Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
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Aortic dissection may be associated with renal disease. The presentation, especially in the later stages of the process, includes proteinuria, hematuria and impairment of renal function. Thus the clinical picture may be confused with glomerulonephritis or hypertension. We present a case of ischemic nephropathy resulting from involvement of the right kidney by an aortic dissection. The pateint presented with the nephrotic syndrome some two and a half months after the probable time when the aortic disection had occurred. At that time the initial back and flank pains had disappeared. Ultrasound examination revealed a smaller right kidney, compared to the left one. Imaging techneques, initaited for suspected renal artery stenosis, revealed aortic dissection involving the right renal artery starting from the descending aorta, distal to the origin of the left subclavian artery and extending down to the right common iliac artery; occluding the right renal artery. The medical literature is reviewed for patients presenting with ischemic nephropathy and the mechanisms of proteinuria discussed. We conclude that ischemic nephropathy can clinically mimic glomerulonephritis and can be missed if it is not included in the differential diagnosis of patients who present with heavy proteinuria and hypertension.
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PMID:Missed renal infarction presenting as the nephrotic syndrome: a case report. 1766 Jun 58

Numerous anatomical and functional changes occurring in the aging kidney lead to reduced glomerular filtration rate, lower renal blood flow and impaired renal autoregulation. The elderly are especially vulnerable to the development of renal dysfunction and in this population acute renal failure (ARF) is a common problem. ARF is often iatrogenic and multifactorial; common iatrogenic combinations include pre-existing renal dysfunction and exposure to nephrotoxins such as radiocontrast agents or aminoglycosides, use of NSAIDs in patients with congestive cardiac failure and use of ACE inhibitors and diuretics in patients with underlying atherosclerotic renal artery stenosis. The aetiology of ARF is classically grouped into three categories: prerenal, intrinsic and postrenal. Prerenal ARF is the second most common cause of ARF in the elderly, accounting for nearly one-third of all hospitalized cases. Common causes can be grouped into true volume depletion (e.g. decreased fluid intake), decreased effective blood volume (e.g. systemic vasodilation) and haemodynamic (e.g. renal artery stenosis, NSAID use). Acute tubular necrosis (ATN) is the most common cause of intrinsic ARF and is responsible for over 50% of ARF in hospitalized patients, and up to 76% of cases in patients in intensive care units. ATN usually occurs after an acute ischaemic or toxic event. The pathogenesis of ATN involves an interplay of processes that include endothelial injury, microvascular flow disruption, tubular hypoxia, dysfunction and apoptosis, tubular obstruction and trans-tubular back-leak. Vasculitis causing ARF should not be missed as this condition is potentially life threatening. The likelihood of a postrenal cause for ARF increases with age. Benign prostatic hypertrophy, prostatic carcinoma and pelvic malignancies are all important causes. Early identification of ARF secondary to obstruction with renal imaging is essential, and complete or partial renal recovery usually ensues following relief of the obstruction.A comprehensive medical and drug history and physical examination are all invaluable. Particular attention should be paid to the fluid status of the patient (skin turgor, jugular venous pressure, lying and standing blood pressure, urine output). Urinalysis should be performed to detect evidence of proteinuria and haematuria, which will aid diagnosis. Fractional excretion of sodium and urine osmolality may be measured but the widespread use of diuretics in the elderly gives rise to unreliable results. Renal imaging, usually ultrasound scanning, is routinely performed for assessment of renal size and to exclude urinary obstruction. In some cases, renal biopsy is necessary to provide specific diagnostic information. The general principles of managing ARF include treatment of life-threatening features such as shock, respiratory failure, hyperkalaemia, pulmonary oedema, metabolic acidosis and sepsis; stopping and avoiding administration of nephrotoxins; optimization of haemodynamic and fluid status; adjustment of drug dosage appropriate to glomerular filtration rate; early nutritional support; and early referral to nephrologists for diagnosis of ARF cause, timely initiation of dialysis and initiation of specific treatment. The treatment of prerenal and ATN ARF is largely supportive with little evidence of benefit from current pharmacological therapies. Despite advances in critical care medicine and renal replacement therapy, the mortality of ARF has not changed significantly over the last 40 years, with current mortality rates being up to 75%.
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PMID:Management of acute renal failure in the elderly patient: a clinician's guide. 1854 Jun 87

