referat metodologia cercetarii stiintifice

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REFERAT METODOLOGIA CERCETARII STIINTIFICE VENELE RENALE- CONTRIBUTIA LA STUDIUL ANATOMO CLINIC AL VASCULARIZATIEI RENALE MEDICINA DENTARA I GRUPA IV POPA ALEXANDRA GABRIELA

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Page 1: Referat Metodologia Cercetarii Stiintifice

REFERAT METODOLOGIA CERCETARII STIINTIFICE

VENELE RENALE-CONTRIBUTIA LA STUDIUL ANATOMO CLINIC AL

VASCULARIZATIEI RENALE

MEDICINA DENTARA IGRUPA IV

POPA ALEXANDRA GABRIELA

SUMMARY

Cap.I. Working Hypothesis .................................................................................. ........ pg.3Cap.II. General Part ................................................................................................ ..... pg.4Chapter III. Material and Methods ................................................................................ pg.7

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V.1. Clinical and laboratory study - Study of the correlation between HRV through direct vascular injury by renal vascular anormalities neastomosated congenital or acquired and the lesions Vascular indirect (vascular compression) by assessing HRV in hypertension nefrogenes shareV.2. Anatomic-pathological study of preparations obtained during the nefrectomiesV.3. Experimental studies on animals of laborator experience Cap.IV. Results ............................................................................................... ........... pg 10Cap.VII. Discussion results ......................................................................................... pg.11CapVIII.Conclusions...................................................................................... ............ pg.13Selective Bibliography ……………………………………………………………….pg.15

Chapter I Working hypothesis Anatomy vascularisation of the kidney is a diversity complex both because of segmentation, ramification renal artery, and because the etiology of vascular network echo disease. In recent decades, with the development of means of investigation and discovery system reninăangiotensină - aldosterone (Page-1940, Braun-Menendez-1939), concluded that some of hypertension treated the key is actually secondary to well-defined lesions, often the kidney. Furthermore, HTA nefrogene occurs in many renal diseases, especially in their stages advanced. As to etiology, it recognizes: - HTA renoparenchimatoasă - renovascular hypertension. HRV determined by unilateral or bilateral stenozarea artery / renal artery or main branches is the may curable hypertension and involves one of the forms of chronic renal insufficiense potential of curability. But not all renal artery stenosis causes hypertension pressure, whereas activation of the renin-angiotensin depends on the severity of stenosis and the hemodynamic relevance. Number of cases of HRV is relatively small, by compared with alarming frequency and always growing essential hypertension, but their interest is precisely in curable nature which gives them a special status. Beginning from these realities, working assumption is based on demonstration of

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correlations between the vascularisation of impairment, individual model affections it with the emergence of kidney disorders due the vascularisation impairment and the need to establish clear of diagnosis for the effectiveness of therapeutic means.

REZUMATAnatomia vascularizaTiei renale constituie o diversitate complexă atât datorită segmentării, ramificării arterelor renale, cât si datorită răsunetului retelei vasculare în etiologia unor maladii. În ultimele decenii, odată cu dezvoltarea mijloacelor de investigatie si cu descoperirea sistemului reninăangiotensină-aldosteron (Page-1940; Braun-Menendez- 1939), s-a ajuns la concluzia că o parte din hipertensiunile considerateca esentiale sunt de fapt secundare unor leziuni bine definite, de cele mai multe ori renale. Pe de altă parte, HTA nefrogenă apare în foarte multe boli renale, mai ales în fazele lor avansate. Din punct de vedere etiologic, se recunoaste :- HTArenoparenchimatoasă, - HTA renovasculară. HRV, determinată de stenozarea unilaterală sau bilaterală a arterei / arterelor renale sau a ramurilor principale este cea mai curabilă hipertensiune arterială si implică una din formele de insuficientă renală cronică potential vindecabilă.Dar, nu toate stenozele de arteră renală determină hipertensiune arterială, întrucât activarea sistemului renină-angiotensină depinde de severitatea stenozei si de relevanta hemodinamică. Numărul cazurilor de HRV este relativ restrâns, prin comparatie cu frecventa alarmantă si mereu crescândă a hipertensiunilor esenŃiale, dar interesul lor constă tocmai în caracterul curabil ceea ce le conferă un statut aparte.Pornindde la aceste realităti, ipoteza de lucru are la bază demonstrarea unor corelatii între vascularizatia renală, modelul individual al acesteia cu aparitia unor afectiuni renale datorate tulburărilor de vascularizatie renală precum si necesitatea stabilirii certe adiagnosticului pentru eficienta unor mijloace terapeutice.

