Nonspecific infections of the genitourinary tract.
The acute pyelonephritis is a nonspecific infectious disease that involves the pelvis of
the kidney, calyces and parenchyma, particularly its interstitial tissue.
Depending where the inflammatory process has started, nephropyelouretritis and
urerteropyelonephritis are differed. The results are equal.
The interstitial tissue distraction goes at first than it spreads on tubules and glomeruli. It
should be differed from the allergic interstitial nephritis when there is no destruction in
the pelvis of the kidney.
20-40% of the patients with the renal diseases suffers of the pyelonephritis. The short
urethra in girls and women and its close proximity to the anus allow the periurethral
pathogenic bacteria easy ascend from the urethra especially because of defloration,
pregnancy, delivery, postpartum period. The primary and secondary pyelonephritis are
distinguished. The primary pyelonephritis means no dysfunction for the urine outflow; the
secondary pyelonephritis goes with urostasis.
Classification.
1/ The unilateral and bilateral.
a/ Acute /purulent, serous/
b/ Chronic;
c/ Relapsing course.
2/ By the mode of bacteria pathway there are differed:
3/ a/ hematogenous /ascending/;
b/ urogenic /ascending/;
c/ urolithiasis /infected urinary stones/;
d/ tuberculosis of the kidneys;
e/ the other renal diseases.
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By the course, age, stage of the organism there are differed:
1/ the pyelonephritis of newborn;
2/ the pyelonephritis of the aged patients;
3/ the pyelonephritis of the pregnant women;
4/ the pyelonephritis in diabetes mellitus patients.
The acute pyelonephritis may be complicated with purulent nephritis, carbuncle of the
kidney, the renal abscess, renal insufficiency. The chronic pyelonephritis tends to progress
with the development of the malignant arterial hypertension, terminal renal insufficiency
/azotemia/, broadened necrosis of the renal parenchyma.
Ethiology and pathogenesis.
The pyelonephritis arises because of entry of the bacteria into the kidneys and
development of the inflammatory process within the interstitial tissue, renal pelvis and
calyces.
The principal causative agents are E.Coli, Staphylococci, Vulgar Proteus, Enterococci,
etc. Due to urine pH changes or antibiotics instillations these bacteria transform into Lforms and protoplasts. When the conditions become better they transfer back to the
vegetative form. That’s why there is no growth at the culture mediums while laboratory
diagnosis and there isn’t an effect of common treatment. The peculiarity of the
pyelonephritis is mixed infections with the resistant bacterial strains. The most common
association is Proteus with Pseudomonas Auruginosa /Blue pus bacillus/ not so frequent
the Hemoliticus strains of the E.Coli, Enterococci and staphylococci.
The massive infection diminished urodynamics, general immune dysfunction promote the
bacterial adhesion. There are major of entry of bacteria into the genitourinary tract.
A. Hematogenous spread.
Infections spread from the distant place /while otitis, tonsillitis, bronchitis, pneumonia,
osteomyelitis, mastitis, furunculosis, wounds.
B. Urinogenic spread.
Infection goes at the ureter from the bladder because of the vesicoureteral reflux. The
pelvicovenous, pelvicolymphathic, fornical and tubular refluxes may occur.
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C. Ascending infection.
Ascending infection from the ureter at the subepithelial tissue passes direct into the
interstitial tissue of the kidney.
D. Lymphatogenous spread.
The infection by means of the lymphatic channels probably occurs but it is rare. The
promote factors are general /avitaminosis, supercooling, overheating, other infection
diseases, gastric ulcer, etc./ and local /intravesical obstruction, neuromuscular dysplasia of
ureter, benign prostate hyperplasia, etc/.
The iatrogenic pyelonephritis is possible after the instrumental research.
Pathomorphology.
The interstitial nephritis may be considered as the independent nosology. But it is
considered commonly as the initial phase of the abacterial pyelonephritis.