In patients with severe hypertension a search for a renal cause, particularly for a renal artery stenosis, needs to be undertaken with 24-hour blood pressure measurement, urinary examination, determination of renal function and duplex sonography of the kidneys.--Sympathetic hyperactivity, which is associated with an increased cardiovascular risk, may already be found in an early stage of renal diseases. There is evidence that administration of an ACE inhibitor or an angiotensin receptor antagonist (ARB) may induce a decrease of sympathetic hyperactivity as well as a reduced rate of adverse cardiovascular events in patients in renal failure.--In patients with renal disease and high proteinuria antihypertensive therapy with ACE-inhibitors or ARB delays the progression of chronic renal failure. Combined therapy of ACE-inhibitors plus ARB may reduce proteinuria more than that would be the case with either of these drugs alone. However, there is no evidence that combination of these two drugs improves renal function more than monotherapy.--Renal artery stenosis of > 70% should be treated by dilatation, if there is evidence of fibromuscular dysplasia. Dilatation and/or stent implantation in an atherosclerotic renal artery stenosis of > 70% should be performed if indicated by the patient's clinical state. i.e. severe hypertension has proved to be resistant to triple drug antihypertensive therapy or pulmonary edema has occurred frequently. Preservation of renal function by angioplasty of an atherosclerotic renal artery stenosis remains a challenge. However, exact criteria for such intervention need to be established. But so far there have not been adequate data from controlled prospective trials.
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PMID:[The kidneys and hypertension]. 1877 Apr 87

Hyponatremic hypertensive syndrome is a manifestation of severe hypertension related to renal ischemia. The most common underlying cause of hyponatremic hypertensive syndrome in adults is severe atherosclerotic reno-vascular disorder while in children the most common cause of hyponatremic hypertensive syndrome is unilateral congenital renal artery stenosis due to some form of arterial dysplasia. An excessively stimulated renin-angiotensin-aldosterone system is mainly responsible for heavy polyuria, renal electrolyte loss and proteinuria. The neurological manifestations of hyponatremia and/or hypertensive encephalopathy are the main presenting symptoms, and they are not always in linear correlation with the degree of hyponatremia and/or hypertension. The cornerstone of management is the treatment of underlying hypertensive disease, but the correction of hyponatremic dehydration and safe decrease of blood pressure are essential in the emergency phase of hyponatremic hypertensive syndrome. The optimal antihypertensive therapy depends on the underlying condition. Revascularization, either surgical or by percutaneous transluminal angioplasty, is recommended for children with renal artery stenosis. Pharmacological treatment based on ACEI and/or ARB is the most efficient antihypertensive therapy for those with ischemic reno-parenchymal disorder. Nephrectomy is required if an affected kidney contributes less than 10% of the global renal function, if percutaneous transluminal angioplasty fails and the operative risk is too high, or in the case of extensive tumorous lesions.
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PMID:Hyponatremic hypertensive syndrome. 1892 57

Three children under the age of 3 years presented with malignant hypertension, proteinuria, and acute kidney injury. Takayasu's arteritis was diagnosed on the basis of clinical symptoms of weight loss and low grade fever in conjunction with elevated sedimentation rate and radiographic evidence of aortic and renal artery stenosis. One patient had a renal biopsy which showed arteriolar sclerosis and focal glomerulosclerosis. All three patients required multiple antihypertensive agents, ultimately including angiotensin receptor blockers and/or angiotensin converting enzyme inhibitors. The vasculitis was treated with pulse corticosteroids followed by cyclophosphamide in one patient and mycophenolate mofetil as maintenance therapy in all. Follow-up has ranged from 2 to 8 years. Although global renal function has normalized in each patient, two have unilateral non-function of one kidney. The last patient has persistent aortic and renal artery stenosis with complex collateralization requiring ongoing medical and anticipated surgical management.
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PMID:Renal manifestations in toddlers with Takayasu's arteritis and malignant hypertension. 2006 41

A 25-year-old female at 10 weeks of her first pregnancy abruptly developed severe hypertension as high as 230/160 mmHg and thus was referred to our hospital. Her past history was unremarkable and no medication or supplement was prescribed. The laboratory findings revealed that plasma renin activity was 59.0 ng mL hr and plasma aldosterone concentration was 1700 pg mL together with serum creatinine of 0.42 mg dL and serum potassium of 2.8 mEq L. Urinalysis revealed insignificant findings. Her hypertension was extremely resistant to antihypertensive agents, including hydralazine, alpha-methyldopa, and alpha beta blocker, leading to suspicion of secondary hypertension as a cause. Adrenal tumor was not detected but Doppler ultrasonography suggested the constriction of the right renal artery consistent with renovascular hypertension. Considering the following imaging test and medications, the patient and her family decided to abort the pregnancy. 3D-CT and MR angiography showed stenosis of the right renal artery, therefore, percutaneous transcatheter renal angioplasty was performed, resulting in normalization of the blood pressure without antihypertensives. Two years later she successfully gave birth uneventfully. Her hypertension was presumably irrelevant to preeclampsia because it occurred at 10 weeks of pregnancy and proteinuria was not associated. The stenosis of the right renal artery was probably due to fibromuscular dysplasia, which is one of the major causes of renal artery stenosis in young women. This patient was such a case and presented a difficult decision on how to treat and whether or not to abort. We will discuss the mechanism of hypertension in pregnancy and the advantages and disadvantages of available treatments for such cases.
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PMID:[Case of fibromuscular dysplasia revealed by the emergence of severe hypertension in the early phase of pregnancy]. 1960 60

