartan therapy, 6 and 3 months before the start, and at 3, 6, 12, 18 and 24 months thereafter. A tendency analysis by linear regression comparing two slopes before and after treatment was realized. A decrease in mean blood pressure and proteinuria, from 106.7+/-0.9 to 98.2+/-2.1 mmHg and from 1253.9+/-188 to 91.2+/-33.7 mg/24 h, P<0.05, respectively, was observed after introduction of losartan. A progressive increase in creatinine clearance was observed after the third month of losartan treatment. No significant changes were seen in haematocrit or serum potassium levels. We can conclude that a progressive decrease in mean arterial pressure associated with a decrease in proteinuria was observed during long-term follow-up. Based on the capacity of losartan to improve renal function, this drug could be decisive for the treatment and prevention of chronic allograft nephropathy.
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PMID:Angiotensin II type 1 (AT1) receptor antagonists in the treatment of hypertension after renal transplantation. 1136 38


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