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)

If proteinuria is of sufficient amount, and persists for long enough, then a series of consequences arises which is called the nephrotic syndrome. The most notable consequence of massive proteinuria is salt and water retention leading to edema formation. This edema is found in association with proteinuria usually greater than 3.5 g/day, accompanied by hypoalbuminemia, usually less than 25 g/l. The underlying disease is usually a glomerulonephritis, albeit in rare situations severe renal artery stenosis can lead to proteinuria by hyperfiltration. Two theories have been proposed. In the classical "underfill" theory edema is considered to be secondary to salt retention resulting from renal hypoperfusion. According to this theory the primary event is the decrease in plasma volume due to the diminution of plasma oncotic pressure resulting from hypoalbuminemia, causing transfer of fluid from the plasma to the interstitial space "underfilling" the blood compartment and resulting to secondary renal sodium retention. This mechanism applies mainly to the nephrotic syndrome associated with minimal change disease observed in children. By contrast, in most adults with the nephrotic syndrome due to minimal change disease or other glomerular lesions such as membranous or proliferative glomerulonephritis, an initial plasma volume expansion is observed. Therefore, the primary event responsible for the sodium retention is a renal intrinsic excretory defect, which leads to extracellular fluid expansion and edema formation. Therapy is specific for the specific glomerular disease and symptomatic for the edema (diuretics), anticoagulation therapy for prevention of venous thrombosis and embolism, antibiotics for infections, and most of all, omission of triggering factors such as specific xenobiotics.
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PMID:[Edema and the nephrotic syndrome]. 1560 57

Renal artery stenosis (RAS) is a common cause of secondary hypertension, with the activation of the renin-angiotensin-aldosterone system being the pathophysiologic hallmark of the disease. Renovascular hypertension, ischemic nephropathy, proteinuria, and flash pulmonary edema are the main clinical syndromes associated with RAS. The prevalence of RAS is on the rise, owing to an increasing prevalence of diabetes and atherosclerotic disease among our aging population. This rise in RAS prevalence poses major challenges for clinicians making diagnostic and treatment decisions. Although renal angioplasty is of proven benefit in fibromuscular dysplasia, randomized trials in atherosclerotic RAS have not shown any advantage for revascularization over medical therapy in terms of blood pressure control or renal function preservation. Angioplasty and surgical interventions should be reserved for patients with preserved kidney size and hemodynamically significant stenosis.
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PMID:Challenges in the diagnosis and management of renal artery stenosis. 1591 98

Atherosclerotic renovascular disease (ARVD) is defined as a reduction in glomerular filtration rate in patient with significant renovascular bilateral occlusive disease or unilateral in a solitary kidney. ARVD is a frequent and potentially avoidable cause of end stage renal failure and the need for replacement therapy among person above 50 years old. Use of balloon angioplasty with stenting or surgical repair has been shown to improve renal potency, but there is no clear evidence that it prevents further progressive decline of renal function or blood pressure, compared to medical therapy alone. It is now recognized that severity of histopathologic damage is an important determinant and predictor of renal functional outcome. Proteinuria increases with declining renal failure and reflects the severity of parenchymal damage. Proteinuria and high renal resistance index are associated with glomerular damage and altered intrarenal perfusion. They aren't linked to renal artery stenosis (RAS) grade. Recent study indicate that abrupt decline in renal function reflects reversibility after revascularization. This should probably be undertaken in RAS patients with rapidly deteriorating renal function, refractory hypertension and in whom plasma creatinine concentration has increased by >20% during one month long administration of angiotensin-converting enzyme inhibitor. Renal biopsy may be useful to evaluate patient who will have advantage from revascularization.
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PMID:[Predictors of successful renal artery revascularization in atherosclerotic renovascular disease]. 1624 36