Chapter II.

GENERAL PART Summary, kidney fulfills the following roles in human body: 1. excretion function of the body substances or depuration useless endogenous and exogenous, 2. role in maintaining acid-base balance, 3. role in maintaining osmotic balance, 4. endocrine-metabolic function

Renal vasculature Irigation pressure ensures kidney arteries kidney, lateral branches of abdominal aorta, usually the both. Referring on the number usually there is only one renal artery for each kidney, but there are often variations of this vessel. In general they concern how the branch arteries, where they deal with kidney and number variants (supernumerary).

Variability of arteries kidney is greater than the renal vein. Explanation may be given by the existence of different sources of pressure irrigation of the kidney during development. Thus, during ontogenesis kidney receives blood from the artery arteries loan sacral, common iliac artery and the lumbar region of the three arteries of the adrenal gland of which the most caudal renal artery becomes final, the persistence of some of these ship explain deviations from normal body irrigation, that the presence of accessory arteries of the kidney. From renal arteries in the hill of the kidney neighborhood, go into a common terminal branches, four branches are placed pre-skin

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(before the renal pelvis) and one is retro-skin (must avoided pielotomia rear). All these arteries are anatomical terms in terminal arteries.Here, the renal arteries give rise artery segmentation interlobes or peripiramidale.They are in number about 100 in a kidney. Kidney bertin entered the columns (one around 4.5 each pyramid) and the FENE pyramid going forward from the papillary to their base. He arrived at the pyramids To Malpighi interlobes arteries inflects right angle forming curved arteries, they do not anastomosating between them. Arteries arched branch and give interlobulare arteries. The transition from curved to the arteries is a interlobes ramification a sudden and very rich. Nointerlobulare arteries are not anastomosating between them, with all their numbers very large (tens of thousands). They have formed an average of Several lines of Mioc, elastic and collagen fibers. Lamina external elastic is absent. Interlobulare arteries are placed radial, cross Ferrein cortical among pyramids, and reach fibrous capsule of kidney, and some even penetrate, into the anastomosating arteries of adipos perirenales . From capsule of the arteries come off the dishes interlobulare related to penetrate the vascular pole of renal corpuscles and is capilarisating to form of the renal glomerules.The kidney glomerules continues to effent dish. Kidney veins are similar to the provision of arteries, however they present some differences. It describes veins of the paranchim and veins of the fat capsule. In the parenchymal veins form a venous arch suprapiramidal continuous, consisting of arched veins. They are related together by anastomosis. This arcade is suprapiramidalecollect blood from the kidney, the vein downward and upward. Venous circulation of the kidney is not completed, as the pressure, with the various territories venous communication or anastomosis. The veins are the veins downward interlobulare. In near the base of the pyramids is recurbating passing the arched veins. Ascending veins originate capillaries surrounding renal tubules and is called venue straight. Arched veins accompanying arteries of homonyms. He reached the columns right kidney is incurbating and down through the columns. They are the veins that interlobules collected affluentscolumns of Bertin, and reached the sinus are united in the small calice piece of sinus vein branches. Have a paths varied, some of which are located before other return arterial branches. Sinus branches unite and form renală.Ca vein and renal arteries, veins have variations that may especially in number. Data on lymph vascularisation kidney are contradictory. Clearly no glomeruls and no marrow not state the existence of three classical limfatics.The description of the perivascular lymphatic capillary networks located: the sine kidney form of collecting, the fibrous capsule and the fat capsule.