Long-term allograft survival poses a major problem in pediatric renal transplantation, with allograft nephropathy being the principal cause of graft failure after the first post-transplant year. The mechanisms of nephron loss resulting in graft dysfunction are multiple, comprising both immunologic factors such as acute and chronic antibody- or T-cell-mediated rejection and non-immunologic components. The latter include peri-transplant injuries and renovascular lesions (renal artery stenosis, thrombosis) as well as cardiovascular risk factors such as arterial hypertension and hyperlipidemia. Another relevant issue leading to progressive nephron loss and declining kidney transplant function is acute and chronic nephrotoxicity induced by the calcineurin inhibitors (CNIs) ciclosporin (cyclosporine microemulsion) and tacrolimus. Furthermore, the presence of an abnormal lower urinary tract as well as bacterial (recurrent pyelonephritis) and viral (cytomegalovirus [CMV], polyomavirus [BK virus; BKV]) infections are crucial factors involved in the incidence of chronic allograft dysfunction and graft failure. Renovascular lesions and lower urinary tract obstruction are typical indicators for surgical intervention. The aim of treatment in pediatric patients with renal failure secondary to a dysfunctional lower urinary tract is to create a sterile, continent, and nonrefluxive reservoir. Surgical techniques such as bladder augmentation and the introduction of intermittent catheterization and anticholinergic therapy have significantly improved graft outcome. Arterial hypertension, another factor responsible for graft function deterioration in pediatric renal transplant recipients, is controlled preferably by the use of angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists, which are known to possess nephroprotective properties in addition to their potent antihypertensive effects. Although treatment of subclinical rejection with augmented immunosuppression has been associated with better graft survival, an increase of the immunosuppressive level to avoid subclinical rejection should be weighed against the risk of infection. The majority of viral infections affecting kidney allografts are caused by CMV and BKV. Antiviral CMV prophylaxis or pre-emptive therapy with ganciclovir has been shown to have beneficial effects in the pediatric renal transplant population. Treatment of BKV-induced nephropathy is based on reduction of the immunosuppressant therapy, although specific antiviral agents such as cidofovir and leflunomide are known to inhibit BKV. However, cidofovir itself is nephrotoxic and should therefore be administered cautiously to pediatric renal transplant patients. Since CNIs are likewise known for their nephrotoxic effects, especially with long-term use, alteration of the immunosuppressant regimen is necessary in case of deteriorating graft function due to CNI-induced histopathologic changes. Complete CNI avoidance seems inappropriate because, in this situation in pediatric renal transplant recipients, other relatively potent immunosuppressant agents such as lymphocyte-depleting antibodies, which are frequently accompanied by a higher incidence of infections, are needed for rejection prophylaxis. CNI withdrawal and switching of the immunosuppressant regimen from CNI therapy to sirolimus may be an option for some pediatric renal transplant patients with less advanced graft function deterioration. Nevertheless, potential adverse events such as aggravation of proteinuria, hyperlipidemia, myelosuppression, and hypergonadotropic hypogonadism have to be considered, and controlled studies are lacking. At present, an immunosuppressant maintenance therapy composed of low-dose tacrolimus or ciclosporin (CNI minimization) and mycophenolate mofetil with low-dose corticosteroids appears to be the most promising strategy to adopt in pediatric renal transplant recipients at low or normal immunologic risk.
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PMID:Treatment strategies to minimize or prevent chronic allograft dysfunction in pediatric renal transplant recipients: an overview. 1987 24

Renal artery stenosis (RAS) is a progressive disease and may lead to chronic kidney disease by deterioration of renal functions. Endothelial dysfunction is an important causative factor for kidney damage after RAS revascularization. Nebivolol, a new generation beta blocker induces endothelium-related arterial relaxation by nitric oxide (NO) and may improve endothelial dysfunction. This pilot study tested the effect of nebivolol on the glomerular filtration rate (GFR) in a series of 33 patients with severe RAS (>70%) who underwent revascularization. After revascularization, nebivolol was added to antihypertensive treatment in 17 randomly selected patients while 16 patients (control group) continued their standard treatment. Estimated glomerular filtration rate (eGFR), proteinuria as well as nitrite and nitrate levels were measured at baseline and 6 months after the revascularization procedure. Six months after revascularization, eGFR increased from 44.8 to 50.6 ml/min in the nebivolol group. In contrast, eGFR did not change in the control group. Nitrite/nitrate levels decreased to a significant extent both in the nebivolol and in the control group. Proteinuria decreased more in the nebivolol group compared to the control group. These pilot data support a full-fledged clinical trial, testing whether nebivolol may be beneficial in the post-revascularization phase in patients with RAS.
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PMID:Nebivolol improves renal function in patients who underwent angioplasty due to renal artery stenosis: a pilot study. 1995 27