A 48-year-old man presented with malignant hypertension and massive proteinuria. Renal angiography showed complete obstruction of the left renal artery and 99mTc-mercaptoacetylglycine (MAG3) renography showed a nonfunctioning left kidney. Percutaneous transluminal renal angioplasty of the left renal artery was unsuccessful; hence, the patient underwent left nephrectomy because of uncontrolled hypertension and proteinuria. Histological examination of a right kidney specimen revealed lesions of focal segmental glomerulosclerosis with benign nephrosclerosis. In contrast, histology of the left kidney showed typical ischemic kidney with hypertrophy of arteriolar smooth muscle cells. The patient responded favorably to the nephrectomy, as his blood pressure and urinary protein dramatically decreased with no antihypertensive medication. This case illustrates the heterogeneous effect of the renin-angiotensin system on either kidney in patients with renovascular hypertension due to unilateral renal artery stenosis.
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PMID:Renovascular hypertension: a unique cause of unilateral focal segmental glomerulosclerosis. 1675 56

A case report in the journal Pediatric Nephrology describes a 15-month-old girl with the syndrome of hypertension and hyponatremia (HH syndrome) due to underlying unilateral renal artery stenosis. This syndrome is typically associated with hypokalemia and severe volume depletion and sometimes proteinuria, all of which, along with hypertension and hyponatremia, are usually corrected by resolution of the underlying renal ischemia. Gross and probably sudden activation of the renin-angiotensin system in response to renal ischemia is central to the pathophysiology although the cardiac atrial and B-type natriuretic peptides probably contribute also. Initial control of the severe hypertension may, in some cases, require careful volume repletion prior to introduction of blockade of the renin-angiotensin system in order to avoid first-dose hypotension, after which correction of the underlying renal ischemia is required. Whereas the syndrome has rarely been reported in children, it is possible that, as in adults, this reflects its lack of recognition by clinicians. The HH syndrome due to unilateral renal ischemia in children may be much more common than we think.
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PMID:Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children--more common than we think? 1677 97

Ulcerative colitis is rarely associated with immunoglobulin A nephropathy (IgAN). The development of IgA nephropathy complicates further the clinical course of patients with ulcerative colitis. A 72-year old man with a 30-year history of ulcerative colitis requiring colectomy and modest renal insufficiency secondary to complications of nephrolithiasis and renal artery stenosis developed glomerular hematuria, proteinuria and progressive renal failure. Percutaneous kidney biopsy revealed IgAN with extensive glomerular and interstitial sclerotic changes. After resection of a chronically infected ileo-rectal pouch, renal function improved, while hematuria and proteinuria gradually disappeared without specific treatment of the IgAN. The manifestations of IgAN complicating ulcerative colitis can be improved with effective treatment of the bowel disease even when there are extensive sclerotic changes in the kidneys.
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PMID:Immunoglobulin A nephropathy complicating ulcerative colitis. 1686 9

Hypertension and episodic pulmonary oedema are known complications of bilateral renovascular disease. However, significant proteinuria has not been reported in this setting. We describe a patient who presented with recurrent pulmonary oedema and nephrotic syndrome, and was found to have bilateral renal artery stenosis. Percutaneous angioplasty and stenting led to a complete resolution of both, confirming a causal relationship. This is perhaps the first report documenting the rare combination of nephrotic syndrome and flash pulmonary oedema due to bilateral renal artery stenosis.
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PMID:Nephrotic syndrome and recurrent pulmonary oedema in bilateral atherosclerotic renal artery stenosis: resolution following renal angioplasty and stenting. 1720 79

The diagnosis of antiphospholipid syndrome (APS) relies on clinical and laboratory criteria, which have been recently outlined in specific consensus conferences. Renal involvement in APS is not infrequent and includes different clinical patterns. For clinical purposes a distinction can be made between large vessel and microvascular involvement. Renal artery stenosis is frequent in APS. In case of microvascular involvement with an acute clinical course a differential diagnosis with other thrombotic microangiopathic diseases has to be made, taking in account thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, malignant hypertension, drug nephrotoxicity (cyclosporin) and others. The disease is often chronic, with hypertension, different degrees of renal insufficiency and mild proteinuria. In patients with systemic lupus erythematosus and antiphospholipid antibodies the prognosis of kidney disease is generally poorer than in lupus alone. Finally, the kidney is almost invariably a target in catastrophic antiphospholipid syndrome. Anticoagulation is the therapy of choice, especially in arterial stenosis and acute disease, but is probably also indicated in chronic and subacute patterns. The role of immunomodulatory therapy has to be assessed.
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PMID:[Antiphospholipid syndrome and kidney]. 1745 26