Renovascular hypertension (HRV) Renovascular hypertension is defined as a secondary afection of renal arterial lesions can be corrected by restoring movement of blood pressure or kidney nephrectomy. Initially, name of renovascular hypertension was referred only to that caused by renal artery stenosis, which causes renal ischemia, acception largely maintained today. Is part of secondary hypertension were included in terms of the high nefrogene etiologic along with hypertension major renoparenchimatoasă. The causes of the renovascular hypertension is atherosclerosis and dysplasia fibromuscular average. Atherosclerosis is incriminated in 60-80% of cases with renovascular hypertension. The lesion is represented, ultimately, the formation of plaques that lower ateromatoase arterial lumen. Injuries are common in ateromatoases men over 50 years, smokers. Appear in third proximal renal artery, sometimes even ostiumul artery stenosis (diferentiention between plates and the proximal ateromatoases hostile is important to perform angioplasty). Evolution-the absence obstruction-treatment is gradually to complete. The estimated that 15% of patients with CKD are affection causal HRV. Fibromuscular dysplasia is present in 33% of cases of renal artery stenosis. Etiopatogenia is known, is take into discussion the role nefroptoses and smoking. Appears to younger individuals with a

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marked predisposition women. It rarely affects more frequently bilateral renal artery right, especially the distal portion main trunk and, frequently, grab branches intrarenal segmentation. There is under 4 morphopathological forms as follows: 1. Fibroplazia (dysplasia) intimate, whose support is pathological holds circumferential collagen accumulation, the reduction lumen. The adults appears in children and young people, representing 5-10% of dysplasia lesions. 2. Fibromusculară hyperplasia - a rare lesion (3% of dysplasia); is to support true smooth muscle hyperplasia, is in children and young adults. 3. Fibroplazia (dysplasia) average - the most common, representing 80% of dysplasia, more common in women young (20-50 years). Pathology, rings appear fibrotic pressure stenotics, interspersed with dilatations type aneurysm. Characteristic appearance on arteriography is the "string of beads "(string of beads). 4. Fibroplazia (dysplasia) perimediei. Represents 10-15% of dysplasia, occurs more often in young women and especially right kidney. Renal artery agenesis is based on development embryological aberration of the three groups of vascular channels primitive: cranial, middle and caudal, part of which will degenerate after migration of the kidney .Infarctul artery posttraumatic may be the consequence of a lower back contusion violent, with or without rupture of the kidney, which resulted in a renal artery thrombosis. Often post-traumatic heart is installed after postoperative interventions relating in particular within the cardiovascular, (mitral stenosis, aortic aneurysm, etc..), or path excretor kidney (partial nephrectomy, nefrotomia, section vessels and less polar pielotomia) Hypertensive Nefroscleroza be classified in benign or malignant, depending on the method of evolving lesions secondary hypertension, maintaining blood pressure caused by a long time - systolic pressure over 160 mmHg and the diastolic above 90 mmHg.

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Chapter III MATERIAL AND METHOD Concluding the set, this work aims towards clinical and anatomical study of morphopathological vascularisation renal alteration in terms of movement of bloodthrough the kidneys direct vascular lesions, renal vascular abnormalities nestenozantes and congenital or acquired vascular lesions indirect (vascularcompression), and their echo with renovascular hypertension with clinical methods, pathological, imaging and experimental. 1. Clinical and laboratory study-study corelated between HRV through direct vascular injury by renal vascular abnormalities nestenosated congenital or acquired and the lesions Vascular indirect (vascular compression) by assessing HRV ratio of hypertension nefrogene 2. Anatomic-pathological study of preparations obtained after the nefrectomies 3. Experimental studies on experience and laboratory animals The survey was conducted on a total of 493 patients, supplemented by pathological analysis of 217 prepared obtained from nefrectomies and a total of 20 of laboratory animals. Clinical and laboratory III1.Studiul of patients with HRV by direct vascular injury by renal vascular abnormalities nestenosate congenital or acquired and the lesions vascular indirect (vascular compression) in the light share HRV in hypertension nefrogene stuff The lot includes a total of 493 patients aged between 15-70 years, the hospital examination in Oradea, Section of Nephrology and Hospital C.F.R. Oradea, Section of Nephrology, during 2000 to 2005. Selection lot was based on two criteria, the the one hand the lack of response to treatment in patients with hypotensive long evolving hypertension, and on the other patients in that hypertension was discovered by chance at some other afections. We found that hypertension is refractory to treatment conditions under which the medicinal values above 170/110 mmHg to maintain the patient who receives an optimal dose of 3 to 4 antihypertensive usual. These patients diagnosticated with hypertension are nefrogene.

