9 nefropatii tubulo inters ti ti ale engl

8/3/2019 9 Nefropatii Tubulo Inters Ti Ti Ale Engl

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TUBULO-INTERSTITIAL

NEPHROPATHY

Conf.Dr. Mircea PENESCU


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Definition. Classification

Interstitial Nephropathies are acute or chronic renal pluriethyologicaldisorders, 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

Ethyologic and morphologic criteria

- Secondary to infections ITN

- Tuberculosis ITN

- Leprous ITN


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- ITN : - 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


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Pathogeny

The majority of TIN are determined by infectious or toxic factors, actingdirectly on tubuli and interstitia

Involved germs are acting either directly on renal structures, or through theendotoxines they are eliminating in the circulation.

Medication and toxic substances are acting on certain zones of the kidney, so

they have special tropismThe involvement of the immune mechanisms in the genesis of TIN is onlypartially demonstrated:

- induction through experimental patterns on animals through

certain immunologic methods- composition of the inflammatory infiltratelimphocythes

plasmocythes

- frequent translation from acute into chronic forms

- immunologic mechanism can perpetuate the inflammatory

response even in case the initial response was not immunologic


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FisiopathologyAnathomo functional particularities responsible for making kidneysvulnerable 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 theactivation of the complement

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


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Pathologic Anatomy

Macroscopy

- 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

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


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Pathologic Anatomy (2)

Glomeruli and vases frequently appear as normal or sometimes acertain 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) goingup 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


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Fig. 1.. Chronicpielonephritis is suggested by tubulo-interstitial fibrosis and glomerularscars, irregularly distributed, in alternance with healthy (intact) zones . There is to benoted a disproportion between the tubul interstitial inflammation always evidenced and

the discreet glomerular involvement (jones Silver coloration ; X 100 )


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Fig. 2.Glomerular scars evidenced with focal and segmental location in the course of a PNC throughreflux-nephropathy. Signifiquant signs for the diagnosis of this . Are the periglomerulal scarsfourrounding relativecy intacts glomeruliand the tighteness of the capsula Bowman. The increasedglomeruli can appear in this form of secondary GNFS the pattern of the tubulo-interstitial scarsis

regional geografic pattern (Jones Silver coloration; x 120)


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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)


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Symptomathology

Clinic 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 syndromefever, asthenia, cephaleea,

moderate perspirations, arthralgias, mialgias, loss of weigh

- digestive syndromeanorexia, nausea ,

gastrointestinal disorders


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Symptomathology (2)Renal functional disorders

- reno-urinary painsleading up to a nephriticcolica, 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 painsunilateral 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


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Paraclinic investigations

Urine examination

- 24 hours urine volume is variable pending on the stage of

the 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)


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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


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Imagistic examinations

-Radiologic examination- Simple renal radiography shows:

kidneys assimetric in shapes, difference being over 1,5 cm-- irregular contour

-- possible calcifications

- 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 scintigraphia-- renal assymmetric dimensions

-- weak non-homogeneous interception of the radiopharmaceutical

- Sonographyevidences dimensions of the kidneys, echostructures of theparenchyma and the reno-urinary cavities


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Renal Biopsy

To 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

- periglommerular hyalinousis

- proliferative endarteritis


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Main ethyopathogenyc and clinic forms of interstitialnephropathies

Interstitial nephropathies through obstructive uropathy

Tubulo-interstitial nephropathies of medical causes

- infectious tubulo-interstitial nephropathies (pyelonephritis)

- toxicmedicinal 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 (infiltrativeNTI)

Tubulo-interstitial nephropathies in hereditary diseasesInterstitial nephropathies of unknown causes (chronic primitive interstitialnephropathies, xantogranulomatous pyelonephritis, balcanic endemicnephropathy).


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Interstitial nephropathy through obstructive

uropathyDefinition.Interstitial nephropathy through obstructive uropathy comprises

functional disorders and structural alteration of the kidney as a result of theexistence of an inner obstacle , mechanic or functional, within the urinarytract.

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


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Main causes of obstructive uropathy

Heterogenous (foreign) bodies: calculus, clots, necroused papillas

Inflammationfibrosis 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


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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

- posttraumatic paraplegia

- tabes

- diabetic polyneuritis

- vascular cerebral strokes


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Clinical forms of nephropathy through

obstructive uropathies

Interstitial nephropathy through unilateral ureteral

obstruction

Complete obstruction of the ureter induces the first 6 hours completely

reversible functional disorders and the first 6 days functional but alsostructural 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.

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.


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Interstitial nephropathy through unilateral uretheral

obstacle

Fisiopathology. 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 accumulatingup 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

Microscopically, there are tubular and glomerular injuries, vases and interstitium

structure; there is also a diffuse extensive and rare fibrosis.