The renin-angiotensin-aldosterone system (RAAS) plays an important part in the pathogenesis of arterial hypertension and the complications it causes in organs (the heart, the circulatory system, the brain, the kidneys), heart failure and kidney diseases. Materials that block the most upstream point of the RAAS cascade (ACE inhibitors - ACEI, AT1,-receptor (AT1R) blockers, aldosterone receptor blockers) have greatly expanded our options in the treatment and primary and secondary prevention of cardiovascular and renal diseases. ACEI and AT1R blockers interrupt the normal feedback provided by the release of renin into the circulatory system from the kidneys. After they are applied the reactive increase in active circulating renin leads to increased creation of angiotensin I and angiotensin II and the subsequent return of aldosterone secretions to pre-treatment values ("escape" phenomenon). The possible negative effect of these intermediary products of an incomplete blockade of RAAS on organ complications lead to an effort to develop a material that could block the renin-angiotensin cascade at its first stage--i.e. a renin blocker. The first efforts with renin antibodies or peptide analogues of renin prosegments failed to satisify the basic requirements for long-term medication--effectiveness when used orally. In recent years the first non-peptidic, oral renin ihibitor providing sustained effects has been developed, aliskiren fumarate. Aliskiren reduces BP depending on the dose (50-300 mg/day) in monotherapy or in combination with hydrochlorothiazide. Aliskiren lowers plasma renin activity (PRA) and neutralises the activation of the RAAS triggered by hydrochlorothiazide. Ambulatory BP monitoring has shown that taking the medicine once a day has a 24-hour effect and its continued residence in the kidneys suggests renoprotective effects. The compound is in the third stage of clinical tests as a monotherapy or in combination for the treatment of hypertension. It has also been shown to have an influence on the regression of cardiac hypertrophy (Aliskiren in Left-Ventricular Hypertrophy trial - ALLAY), the treatment of heart failure (Aliskiren Observation of Heart Failure Treatment trial - ALOFT) and diabetic (Aliskiren in the Evaluation of Proteinuria in Diabetes trial - AVOID). In April 206, the FDA permitted the use of aliskiren in the USA for the treatment of high BP and it is currently undergoing testing in Europe. The renin inhibitor has minimal undesirable side effects, like AT1-receptor blockers. The slightly lower effectiveness ofaliskiren than AT1-receptor blockers in reducing BP is caused by the fact that it does not block bradykinins. It is recommended as a monotherapy for clinical use or in combination with other antihypertensive medicines for conditions with high levels of PRA including its rise after diuretics, ACEI and AT1-receptor blockers. Aliskiren could therefore be used primarily with young patients, Caucasians, persons with ACEI intolerance, and also in diseases where angiotensin II is involved in the pathogenesis and the secondary prevention of cardiovascular disease. It is also safe for persons with concurrent renal problems, because it is mainly removed by the liver without great interference with other materials. Like ACEI, the renin inhibitor has a vasodilatory effect which could potentially improve the elasticity of arteries. The medicine has the same limitations and contraindications as ACEI and AT1R blockers, such as pregnancy and bilateral renal artery stenosis. A definitive assessment of the benefit of this new class of medicines and its broad application in the treatment of cardiovascular and other diseases will require demonstration of its long-term effect on morbidity and mortality, as well as comparison with other RAAS blockers in long clinical studies, which represent research programmes lasting another 7 to 8 years.
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PMID:[Does the rennin inhibitor aliskiren offer promising novel opportunities in the treatment of cardiovascular diseases?]. 1757 67

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


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