Methodology Review Clinical examination was carried out systematically in all the pacientes followed by laboratory examinations and laboratory radioimagistics. Evaluation Criteria Favorizating were factors in the emergence of hypertension followed by rocked of personal and family history, age, gender and combination of various symptoms and their correlation with aspects radioimagistics and other laboratory abnormalities and specific binding. - Patient distribution by age; - Distribution of patients by degree provenience; - Patient distribution by sex; - Heredo-side corelation between history and personal HRV etiology; - Corelations between clinical symptoms with HRV etiology; - Presence of breath, or systolic-diastolic abdominal sistolo as a positive diagnostic tool; - Assessing the results of laboratory investigations required as evidence of a positive diagnosis;

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- Corelations of the results of special laboratory investigations and etiology of HRV.

III.2. Anatomic-pathological study of preparations obtained after the nefrectomies It took a total of 217 study biological preparations ( kidney and renal pelvis) obtained after the nefroctimies made the period 2003 - 2005 the Department of Urology Hospital Clinical Oradea and processed in the Laboratory Pathological Anatomy of the same hospital. The study consisted of macroscopic examination of the play operators as well as microscopic examination of preparations biological. Sampling of biological material for microscopy was executed in pathological anatomy laboratory of Clinical Hospital Oradea is an essential step for the study histology and pathology.

Methodology Review After studying foreign configuration I prepared dishes kidney as deep as possible in sine kidney. To study microscopic been done to section with microtome at 4.8 microns, depending on the structure considered. Coloring blades was done with hematoxylin-eozine but I used and special coloration Van Gieson for the conjunctiv tissue, HE, PAS for hialin, etc. The coloration blades and their study has made in the laboratory of pathological anatomy of Hospital Oradea.

Evaluation Criteria -distribution by gender nefrectomies nephrectomised; -nefrectomies of the age distribution of persons nephrectomised; -distribution nefrectomiilor after urological diagnosis; -nefrectomies distribution by sex, age group and urological diagnosis; -correlations between anatomical lesions and kidney pathology nefrectomies;

III.3. Experimental studies on experience and laboratory animals Research project titled Goldblatt hypertension with two kidney was performed in the University of Medicine and Pharmacy Timisoara, in Biobaza Surgery Center Laparoscopic and Microsurgery,, Pius Branzeu '. In 1934, Goldblatt has shown by experimental work pensare a renal artery that drives fast blood pressure is investigating the behavior of blood pressure in rats at different times after applying a pensare a kidney artery stenosis. Luan the study were 20 Wistar rats weighing between 250-300 g, were in group A and group group B, each lot consisting of 10 rats of each sex male. Measuring and recording blood pressure values of was possible using a simple device consisting in Physiology Laboratory at the University of Medicine and Pharmacy, Victor Babes ", Timisoara by Dr. Ordodi V.L.

Method To conduct surgical techniques, the animals were anesthetized with Isofluran in conc. 3% for induction anesthesia and 1.2% for maintaining them over the experiment.For the renal artery clipping were used microclipuri with microaproximatorului in order to obtain a hemodynamically significant stenosis with narrowing renal artery lumen of approx. 70-80%. To measure TA has used the carotid artery catheterization left.Tuturor experience animals were conducted measurements of the TA, starting at 4 o'clock renale.At the artery 2 months after clipping the commencement of the experiment, was charged nephrectomy kidney release the animals in group A and in 3 months nephrectomy release kidney BS-group animals continued to TA measurement yet 2 months of completing the group nefrectomiei A and group B at 1 month after removal of the kidney release. .

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Chapter IV RESULTS IV.1. Clinical and laboratory study Following data from history, clinical picture, physical examination in conjunction with laboratory investigations specific binding and was diagnosed with hypertension Renovascular for the 122 patients. Summary from clinical trials on a batch of 493 patients selection (HTA toughness 3-4 usual antihypertensive), 122 patients (24.7%) have hypertension renovascular. According to the classification of etiology, 19.6% of patients have a bilateral stenosis of small vessels due a complex essential hypertension, 22.3% with bilateral stenosis small vessels due to malignant hypertension, 36.8% with occlusion incomplete unilateral renal artery that ateromatoasă, 4.1% of dysplastic unilateral renal artery stenosis, 0.8% with as aberrant lower polar vessel, 6.5% with extrinsic compression artery stenosis because renal

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cysts and 9.9% by Renal artery compression due to renal tumors.

