TUBULO-INTERSTITIAL

NEPHROPATHY
Conf.Dr. Mircea PENESCU

Definition. Classification
Interstitial 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

Ethyologic and morphologic criteria

- Secondary to infections ITN
- Tuberculosis ITN
- Leprous ITN

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

Pathogeny
The 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

Fisiopathology
Anathomo 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
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

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

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

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 )

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)
(

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)

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 syndrome fever, asthenia, cephaleea,
moderate perspirations, arthralgias, mialgias, loss of weigh
- digestive syndrome anorexia, nausea ,
gastrointestinal disorders

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

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)

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

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

- Sonography evidences dimensions of the kidneys, echostructures of the

parenchyma and the reno-urinary cavities

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

Main ethyopathogenyc and clinic forms of interstitial

nephropathies
Interstitial 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).

Interstitial nephropathy through obstructive

uropathy
Definition. 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

Main causes of obstructive uropathy

Heterogenous (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

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

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 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.
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.

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 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
Microscopically, there are tubular and glomerular injuries, vases and interstitium
structure; there is also a diffuse extensive and rare fibrosis.

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 hydronephrosis in the case of
unique ureter.

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

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 spreaded
on 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

Acute pyelonephritis
Pathologyc anatomy
Macroscopy:
- 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 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 by
purulent secretions

Microscopic:
- acute inflammation with interstitial edema and focal infiltration with
polinuclear 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

Fig 4. Pielonefrita acuta este diagnosticata prin evidentiere agregarilor

intratubulare de neutrofile polimorfonucleare, inconjurate de inflamatie
interstitiala continand PMN, limfocite, plasmocite; inflamatia este predominanta
la nivelul tubulilor. (Coloratia Jones Silver , marirea X 200).

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

Acute pyelonephritis. (3)

Positive diagnosis
- anamnesis evidencing the presence of favoring factors
- infectious syndrome
- lumbalgias , nephretic colics
- cystic syndrome
- urine exam evidencing discreet proteinuria
- leucocyturia pyuria, 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

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 be
closely 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 of
the cortical infective centers through the capsule into the
perirenal space.
- Papillary Necrosis at the same time a complication and a
clinical form
- Sepsis, as a consequence of massive pouring of germs into
the blood circulation
- Acute Renal Failure, due to the severe APN

Hematogenous interstitial nephritis (hematogenous acute

or descendent PN)
Ethyopathogeny. Insemination of the renal parenchima is induced
through descendent hematogenous way, with germs originating
either 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 the
localization of the germs, being similar to those found in ascendant
APN
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.

Haematogen interstitial nephritis(2)

Symptomatology is marked by sepsis and only systematic examines of
urines 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

Pyelonephritis due to Candida albicans

Causes: abuse of antibiotherapy , prolonged corticotherapy
Location. Children, pregnant women, aged patients with consumptive diseases or
immunitary 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 perirenal space,
disseminating in the whole kidneys (cortical and medullar) abscesses with draining in
the renal excretory duct
Symptomatology could be dramatic, with respect to the aspect of unilateral or
bilateral APN with papillar necrosis.
- Some other times, patients show prolonged sub feverishness
lumbagos or even repeated nephritic collics, leading to confusions
with renal tuberculosis

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,
lymphocytopenia
Evolution. In the absence of a specific treatment, kidneys are destroyed
Treatment must be established as soon as possible, aiming to eradicate infecting favorable
circumstances:
- 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)

Treatment of acute pyelonephritis

General treatment management
Essential principles of the therapy of APN :
- Antibiotic treatment before the identification of the germs, 34g/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 evening
Presence of a septicemia complies with administration of 2 antibiotics:ampicylin 34g/day x20 days plus gentamycin 80 mg/each 8 hours x 10 days

Treatament of acute pyelonephritis (2)

APN in pregnancy. In case of APN in pregnant women, ampicylin,certain
cephalosporines and carbenicylin could be used, as well as furantoin, but
paing great attention to its administration.
Contra-indicated medicines are:
tetracycline severe risks both for mother (jaundice or ARI) and
child (drug being deposited in the bones tissues and dental buds)
sulphamides, cortimoxazole mostly, due to the antifolic and
teratogene action of the trimetroprim
streptomycine and kanamycin for their toxic effects on the cranial
nerves of the child
Rifampycin, toxic during the first quarter of pregnancy
quinolones that must be avoided both the first 3 monthes and after
the 8 month; nalidixic acid induces fetal jaundice through inhibiting
glucuronyltransferase
Cloramfenicol, is medullarly hematotoxic both for mother and child

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
Escherichia coli
32,8
Enterococcus
32,6
Streptococcus
9,3
Proteus mirabilis
7,2
Klebsiella
4,2
Pseudomonas aeruginosa
3,8
Staphylococcus aureus
2,6
Alkaligenes
2,2
Aerobacter cloacae
2,6

Kienitz
35
17
15
7
4
9
-

Legrain
60
10
10-20
5-10
5-10
2,5
-

Ursea
68,5
4,6
0,4
3,6
12,3
1,8
0,5
1,4
1,6

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
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 shape
kidneys
Irregular appearances
Reduced parenchymatous index
Calice distortions
Izotopic + sonographyc explorations:
Morphologycal and functional
inequality between kidneys
Hypocapting areas
Renal biopsy:
Inflammatory infiltrate and areas
of sclerosis in the interstitium,
alternating with healthy areas
Distroyed tubules , with
pseudothyroidian aspect

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

CPN treatment
Principles:
- treatment of the urinary infection antiinfectious 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 disorders fiziopathologycal 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 reduced
dosage given between several monthes up to 1 year, or intermitently 7-10 days /
monthly in high doses.

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 active
metabolits form
-- not to precipitate in the urine, irrespectively of the pH
-- to be properly tollerated
-- to induce the lowest possible microbial resistance

Drug medicine induced 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 of
analgetics.
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 necrosis
Macroscopy:
o Kidneys are reduced in shapes, with adherent capsula, wrinkled by
whitish stripes
o The surface of the kidneys appears as irregular with retractile scars
o Cysts , papillar necrosis ,calcifications, papillar scars

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 such
as 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.

Fig 5. Fragment de papila medulara necrozata prezent in urina

Fig 6. Necroza papilara in nefropatia la analgetice.