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Infections of the urinary tract Urinary Tract Infection

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Infections of the urinary tract Urinary Tract Infection Powered By Docstoc
					296                                                                                                                 ın
                                                   Chapter 4. Pathophysiology of kidneys and urinary system ( I. Hul´ )


moderate and asymptomatic proteinuria. Even be-
fore proteinuria appears carbohydrate intolerance is
almost in all cases present. The glomerular filtration       4.10        Infections of the urinary
rate is normal or increased.                                            tract
  When the proteinuria appears during the diabetes,
glomerular filtration begins to decrease. Very exact
regulation of glucose level in peripheral blood can sig-
nificantly delay the appearence of diabetic nephropa-           In most cases of urinary system infections is bac-
thy.                                                        teriuria present. Bacteriuria is a condition where
                                                            in the midstream urine more than 105 bacteria are
4.9.6     Hereditary glomerulopathies                       found. Less amount of bacteria may also indicate in-
                                                            fection if the urine was obtained by catheterization or
4.9.6.1   Alport’s syndrome (hereditrary                    by suprapubic aspiration. Bacteriuria however, migt
          nephritis with deafness)                          be absent in some cases, thought the urinary system
Pathogenesis of this condition is not known ex-             infection is evident. This situation may occur follow-
actly. There is a disorder of glycoprotein, non-            ing or during the antibiotic treatment, during high
collagenous components of glomerular and tubular            urea concentration in urine and when the pH of urine
capillary basement membrane synthesis. The clini-           is low.
cal manifestation is haematuria and proteinuria. The
microscopic picture shows commonly focal and dif-           4.10.1       Cystitis, acute pyelonephritis,
fuse glomerular proliferation with segmental sclero-                     urethritis
sis.
                                                            Various types of microbes might be the underlying
4.9.6.2   Fabry’s disease (hereditary dystopic              cause of these diseases. Ninety per cent of acute
          lipidosis)                                        urinary tract infections are caused by Escherichia
                                                            coli. Further Gram-negative microbes, as Proteus,
is an inherited disorder of glycosphingolipid meta-         Klebsiella, Enterobacter and Pseudomonas may be
bolism with accumation of trihexosylceramide in the         responsible for urinary infections. They participate
tissues of eye, skin, cardiovascular system and kid-        in nosocomial infections. Among the Gram-positive
neys. In glomeruli, tubules and in renal interstitium       cocci the enterococci and staphylococcus saprophyti-
typical foam cells are found with lipid vacuoles and        cus occur most commonly. The viral infections may
excentric location of nucleus. Clinical manifestation       be the cause of cystitis and pyelonephritis.
of disease are: haematuria and proteinuria with pro-           Under physiological circumstances the urinary
gressive development, resulting in renal failure.           tract cannot be settled by micro-organisms. The
                                                            urine dispose of direct antibacterial effects. The high
4.9.6.3   Congenital nephrotic syndrome                     urea content and the high osmolarity of urine kill di-
                                                            rectly the pathogenic germs. The prostatic secretion
is a fatal hereditary disease, inherited as an auto-
                                                            has also antibacterial activity. The polymorphonu-
somal recessive trait, manifested by nephrotic syn-
                                                            clear leucocytes in the urinary bladder wall also have
drome in first weeks of life. The synthesis of glomeru-
                                                            a protective function.
lar and tubular basement membrane components is
                                                               Favorable conditions for infection arise if obstruc-
pathologically altered. Large amount of proteins
                                                            tion occurs. Tumors of urinary tract, urinary cal-
cross the impaired basement membrane. The pro-
                                                            culosis and hypertrophy of prostata may lead to hy-
teinuria of non-selective type is very massive. The
                                                            dronephrosis and urinary tract infections. In these
disease leads to renal failure. Concomitant infection
                                                            cases the concomitant infection accelerates the renal
is commonly fatal.
                                                            tissue destruction.
                                                               Vesicoureteral reflux facilitates sometimes the de-
                                                            velopment of infection. The reflux of urine may at-
4.10. Infections of the urinary tract                                                                       297