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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.

- Uncomplete obstruction , with the maintenance of the diuresis.

Uncomplete obstruction on the common way leads to the progresive

appearance of bilateral or unilateral hydronephrosisin the case ofunique ureter.


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Reflux nephropathy

Reflux 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


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Tubulo-interstitial nephropathy of medical cause

Infectious 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 spreadedon ascendent or descendent (haematogen) path.

Ascendent acute pyelonephritis

- Ethyopathogeny: two categories of elements: microbian

determinants 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


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Acute pyelonephritis

Pathologyc anatomy

Macroscopy:

- kidneys are edematous, of enlarged volume with multiple

abscesses visible on the surface and that occasionally pierce thecapsule

- surface of the kidney shows plots of congestion and paleness

- on section , can be noted triangular areas, grey, radially

arranged , with the pear in the papilla, as well as abscesses in the

cortical

- pyelo-caliceal branch shows dilationed congested and covered bypurulent secretions


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Microscopic:

- acute inflammation with interstitial edema and focal infiltration withpolinuclear and little abscesses

- necrosis of the tubular epithelia, granulose cylinders in the lumen

- in severe forms, glomeruli invaded by PMN (invasive glomerulitis)

- thrombosis of the segmentary capillaries,sometimes accompanied by

breakes of the capsular and capillary basal membranes, with messangial

celullar proliferation

- in severe forms , can be seen the exclusion of the circulation through

obliteration of medium size arteries , surrounded by ischemiac areas

- lesions are plotted , explaining the discrepancy between clinic picture and

results of the renal puncture biopsy.

- if disease is not controlled , extended renal suppuration forms appear

leading to melting away the Bertin pyramid , with high deadly risk

- healing is accompanied by the apparition of linear scars with retraction

in the medulla


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Fig 4. Pielonefrita acuta este diagnosticata prin evidentiere agregarilorintratubulare de neutrofile polimorfonucleare, inconjurate de inflamatieinterstitiala continand PMN, limfocite, plasmocite; inflamatia este predominantala nivelul tubulilor. (Coloratia Jones Silver , marirea X 200).


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Acute pyelonephritis. (2)

Symptomatology.

Beginning

Phisic examination

Paraclinic investigation:

- urine

summation examination;

- examination of the 24 hours urines;

- bacteriological examination (urinary culture, haemoculture);

- renal functional examination;

- blood examination.

- radiologic examination:-- renal simple radiography

-- urography

- renal biopsy


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Acute pyelonephritis. (3)

Positive diagnosis

- anamnesis evidencing the presence of favoring factors

- infectious syndrome

- lumbalgias , nephretic colics

- cystic syndrome

- urine exam evidencing discreet proteinuria- leucocyturiapyuria, leucocytar cylinders, pozitives urinary

cultures

- enlarged kidney volume evidenced due to the radio-urography

Differentiation diagnosis with:

- cystitis, cystopyelitis, renal litiasis- renal tuberculosis

- feverish diseases (malaria, typhos fever, sepsis, meningitis)

- basal pneumonia

- acute pancreatitis


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Acute pyelonephritis. (4)Evolution and evaluation of APN. Correctly treated, ascendant APN has a

favorable evaluation, as it can cure, spontaneous, but in this case it exists the risk

of becoming chronic. All favorable factors must be removed, and the patient will beclosely supervised and controlled for 1-2 years, by regular urine examinations.

APN complications are:

- Pyonephrosis, usually secondary to obstructive elements

- Perynephretic Phlegmon, appearing due to transspassing ofthe cortical infective centers through the capsule into the

perirenal space.

- Papillary Necrosisat the same time a complication and a

clinical form

- Sepsis, as a consequence of massive pouring of germs intothe blood circulation

- Acute Renal Failure, due to the severe APN


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Hematogenous interstitial nephritis (hematogenous acuteor descendent PN)

Ethyopathogeny. Insemination of the renal parenchima is inducedthrough descendent hematogenous way, with germs originatingeither in infectious proximal centers, or in far distance ones .

- involved germs: Staphylococus Aureus, Enterococcus

Pseudomonas aeruginosa, leptospire, ricketsii, brucelle

- gram negative germs (Escherichia coli, Proteus, Klebsiela)

Pathologycal anatomy. Lesions appear in 3-7 days from thelocalization of the germs, being similar to those found in ascendantAPN

Microscopy:

- plotted acute inflammation centers, abscesses, tubes destructions

or thickened tubes (tubullis) distended by the leucocytes contents

or the cylinders

- in the medullar vesgels, the first 3 days appear thrombi,

resulting in septic infections

- the process diffuses radially towards the cortex.


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Haematogen interstitial nephritis(2)

Symptomatology is marked by sepsis and only systematic examines ofurines could evidence the presence of the germs in the kidneys.