The role of renin-angiotensin-aldosterone system (RAAS) in regulating the volume and composition of extracellular fluid, blood pressure (BP) as well as onset and progression of cardiovascular and renal diseases has been studied for more than 150 years. The compounds that block the vital stages of the RAAS cascade, such as ACE-inhibitors (ACEI), AT1-receptor blockers (ARB) and aldosterone receptor antagonists, importantly extended our treatment options. However, the positive therapeutic effects of these compounds also have certain negative consequences. Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ('escape' phenomenon). These possible adverse effects of the intermediary products of incomplete RAAS blockade leading to organ complications have facilitated the efforts to develop compounds blocking the initial stages of renin-angiotensin cascade--i.e. direct renin blockers. After several years of unsuccessful attempts, the recent years have seen development of the first non-peptide, orally long-term effective renin inhibitor, aliskiren fumarate. In monotherapy or in combination with other antihypertensives (hydrochlorothiazide, ARB, ACEI), aliskiren reduces BP in a dose-dependent manner (75-600 mg/den). Aliskiren reduces plasma renin activity (PRA) and neutralises hydrochlorothiazide-induced RAAS activation. Once daily administration of the drug leads to longer than 24-hour activity and its prolonged blocking effects on the kidneys are the basis for its renoprotectivity. In addition to the significant antihypertensive effect, clinical studies also showed a range of organoprotective properties in patients with left ventricle hypertrophy (ALLAY study), heart failure (ALOFT study) and diabetic nephropathy (AVOID study). Similar to other AT1-blockers, aliskiren has a minimum of adverse side effects. Aliskiren for hypertension therapy was launched in clinical practice in USA in 2007 (Tekturna and combination formulation TekturnaHCl, respectively) and shortly after that in European Union as Rasilez. In the Czech Republic, aliskiren (Rasilez) was released for clinical use by diabetologists and nephrologists in patients with hypertension and concomitant diabetes, nephropathy and proteinuria in doses of 150-300 mg per day on 1. 8. 2009. It is recommended as monotherapy or in combination with other antihypertensives to treat conditions with elevated PRA, including PRA elevation following diuretic, ACEI or ARB administration. Aliskiren might be used in patients who do not tolerate ACEIs as well as in patients in whom angiotensin II participates in the pathogenesis of their diseases. Reno-protective properties leading to a reduction in proteinuria and delaying renal failure progression were observed in patients with diabetic as well as non-diabetic nephropathy. The drug is the subject to similar precautions and contraindications as ACEIs and ARBs, i.e. pregnancy and bilateral renal artery stenosis. To make meaningful conclusions about the so far positive contribution of this new treatment class and its broad applicability for the therapy of hypertension and other cardiovascular diseases, it will be imperative to assess its long-term effects on morbidity and mortality as well as to compare these agents with other RAAS blockers in long-term clinical studies; this represents a research effort for another 7-8 years.
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PMID:[Direct renin inhibitor aliskiren in the treatment of cardiovascular and renal diseases]. 2032 82

Renal artery stenosis (RAS) is a disease which might present as hypertension, renal insufficiency or proteinuria and even as nephrotic syndrome. While 90% of cases are secondary to atherosclerosis, the rest of the cases are usually related to fibromuscular dysplasia. Recently, RAS has also been documented in patients with the antiphospholipid syndrome (APS). Although cases of nephrotic syndrome induced by RAS have been published, cases of patients with APS and nephrotic syndrome attributed to RAS were not reported in the literature. In this paper, three young male patients with APS, hypertension and significant proteinuria secondary to RAS are presented. The patients were treated with nephrectomy or revascularization in addition to prior treatment with warfarin, with improvement of the hypertension and the proteinuria. The relationship between renal artery stenosis, nephrotic range proteinuria and APS is reviewed. We suggest that renal artery stenosis should be included in the differential diagnosis of the nephrotic syndrome and that APS should be included in the differential diagnosis of renal artery stenosis especially in young male patients with proteinuria.
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PMID:Renal artery stenosis with significant proteinuria may be reversed after nephrectomy or revascularization in patients with the antiphospholipid antibody syndrome: a case series and review of the literature. 2066 31


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