IV.2. Anatomic-pathological study of preparations obtained after the nefrectomies Distribution over nefrectomiilor showed that 35% is due Grawitz tumors, followed by pionefroze (25.8%) and of hydronephrosis (11.9%). After examining the macro and microscopic changes were highlighted characteristic vascular nephropathy in 19 patients (8.7%).

IV.3. Experimental studies on experience and laboratory animalsIn this study we studied the behavior blood pressure in Wistar rats over 4 months after application of a clamp on renal artery of a kidney. S found that blood pressure began to rise after a within 4 hours of clipping mentaining is built on during the 2 months of observation. Nephrectomy kidney release made at the end of 2 months of clipping determined normalizing blood pressure. Nephrectomy A later release kidney at 3 months of the clipping TA does not result in normalization.

Chapter V. DISCUTION RESULTS Ducher M. et al. (2005) conducted a screening on 336 patients for resistant renal artery stenosis ateromatoasă 2 antihypertensive agents focusing on personal and family history, living environment, attitudes behavioral presence alongside breath systolic laboratory investigations. Prevalented artery stenosis ateromatoasă was 15%. In the study, 43% of the pacients with hypertension and nefrogene 40.1% of the HRV pacients declares the existence in history family of hypertension. The literature specialist, Maxwell states 41%, 30.9% and Proca Hunt 3 also considers one of the patients have a history family hipertensive. Although hypertension often missing in patient's family with HRV, detect dysplasia fibromusculare first-degree relatives drew attention to the family character, though few cases are cited. The collection of breath-sistolo systolic or diastolic paraombilical, subxifoidian or lumbar (L2) is a sign valuable diagnostic positive for HRV, especially for the by fibromusculară dysplasia. This sign was detected in a total of 84 pacients with hypertension nefrogene (17.03%). Of these there are to make investigations special number of 59 patients representing 70.23% of all patients with systolic or presence breath sistolodiastolic and 48.36% of all patients with HRV. Maxwell recorded the presence of breath in proportion 50%, Julius Milliez report quoted by the presence of

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breath in 16% of the normal subjects and in 28% of cases of hypertension. Breath systolic continuously is reported in 80% of cases the artery renal dysplasia fibromusculară by the Hunt and in 57% of Dustan (70, 75, 76). A lot of patients of 47-54 years, Berlung et al. have found the following prevalence of hypertension: primary hypertension-94.0%, HTA renoparenchimatoasă-3.6%, 0.6%-renovascular hypertension, primary aldosteronism-0.1% (77). Stimpel et al. finds in a study of prevalence primary hypertension and 92.9% Renovascular hypertension by 2.1%. Danielson, in a study 1000 patients, 47 are of such secondary hypertension: 10 cases renal artery stenosis, hypertension 21cazuri with the question renoparenchimatoasă, 3 cases with hydronephrosis and 13 cases of endocrine etiology (78). Currently it is estimated that 10-14% of all cases of hypertension is the hypertension and nefrogene HRV holds 5% (for some authors 4%) of hypertension. Khosla and Text consider that option for nephrectomy or revascularization or medical treatment must be taken Taking into account some elements based on the results communicated in the literature as well as the pathogenesis of artery stenosis impairment and their evolution and macro examination time. In microscopic changes were highlighted characteristic vascular nephropathy in 19 patients (8.7%). Of 164 nefrectomii for Grawitz tumors, Proc found severe hypertension only 9 patients (5.4%). Study in laboratory animals is justified, because multiple models can be achieved with applications clinice.În 1939, Page achieved by producing an HTA perinefrită engineering, kidney in cellophane wrapping causing changes hemodynamic hipersecretion with stimulation of renin (101). H. Gavras saralazină mice administered with HRV produced experimentally using the two models Goldblatt ( 2-kidney Goldblatt hypertension Goldblatt hypertension and a kidney). Thus, mice with a kidney HRV is given saralazină to 4 weeks of nephrectomy and was not obtained no effect. If a diet is given in advance without Sodium, hypertension would be maintained but after saralazină TA values decrease in hypertension and renindependentă. If repeat maintained saralazină after being given to drink a solution saline 1%, the result is a non renindependentă hypertension. In model with two kidneys, the test is saralazină HTA renindependentă or reninindependentă, depending on the deplention or sodium load for a period of time (35).