Evolution and prognostication:

- APT could be confused with one of the causal disease

- certain forms are regressing under appropriate treatment,others became complicated with IRA

- others became chronic

- evolutive straight is pending on the virulence of the germs and

the presence of the favorable conditions

- main treatment is the one of the causal disease


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Pyelonephritis due to Candida albicans

Causes: abuse of antibiotherapy , prolonged corticotherapy

Location. Children, pregnant women, aged patients with consumptive diseases orimmunitary deficiencies

Kidneys can be infected through two ways: hematogenous and ascendant

Histology : interstitial nephritis in focus (centers) with granulomatous elements

that may confluence and then produce fistula in the parenchyma or the perirenalspace, disseminating in the whole kidneys (cortical and medullar) abscesses withdraining in the renal excretory duct

Symptomatology could be dramatic, with respect to the aspect of unilateral orbilateral APN with papillar necrosis.

- Some other times, patients show prolonged sub feverishnesslumbagos or even repeated nephritic collics, leading to confusions

with renal tuberculosis


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Pyelonephritis due to Candida albicans (2)

Investigations:- urine examinations: uroculture on Sabouraud medium is

evidencing white colonies with creamy aspect

- urography ; is evidencing confluent cavities and fistular

trajectories

- immune deficiencies : hypogammaglobulinaemias,

lymphocytopeniaEvolution. In the absence of a specific treatment, kidneys are destroyed

Treatment must be established as soon as possible, aiming to eradicate infecting favorablecircumstances:

- well-balancing of an eventual diabetes

- stop to administrating antibiotics and corticoids

- suppressing proximity fungi infections (urethritis, vaginitis)

- selected antibiotic would be Amphotericyn Badministrated as

intravenous perfusion, suggested dose of 0,75-1 mg/kg/day, for 30 days

-Nefrotoxicity of Amphtericyn B complies to its substitution with

another antifungi drug: stamicine or mycostatin or diflucan(fluconazol)


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Treatment of acute pyelonephritis

General treatment management

Essential principles of the therapy of APN :-Antibiotic treatmentbefore the identification of the germs, 3-

4g/day of Ampicilin will be administrated, followed, for some

weeks, by the proper therapy according to antibiogramm

- Attack treatment: cephalosporine (ceftazidim, ceftriaxon, cefuroxim)

tetracycline, carbenicycilin (Pyopen), as single or combined medication

- In severe cases, administration of parentheral antibiotics is recommended,in order to obtain high level sanguine concentrations

- Maintenance treatment: quinolones or sulphamides with prolonged action

In recurrent APN , there are 2 possible treatments:

-- antibiotic treatments for each acute episode, for at least 10-15 days

-- continous treatments: initially 3-4g/day of ampicylin as the attack therapy,

followed by : cotrimoxazole, norfloxacyn,etc.,each morning and eveningPresence of a septicemia complies with administration of 2 antibiotics:ampicylin 3-4g/day x20 days plus gentamycin 80 mg/each 8 hours x 10 days


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Chronic pyelonephritis


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Chronic pyelonephritis

Definition. Chronic pyelonephritis is a bacterial interstitial nephritis

associated with the inflammation of the pelvis, where lesions are situated

predominantly in the renal interstitium and secondary in the tubules.Epidemiology. CPN represents the cause of at least 20 % of the

chronic renal failure.

Aetiology.

Bacteriology in CPN according to various authors

Germen (%) Sarre Kienitz Legrain Ursea

Escherichia coli 32,8 35 60 68,5Enterococcus 32,6 17 10 4,6Streptococcus 9,3 - - 0,4Proteus mirabilis 7,2 15 10-20 3,6

Klebsiella 4,2 7 5-10 12,3Pseudomonas aeruginosa 3,8 4 5-10 1,8Staphylococcus aureus 2,6 9 2,5 0,5Alkaligenes 2,2 - - 1,4Aerobacter cloacae 2,6 - - 1,6


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Symptomatology of PNC

Clinical evidences

General

fever

asthenia, adynamia

loss in weight

headache, migraine

Cutaneous pseudo-addisonian pigmentation

Cardio-vascular

HTA

left ventricle hypertrophy

global cardiac hypertrophy pericarditis

Digestive:

anorexia, vomitis

sabural tongue

hepatosplenomegalia

Bones:

osteopathy

Nephro-urinary:

lumbalgias

nephritic colics

polakiuria

dissuria turbid, fetid urines

Symptomatology of CPN


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Symptomatology of CPN

Paraclinical investigations

Urine examination:

hipo-izo-subizostenuria Lowered urinary osmolarity

Leucocyturia pyuria

Sternheimer-Malbin cells

Leucocytar cylindruria

Macroscopical haemathuria

bacteriuria

Biochemical examination:

diselectrolithemia

acidosis

azotemia

Functional renal exploration

Lowered clearances

natriurezis Deficient concentration tests

Hyperchloremic acidozis

Hematological:

