9 Nefropatii Tubulo Interstitiale Engl
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Post on 08-Nov-2014
<p>TUBULO-INTERSTITIAL NEPHROPATHYConf.Dr. Mircea PENESCU</p> <p>Definition. ClassificationInterstitial Nephropathies are acute or chronic renal pluriethyological disorders, histopathologically carracterised by the predominant involvement of the renal interstitia and tubuli; glomerular and vascular lesions being of minor importance. Ethyologic criteria- TIN microbian infections - Non specific - Specific</p> <p>Ethyologic and morphologic criteria- Secondary to infections ITN - Tuberculosis ITN - Leprous ITN</p> <p>-</p> <p>ITN :</p> <p>- Infectious mononucleosis - Typhoyd fever - Toxoplasmosis - Aspergilosis - Candidosis - Sarcoidosis ITN - Necrosante angeitis ITN: - Wegener granulomatosis - Family chronic granulomatosis - Criptogenic granulomatosis Topographic criteria: - unilateral NTI - bilateral NTI Evolutive criteria: - acute - chronic Ethyopathogenic criteria: - urologic cause - medical cause - unknown ethiollogy</p> <p>PathogenyThe majority of TIN are determined by infectious or toxic factors, acting directly on tubuli and interstitia Involved germs are acting either directly on renal structures, or through the endotoxines they are eliminating in the circulation. Medication and toxic substances are acting on certain zones of the kidney, so they have special tropism The involvement of the immune mechanisms in the genesis of TIN is only partially demonstrated: - induction through experimental patterns on animals through certain immunologic methods - composition of the inflammatory infiltrate limphocythes plasmocythes - frequent translation from acute into chronic forms - immunologic mechanism can perpetuate the inflammatory response even in case the initial response was not immunologic</p> <p>FisiopathologyAnathomo functional particularities responsible for making kidneys vulnerable to certain aggressions : - high blood flow - the capacity of the nephrocytes to decuplate proteic chains - substances that normally are not toxic to pH = 6,8-7,4 levels can became very toxic - fagocythosis is diminished in conditions of raised osmolarity - high concentration of ammonia in the renal interstitia inhibits the activation of the complement</p> <p>Functional consequences of the involvement of medullar structures (Henle ansa, vasa recta, interstitial cells and collecting tubulli) are : - lowering of the concentration capacity of urine - lowering of the renal capacity of preserving sodium - renal acidosis - reduced renal excretion of potassium</p> <p>Pathologic AnatomyMacroscopy- smaller kidneys, unequally dimensioned in shape and weight - irregular surface, with profound scars - capsulla appears as tight, fibrosed, infiltrated - in transversal section white traces appear, going from the papilla to the cortex</p> <p>Microscopy- predominency of lesions in the renal interstitium, to be evidenced mostly in the cortical zone (area) - alternation between inflammatory zones and healthy parenchyma - dominant lesions are in the renal interstitium and secondary ones in the tubes - tubular lesions are of variable degrees, out of simple tumefaction of the tubular epithelial cells up to tubulo-necrosis and tubulo-rhexis</p> <p>Pathologic Anatomy (2)Glomeruli and vases frequently appear as normal or sometimes a certain degree of ischemia can be evidenced Renal papilla is affected in certain ethyologic formes of TIN (analgetic, diabetus melitus, obstruction of urinary tract, siclemya, etc) going up to papillar necrosis The IF examination can evidence different aspects: - presence of anti-MBT antibodies - presence of immune complexes (Ig and C) alongside the MBT and in the renal interstitium - non-specific abnormalities, fibrin in the interstitia linear or granular C3 alongside the MBT</p> <p>Fig. 1.. Chronicpielonephritis is suggested by tubulo-interstitial fibrosis and glomerular scars, irregularly distributed, in alternance with healthy (intact) zones . There is to be noted a disproportion between the tubul interstitial inflammation always evidenced and the discreet glomerular involvement (jones Silver coloration ; X 100 )</p> <p>Fig. 2. Glomerular scars evidenced with focal and segmental location in the course of a PNC through reflux-nephropathy. Signifiquant signs for the diagnosis of this . Are the periglomerulal scars fourrounding relativecy intacts glomeruliand the tighteness of the capsula Bowman. The increased glomeruli can appear in this form of secondary GNFS the pattern of the tubulo-interstitial scarsis regional geografic pattern (Jones Silver coloration; x 120)</p> <p>Fig. 3. PNA Interstitial limfo-plasmocitar infiltrate in ssociation with oedema. Glomeruli are , generraly, preserved, eventualy with minimal alterations, especially in the nephritis to anagestics (Jones Silver coloration; X 100)</p> <p>SymptomathologyClinic Examination Anamnesis - general (septicemias) or local proximity infections - inflammatory diseases in the little basin (mainly to woman) - digestive disorders (constipation, intestinal dyspepsia