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Chapter VI CONCLUSIONS 1. Anatomy vascularization of kidney is a diversity complex both because of segmentation, ramification renal artery, and because the etiology of vascular network echo disease 2. Between hypertension and renal impairment are 3 types of relationship. When Hypertension is due to vascular-renal damage may be the consequence nefroangioscleroza benign or malignant or hypertension renovascular. When hypertension is due to lesions located at level is the consequence of glomerularhypertension and renal interstitialrenoparenchimatoasă. 3. Renovascular hypertension is hypertension caused by stenozarea unilateral or bilateral, partial or total vascularisation renal pressure, potential curable by surgical gesture (vascular reconstructive surgery or nephrectomy). 4. Part of hypertension are considered as essential actually secondary to well-defined lesions, most often kidney, the kidney may become the victim, the cause of HTA. 5. Although the number of cases of HRV is very limited compared with increasing frequency about essential hypertension, timely recognition of secondary mechanism of hypertension lead to enforcement interventions saving kidney surgery or prevent visceralizarea increase blood pressure. For this reason, high pressure caused by decreased renal mechanisms irigation Local firm emerges from large category of essential hypertension. 6. Based on clinical studies and proved that the disease necroptice Renovascular hypertension occurs only when obstruction arterial lumen may cause ischemia. 7. As to etiology, direct vascular injuries by renal artery stenosis caused by atherosclerosis and dysplasia fibers are the most common cause of HRV 8. Although it may appear at any age, onset before after 35 years or 55 years is a sign of recognition. 9. There is no clinical picture to allow individualization HRV in the large group of hypertensive patients. Although There are similarities of clinical symptoms of HRV with the other forms of hypertension, there are some particularities grouped four poles: brain, heart, kidney and peripheral. 10. The data exam of a patient with hypertension which can make diagnosis and elements that have value when are present, their absence excluding the renovascular disease is the collection of breath-sistolo systolic or diastolic paraombilical, subxifoidian or lumbar (L2). In research present the sign is seen in almost half of the pacients with HRV, with statistics that you recorded in a proportion less

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than or greater, depending on the selectionlot taken in the study. 11. The protocol for investigation of a patient with suspected HRV should be included clinical special tests that can evident anatomic substrate of renal ischemia, in addition tests mandatory for all high. In research present, laboratory tests are usually normal or suggest the presence interest secondary target organs in HTA results are in correlation with the literature specialty. 12. Using several techniques urografice (urographia minutes urografia wash-out) enables more evidentien morphological and functional signs, giving urografiei i.v. value of a screening test but a test value selection in HRV for practicing arteriografiei kidney. Sensitized with captopril isotopic Nefroscintigrama help the selection of cases for arteriographia and, with an accurately urografiei top becomes the preferred screening test for HRV. Doppler ultrasound, non-invasive method but consuming time has a high sensitivity and specificity with an accurately establishing the diagnosis in 15% of false + or false. Renal arteriography is a test confirmation established the presence of arterial lesion, position, extent, condition movement of intra-and extrarenală and diferention lesion that the atherosclerotic renal artery dysplasia. 13. Anatomic-pathological study performed on preparations obtained from nefrectomiilor has highlighted the fact that not few of times, HRV clinical picture is masked or is accompanied by clinical manifestations of a resort afection surgery. Data from literature put in evidence the discovery of stenosis during routine necropsiilor and injuries volunteer blood donors fibromusculare renal grafts Renal perfectly healthy and normotensive. 14. While there have been special investigations preoperative indicating a possible HRV, we can say that the origin of renal hypertension can be established retrospectively, after nephrectomy. Extremely important to establish etiology of renal hypertension is still tracking, over more many years,the comportament of blood pressure. Thus, if Hypertension was not influenced by nephrectomy performed for the afection of spring means that surgery is concerned impairment. If blood pressure or normalize improves after nephrectomy is considered the etiology of arterial hypertension is such impairment. 15. Experimental studies on laboratory animals certified pensare a renal arteries that lead to rapid emergence the kidney HTA.Nefrectomia release made at a time of 2 months from the commencement of the experiment is followed by presión and even decrease in their normalization. Nephrectomy kidney after this evolving release of hypertension does not lead to decreased or normalization presión leading to formation of vascular and parenchymal lesions. 16. The corelation all of clinical, radiological and anatomo-pathological evidence the idea that primary impairment the renal vascularisation causes hypertension renovascular, which is actually more common than diagnoses. Pregnancy detection is for each physician who handling a blood pressure recorder and concubă anatomical knodledge diagnosis and clinical morpho-functional.