tain ureters or even renal pelvis. Reflux occurs most     function. Patients with chronic pyelonephritis have
commonly in anatomic aberrations.                        a history of frequent, repeated urinary outflow tract
   Renal disturbances raise the possibility of infec-    infections with impaired renal functions. Their urine
tions appearence. It is not known if renal hyper-        contains pus, leucocyte casts and bacteria. Alter-
tension accelerates the infection occurence. The dia-    ations of renal pelves can be detected by excretion
betic nephropathy has, however, a very close relation    urography. In other cases this finding can be absent
to the urinary tract infections. During the diabetic     in spite of chronic pyelonephritis presence.
nephropathy the chronic pyelonephritis occurs most          Kidneys are of uneven magnitude, with irregu-
frequently and necrosing papillitis is easily develop-   lar, rugged surface. The pathologic process be-
ing. Renal papillae and medulla are very receptive       gins usually in renal interstitium, in medullar re-
to pathogenic microorganisms.                            gion and in renal papillae. Fibrous tissue, lympho-
   Infections of urinary tract can clinically occur as   cytes and plasma cells replace completely the inter-
strictly defined diseases. Bacteriuria per se occurs      stitium and the tubules. In the interstitium, mainly
also in completely asymptomatic patients. Cystitis       in the medulla renis are foci of inflammation. In some
has a rather strict clinical symptomatology. Acute       tubules leucocyte casts occur, in others large amount
pyelonephritis may include the symptomes of the cys-     of eosinophilic material and colloid casts are found.
titis and further signs as fever attacks, nausea, vom-   These tubules are dilated. Proliferative arteritis may
iting, diarhea and tachycardia. Leucocyte casts and      be present. None of these alterations is pathognomic
purulent matter are found in urine. Bacteriuria and      for chronic pyelonephritis. The finding in kidneys de-
pyuria may persist longtime. Haematuria is present       scribed above may appear during diabetic nephropa-
only at the beginning of disease. During urethral        thy and many different nephropathies.
syndrome dysuric troubles are dominant. Infections          The chronic pyelonephritis does not have any typ-
of urinary tract in hospitalized patients occur namely   ical clinical manifestation. Systemic arterial hyper-
in connection with catheterization.                      tension is commonly found stimulating the search
                                                         for the underlying cause. Patient usually visits the
4.10.2       Prostatitis                                 doctor only when the first signs of renal failure ap-
                                                         pear: fatigue, malaise, nausea, tendency to suffusion
Prostatitis includes various types of inflammatory        formation, anorexia, body weight loss, polyuria and
processes comprising acute and chronic inflamma-          nycturia. The progression of pyelonephritis is accom-
tions caused by specific bacteria. Clinical manifes-      panied with decreased glomerular filtration rate an
tations are: sacralgia, and peritoneal pains. Some-      reduced renal blood flow. The picture of uraemia is
times testicular dyscomfort and moderate dysuria         developing. Proteinuria raises to 2 g/day. The renal
are experienced. In additions, microscopic pyuria        ability to concentrate urine decreases. Presence of
and haematuria are occasionally observed.                bacteria, leucocytes, leucocyte casts in urine may be
   The underlying cause of acute prostatitis use to      only intermittent. Renal biopsy can be completely
be the Gram-negative bacterial flora or Staphylococ-      normal.
cus pyogenes aureus. It is difficult to diagnose the          Chronic pyelonephritis need not cause dyscomfort
chronic bacterial prostatitis, because the symptomes     and troubles to patients until the renal functions do
are often inapparent. In uric sediment excessive leu-    not impair substantially. Hypertension makes the
cocyte numbre may be found. The bacteriologic ex-        prognosis of patient worse. During acute infection
amination however, might be negative. Dysuric dis-       or dehydration the renal functions may become es-
orders appear when infection reaches urinary blad-       sentially impaired. The impairment can result even
der.                                                     in uraemia. At the beginning is the impairment usu-
                                                         ally reversible.
4.10.3       Chronic pyelonephritis
                                                         4.10.4     Papillary necrosis
This term indicates the condition developing follow-
ing renal infections. It can occur under the influ-       Renal papillae play a very important role in the
ence of predisposing factors as obstructions, vesi-      pathogenesis of chronic interstitial nephritis. Renal
coureteral reflux and disorders of urinary bladder        papillae have high affinity to bacterial infection. It is
298                                                                                                                ın
                                                  Chapter 4. Pathophysiology of kidneys and urinary system ( I. Hul´ )