- anemia, leucocytosis raised VSH

Radiological:

Asimetrical reduced in shapekidneys

Irregular appearances

Reduced parenchymatous index

Calice distortions

Izotopic + sonographyc explorations:

Morphologycal and functionalinequality between kidneys

Hypocapting areas

Renal biopsy:

Inflammatory infiltrate and areasof sclerosis in the interstitium,

alternating with healthy areas

Distroyed tubules , with

pseudothyroidian aspect


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Radio-urographyc characteristics of CPN

Renal parenchym abnomalies

-global reduction in the shapes of the kidneys, preserving the asymmetry

between them (one being with over 1,5 cm smaller that the other)

- irregular contour , as expressions of the renal scars

- atrophy of a renal pole (segmentary hypoplasya)

- reduced distance from the papilla to the bord (parenchymatous index) due to

cortical atrophy- calcifications :lithyasis, nephrocalcinouzis

Alterations of the excretory cavities (which appear modified)

- little calice appears closer , pushed, but preserving its contour

-pyelocaliceal fan with withered dropping flowers aspect

-papillas shaped as plate , bludgeon, mush room

-papillar necrousis shapped as ring or crab tongs

- pelvis can be hypotonic, with irregular contour,

- urethers are hypotonic

Urinary obstruction : hydronephrosis, hydroureter, bladder residue

Associated signs: lythiasis, vesico-ureteral reflux


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CPN treatmentPrinciples:

- treatment of the urinary infectionantiinfectious treatment

- treatment of the arterial hypertension

- correction of the favourable conditions for infecting of the renal

parenchym- the urological approach

- correction of the renal function disordersfiziopathologycal and

symptomatical treatments

General attitude

Antibiotherapy requirements- identification of the infectious germs and of their sensitivity to

appropriate medication

- elimination of the favourable conditions promoting the infections

- antiinfectious treatment will not be administrated untill at least two

urocultures and one haemoculture would have been taken over

- initial administration of an attack treatment protocole for about 3-4 weeks,

followed by a long term treatment that could be continously administrated in reduceddosage given between several monthes up to 1 year, or intermitently 7-10 days /

monthly in high doses.


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CPN treatment (2)

In selecting appropriate antiinfectious medication some principles must be

observed:

-- to have a proper spectrum, as much as possible , against

the infectious agent found in the urine

-- to be eliminated mostly through the urine, under activemetabolits form

-- not to precipitate in the urine, irrespectively of the pH

-- to be properly tollerated

-- to induce the lowest possible microbial resistance


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Drug medicineinduced toxic tubulli-interstitial

nephropathy. Analgesics nephropathy

Definition. Nephropathy to analgesics is a chronic interstitial nephropathy,

associated with papillar necrosis due to excessive and prolonged intake ofanalgetics.

Pathogenesis. Papillar necrosis is the result of 2 categories of aggressive factors:toxic and ischemiac

Prototype- nephropathy due to phenacethyn (Zollinger and Spuhler).

- hypothesis of the toxic action of associated ingredients to

phenacethyn

- hypothesis of the decreased resistance to renal infections

- hypothesis of immuno-allergycal reaction of the delayed

hypersensitivity

Pathologyc anathomy: bilateral interstitial nephropathy, being characterised by the

compulsory presence of the papillar necrosisMacroscopy:

o Kidneys are reduced in shapes, with adherent capsula, wrinkled bywhitish stripes

o The surface of the kidneys appears as irregular with retractile scars

o Cysts , papillar necrosis ,calcifications, papillar scars


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Analgesyc induced NEPHROPATHY

Pathologyc anathomy (2)

Microscopy:Papillar necrosis and poor inflammatory infiltrate in the interstitia

Brown-golden pigment, intracytoplasmatic,very similar to

lipofuscina

Necrosis of the interstitial cells, of Henle ansas and of capillaries

Brown-black pigment in the necrotic papillas and other tissues suchas cartilages, representing a metabolyte of phenacetyn, 3-amino-7

etoxi-phenasone

Slender calcification of MB thickening of the Henle ansas

Existent healthy areas and necrotic areas the lasts containing

acicular birefringent crystals

Important thickening of the capillaries situated under the pyelic and

uretheral endothelium,as well as in the bladder

Alterations of the renal cortex appear only in more advanced or

more severe stages.


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Fig 5. Fragment de papila medulara necrozata prezent in urina


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Fig 6. Necroza papilara in nefropatia la analgetice.

9 nefropatii tubulo inters ti ti ale engl

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