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Bibliografie selectiv ă 1. Tortora G. -Principles Of Anatomy And Physiology Ed. John Wiley & Sons Inc, 20052. Massry S.G.,Glassock R.J.,-Textbook of Nephrology, Ed. 3, Williams & Wilkins, Baltimore, 19953. Hamburger J.H. et al.- Structure and function of the kidney. W.B. Saunders Comp., Philadelphia, 19714. Graves F.T.- The vascular anatomy and principles of intrarenal access. În Inta-renal Surgery, ed. By J.E.A. Wickam. Ed. Churchill Livingstone, Edinburgh, London, Melbourne and New York, 1984.5. Craig T., Christopher S.- Wilcox-Nephrology &Hipertension, IV ed., Lippincott, Williams & Wilkins, 1999, 50-776. Ursea N. –Tratat de Nefrologie, Vol 1, Ed. Artprint Bucuresti 1994, Cap. 22, pg. 492-5217. Baker L.R.I.- Renal Disease. In: Parveen Kumar, Michael Clark, editors. Kumar & Clark Clinical Medicine. 5th ed. UK : WB Saunders; 2002. p. 587 – 588.8. Gluhovschi Gh.-Rinichiul si hipertensiunea arterială, Helicon, Timisoara, 19969. Ruttiman S., Steinmann E., and Luscher T.F.- Screening for Renovascular Hypertension .Annals of Internal Medicine,1993, volume 118 issue 11 pages 905-90610. Textor S.C.- Renovascular hypertension and ischemic nephropathy. In: Brenner BM, Rector FC, editors. Brenner and Rector's the kidney. Philadelphia, PA: W.B. Saunders; 2004. pp. 2065–2108.11. Mailloux L.U., Napolitano B., Bellucci A.G., Vernance M., Wilkes B.M., Mossey R.T.- Renal vascular disease causing end-stage renal disease: incidence, clinical correlates and outcomes: a 20-year clinical experience. Am J Kidney Dis 1994;24:622-9.12. Hansen K.J., Edwards M.S., Craven T.E., Cherr G.S., Jackson S.A., Appel R.G., et al.- Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg 2002; 36:443–451.13. Svetky LP, Helms MJ, Dunnick NR, et al.- Clinical characteristics useful in screening for renovascular disease.South Med J 1990; 83:743-74714. Ursea N. -EsenŃialul în nefrologie , FundaŃia Română a Rinichiului, 2000, 156-165.15. McLaughlin K., Jardine A.G., Moss J.G.- ABC of arterial and venous disease. Renal artery stenosis, BMJ 2000, 22;320(7242):1124-716. Kaplan NM- Renal vascular hypertension. Clinical Hypertension. Kaplan NM (ed). Baltimore. Williams & Wilkins Co, 1998, pp 301-32317. Goldblatt H., Lynch J., Hanzal R.F., Summerville W.W. - The production of persistent elevation of systolic blood pressure by means of renal ischemia. Journal of Experimental Medicine 1934;59:347-378.18. Proca E.- Tratat de patologie chirurgicală, Editura Medicală, Bucuresti, Vol. VIII - Urologie, Partea I, 1984, pg. 21-38.19. Papilian V.- Anatomia omului, vol. II Splahnologia, ed. A VI-a, reeditare Editura Didactică si Pedagogică, Bucuresti, 1982, pg. 220-235.20. Safian R.D.- Atherosclerotic Renal Artery Stenosis, Curr Treat Options Cardiovasc Med 2003 ;5(2):91-10121. Sinescu I.- Hipertensiunea arterială renovasculară, Urologie Clinică, cap. 33, pg. 357-362, Ed. Medicală AMALTEA, Bucuresti, 1998.22. Ordodi V.L., Mic F.A., Mic A.A., et al.- A simple device for intubation of rats. Lab Anim 2005;34(8):37-9.23. Ciocâlteu Al.- Nefrologie, EdiŃia a doua, 2001, Ed. Infomedica, cap.2:Fiziologia si fiziopatologia rinichiului, pg.26-36; cap.8: Nefropatiile vasculare, pg.523- 561