enterocolitis, megadolicocolon) - endocrine metabolic disorders - exaggerate intake of medication (antinevralgic, sulphamide, antibiotics, etc). General Clinic Simptomathology - infectious syndrome fever, asthenia, cephaleea, moderate perspirations, arthralgias, mialgias, loss of weigh - digestive syndrome anorexia, nausea , gastrointestinal disorders</p> <p>Symptomathology (2)Renal functional disorders - reno-urinary pains leading up to a nephritic colica, suprapubian pains, urinary incontinence or retention of urine - diuressis disorders, meaning polyuria or oliguria - mictioning disorders meaning dysuria, polakiuria Physic examination - pallor and often hiperpigmentated skin - diminished subcutaneous cellular layer - normal or high arterial pressure - local nephro-urinary examination can evidence lumbar pains unilateral or bilateral ptossys, costomuscular and costovertebral pain full points/areas, positive unilateral or bilateral Giordano manoeuvre and sometimes even vesical globe - rectal and vaginal tacts are compulsory</p> <p>Paraclinic investigationsUrine examination - 24 hours urine volume is variable pending on the stage ofthe illness - urinary density is low - collour of the urine is pale with hydruric aspect - proteinuria is ussually from discreet up to moderate - sediment shows leucocyturia, leucocytes, cylinders, glitter cells, haematuria Tests for induced leucocyturia and cylinderuria - Pears-Hutt-Wardener test provoqued through pyrogen injections - Test Katz-Wardener of provoqued leucocyturia and cylinderuria through injections of 40 mg of hydrocortison hemisuccinate - Bacteriologic exam of urine and antibiogram of urine, in case they detect germs have a high value (important for pielonephritis)</p> <p>Paraclinic investigations (2)Renal function tests - urine concentration alterations - urine acidity alterations - natriuresis, going up to natrium diabetis aspect - bicarbonate lakes, leading to acidosys - in more advanced stages,diminished glomerullar filtrate Other laboratory investigations - haemmogram shows normocytar normochrome anemia, moderate leucocitosis - raised speed of sedimentation of haematias - blood ionogramm evidences alterations, in cases of pyelonephrithis - fibrinogen values are moderatly high, attesting the presence of inflammatory process in the kidney - electrophoresis may evidence hyper and hyper - globulinaemia</p> <p>Imagistic examinations- Radiologic examination - Simple renal radiography shows: kidneys assimetric in shapes, difference being over 1,5 cm -- irregular contour -- possible calcifications</p> <p>- Urography -- renal papilas are modified, shaped as plates or knobs -- hydrocalicosis -- reduced parenchimatous index -- polar segmental hypoplasia - Global and selective renal arteriography -- reduced vascularisation -- delayed evidencing of the contrast substance- Renal</p> <p>scintigraphia-- renal assymmetric dimensions -- weak non-homogeneous interception of the radiopharmaceutical</p> <p>- Sonography evidences dimensions of the kidneys, echostructures of the parenchyma and the reno-urinary cavities</p> <p>Renal BiopsyTo be combined, preferably, with microlombothomy: - inflammatory infiltrate in renal interstitia - radial interstitial sclerosis, beginning from the calices - hypertrophy of the tubular epithaelia , with dilatation of the tubes - presence of colloidal cylinders in the tubes, leading to a pseudotyroidian aspect</p> <p>- periglommerular hyalinousis- proliferative endarteritis</p> <p>Main ethyopathogenyc and clinic forms of interstitial nephropathiesInterstitial nephropathies through obstructive uropathy Tubulo-interstitial nephropathies of medical causes - infectious tubulo-interstitial nephropathies (pyelonephritis) - toxic medicinal induced TIN Interstitial nephropathies of metabolic causes [hyperurricemical, hypercalcemical (nephrocalcinosis), oxalic, kalyopenic, renal cystinosis] Immunological interstitial nephropathies Granulomatous tubulo-interstitial nephropathies Tubulo-interstitial nephropathies in haemopathies or neoplasias (infiltrative NTI) Tubulo-interstitial nephropathies in hereditary diseases Interstitial nephropathies of unknown causes (chronic primitive interstitial nephropathies, xantogranulomatous pyelonephritis, balcanic endemic nephropathy).</p> <p>Interstitial nephropathy through obstructive uropathyDefinition. Interstitial nephropathy through obstructive uropathy comprises functional disorders and structural alteration of the kidney as a result of the existence of an inner obstacle , mechanic or functional, within the urinary tract. Obstructive uropathy concept ,versus obstructive nephropathy and hydronephrosis: - obstructive nephropathy : alterations in the structure of the proximal urinary tract, induced by an obstacle situated to this level - nephropathy through obstructive uropathy (obstructive nephropathy) : functional alterations and structural changes of various intensity in the reno-urinary tract Due to the urinary obstructions , there are 3 important consequences: - functional renal failure induces bypyelic hypertension - organic injuries up stream the obstacle , due to stasis - superinduced urinary infection, worsening the lesions</p> <p>Main causes of obstructive uropathyHeterogenous (foreign) bodies: calculus, clots, necroused papillas Inflammation fibrosis installation : - urinary tuberculosis (renal pelvis, ureter , bladder, prostate urethra) - non-specific uretral strictures - peryureteral retroperitoneal fibrosis - interstitial cystitis - post-radiation retraction of the bladder (vesical sclerosis) - prostatic fibrosis, prostatitis - ureteral strictures - traumatic injuries of the ureter - bilharioses Congenital malformations : - pyelo-uretheral dissectasia (disease of colet Syndrome) - cystic distention of the terminal ureter - retrocave ureters - compressions through an abnormal artery - megaureters - bladder col dissease - urethral valves - urethral meatus abnormalies</p> <p>Main causes of obstructive uropathy (2)Tumours - prostate adenoma- prostate cancer - papillomatous tumours of the ureter or bladder - bladder cancer (carcinoma) - secondary retroperitoneal ganglione cancer - cancer infiltration of the little basin and of the retroperitoneal tissue Neurological bladder - post traumatic paraplegia - tabes - diabetic polyneuritis - vascular cerebral strokes</p> <p>Clinical forms of nephropathy through obstructive uropathiesInterstitial nephropathy through unilateral ureteral obstructionComplete obstruction of the ureter induces the first 6 hours completely reversible functional disorders and the first 6 days functional but also structural disorders; but within 3 weeks the kidney being deeply impaired , the renal function is only slightly improved after removing the obstacle. Between 3 weeks and 3 months the complete destruction of the kidney is achieved.</p> <p>Uncomplete obstruction of the ureter, acute of chronic, leads to progressive destruction of the respective kidney within a longer period of time, pending on the degree of pyelic hipertension.</p> <p>Interstitial nephropathy through unilateral uretheral obstacleFisiopathology. Unilateral uretheral obstruction is associated with a raise in renal inflammatory infiltrate with macrophages, responsible for the accumulation of inflammatory cells being the adhesion molecules. Pathological anatomy. Macroscopically, following alterations can be registered: - great distension of the pelvis and pyelocaliceal cavity accumulating up to 3 L of urine - reduction of the renal parenchyma to a simple thin blade, with the erasing of the difference between cortical and meduular - controlateral injuried kidney is hypertrophic</p> <p>Microscopically, there are tubular and glomerular injuries, vases and interstitium structure; there is also a diffuse extensive and rare fibrosis.</p> <p>Interstitial nephropathy through obstacle on the common urinary tract or through obstacle on the unique ureter.Complete obstruction leads to acute urine retention, if reduction is under the bladder or to anuria , if reduction is on unique ureter. It is possible that anuria should be the reflex of a spasm of the Clara preglomerular sphincter Clinically, biologically mechanic anuria induces the clinic aspect of an IRA.</p> <p>- Uncomplete</p> <p>obstruction , with the maintenance of the diuresis. Uncomplete obstruction on the common way leads to the progresive appearance of bilateral or unilateral hydronephrosis in the case of unique ureter.</p> <p>Reflux nephropathyReflux nephropathy means kidney inflammation due to retrograde urinary flux at the level of the Bellini ducts Subsequent to the intrarenal reflux, the epithelia breaks and allows the urine to penetrate in the interstitia, with inflammatory response in case of sterile urine and more ample response in case of infected urine, leading finaly to fibrose. Progressive fibrose and impairment of renal function after resolution of the reflux is a consequence of the renin-dependet-on HTA which is settling down Treatment consists in : - maintaining the urine sterile - avoiding constipation - periodic emptying of the bladder - permictionales cystographies</p> <p>Tubulo-interstitial nephropathy of medical causeInfectious tubulo-interstitial nephropaties Acute pyelonephritis- Definition. Acute pyelonephritis is an acute bacterial disease, both of the renal interstitial tissue and of the pyelon, the infection being spreaded on ascendent or descendent (haematogen) path.</p> <p>Ascendent acute pyelonephritis - Ethyopathogeny: two categories of elements: microbiandeterminants elements and favouring elements - in 1/3 of the acute pyelitis urinary tract is normal - infection is produced in ascendent path ureteral and less often, through lymphatic path, localised initially in the medulla where there are proper conditions for developing an infection</p> <p>Acute pyelonephritisPathologyc anatomyMacroscopy: - kidneys are edematous, of enlarged volume with multiple abscesses visible on the surface and that occasionally pierce the capsule - surface of the kidney shows plots of congestion and paleness - on...</p>
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