very probable that first occurs the papillary damage        that only some of these alterations might be caused
and the chronic interstitial nephritis develops later.     by infection. In tubulointerstitial disturbances are
Papillae may be damaged during arthritis urica, and        non-bacterial factors involved, as: exogenous toxins,
diabetes mellitus. Relatively frequently the papillary     immunologic and metabolic disorders.
lesions occur during treatment with various drugs.            Tubular disturbance is manifested by impaired
Some substances attain just in papillae high concen-       capability of concentration of the urine, by de-
trations affecting with toxic action papillae and the       creased reabsorption of filtered solutes, especially
surrounding area. The effect of phenacetin – a com-         of amoinoacids, phosphates, sodium, chlorides and
ponent of analgesic tablets is well known. It is not       potassium. Tubular alterations appear at the begin-
understood exactly which substances can damage re-         ning separatly, later they become concomitant. The
nal papillae. It is suggested however, that the uri-       structural alterations lead to the progressively re-
nary tract infections might cause papillary lesions.       duced glomerular filtration rate. Tubulointerstitial
   Papillary necrosis appears when the infection is        damage causes secondary glomerular disturbances of
retained in renal pyramids. Participation of a fur-        glomeruli and their involution.
ther factor is necessary to give rise to the papillary        Kidneys have to excrete unnecessary substances,
necrosis. These factors are often: diabetes mellitus,      toxins or drugs from the body. This is why these sub-
chronic alcoholism and blood vessel diseases.              stances cummulate in urine. Various medicaments,
   Clinical manifestations of papillary necrosis are:      the antibiotics above all, can damage the renal inter-
back pains, abdominal pains, and fever. Acute renal        stitium.
failure with oliguria or anuria can occur occasionally.
A sudden impairment of renal functions in patients
with diabetes mellitus or with obstruction of ureters      4.11.1       Nephropathies
signalizes almost in every case the papillary necrosis.
If so, fever or pains are not present.                     4.11.1.1     Phenacetin nephropathy (Analgesic
                                                                        nephropathy)

                                                           It is known that in persons taking large amounts
                                                           of analgesics lesions of renal interstitium and pap-
                                                           illar necrosis frequently are developing. Especially
4.11       Tubulointerstitial                              phenacetin and acetylosalicylic acid can cause papil-
           renal diseases                                  lary necrosis.
                                                              Analgesic nephropathy is characterized by pap-
                                                           illary necrosis and tubulointerstitial inflammation.
                                                           The papillary necrosis occurs usually following
  A large group of diseases exists affecting both           the tubulointerstitial inflammation which causes
kidneys simultaneously, in which morphologic alter-        glomerular filtration rate decrease.
ations in interstitium and in tubules are present.            Papillary damage following phenacetin intake is
Also the functional disturbances are limited rather        due to its metabolite acetaminophen. Its concen-
exclusively to the tubules and interstitium.               tration in papillae is ten times higher than in re-
  Glomeruli and the renal vessel system are usually        nal cortex. High water intake reduces papillary ac-
not involved. Interstitial edema prevails in acute         etaminophen concentration and protects the papil-
form of these diseases, associated often with corti-       lae from necrosis. Acetylosalicylic acid inhibits the
cal and medullar infiltration by polymorphonuclear          synthesis of renal prostaglandins which are impor-
leucocytes. Here are the foci of celullar necrosis. In     tant vasodilating factors. Thus, the acetylosalicylic
chronic forms more outstanding interstitial fibrosis,       acids acts simultanously by its toxic and by indirect
mononuclear inflammatory infiltration with signs of          vasoconstrictive effects increasing so the possibility
atrophy are observed. The tubular lumen is dilated         of renal damage appearing.
and the basement membranes are thickened. In past             Analgesic nephropathy is developing usually if the
was this morphologic finding considered to be the           daily intake of phenacetin, lasting 1 to 3 years, is 1
picture of chronic pyelonephritis. We are aware now,       to 2 g.

				
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