Especially in the cortex the parenchyma shows the extensive tissue destruction by the
acute inflammation. Its surface is rough and deep red colored. The fibrous capsule is
thickened. The polymorphonuclear leukocytes, plasmocytes are tending to pervade the
interstitium and tubules. The infiltration by lymphocytes, erythrocytes, fibrin clots is
present within tubules. Then the connective tissue develops there; the hyaline
degeneration and athrophia progress. Unless inflammation is severe the glomeruli involve
much later. These changes are more common to hematogenous spread.
The renal papillae degenerate at first while the urinogenic infecting. There are the
infiltrations at the renal medulla then the process spreads at the cortex. A small purulent
focus may form there. The infiltration transforms into the sclerotic degention
There are stages of the inflammation of the acute pyelonephritis
1 stage. Serous pyelonephritis
2 stage. Purulent pyelonephritis
Acute pyelonephritis.
1/ Acute serous pyelonephritis.
The primary serous pyelonephritis means the hematogenous infection; the secondary one
occurs because of obstruction and may have especially arrhythmic course.
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Clinical findings. The general symptoms include shaking chills associated with
intermittent fever moderate to excessive sweating, headache, mialgia, artralgia, nausea,
vomiting, the patients appear quiet ill.
The local signs are pains at the lumbar region that irradiates to the upper portion of the
abdomen, into back. The fist percussion over the costovertebral angle overlying the
affected kidney is rather painful /positive Pasternatsky’s symptom/. The overlying
muscles’ spasm, abdominal distention may be marked. The enlarged painful kidney also
may be palpated on first days.
The obstructive /secondary/ type includes the algestic syndrome; hectic fever and renal
colic precedes it. This group of patients commonly suffers on urolithiasis. The enlarged
tough and painful kidney may be palpated.
Diagnosis.
The laboratory findings play the main role. There is bacteriuria. The quantitative
research of culture in 1 ml of urine, kind of pathogen flora, leukocyturia and
Shternheimer-Malbin cells are found out.
There are changes that are typical to any infection at the beginning: leukocyturia /40-60
and more/, erythrocyturia /10-20 to 30-40 in field of vision/, proteinuria /to 1 g/l /. The
early sign is bacteriuria but for its correct interpretation not only the vesical urine should
be inoculated but renal pelvis’s one too. /That is got by means of puncture or
catheterization while operation/. If the research of the cortex, tissue of the renal hilus and
extracted concrement is provided different microflora may be found. Then the bacterial
number in 1 ml of the urine is determined. Healthy people might have the conditionally
pathogenic bacteria /E.Coli, Proteus/ in the urine but not of the higher level than 2 ·10³ in
1ml. The number of the pathogen bacteria exceeds 10*6 per 1 ml of the urine while the
inflammative process at kidneys and urinary tract.
In case of the acute hematogenous pyelonephritis bacteriuria the only sign may be
because the leukocyturia appears in 3-4 days after the beginning of the disease.
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Typically the hemogram shows a moderate decreasing of hemoglobin, leukocytosis with
shift to the left and ESR elevation.
In case of the critical form of the disease with the another kidney affecting, liver
dysfunction, azotemia, hyperbilirubinemia, hyperglycemia, hypo- and dysproteinemia are
observed. But even with present function of the another kidney azotemia develops
because of the pelvic-venous reflux or the calicovenous shunt that is the result of the
occlusion of the upper urinary tract. An urgent operation should be carried out.
The excretory urograms show the enlargement of the infected kidney. The outline of the
ileopsoas muscle is absent sometimes, the diffuse shadow about the kidney and moderate
scoliosis at the side of the disease are present.
There is a slow excretion of the contrast. Calyces are flattered and clubbed, they are
filled with contrast later than normal kidney. The intravenous excretory urogram shows
the significant atrophy of the parenchyma of the affected kidney, its deformation because
of infiltrates and atonia of the ureter.
Chromocystoscopia shows the range even sometimes the cause of the functional loss of
the urine outflow. There can be seen the bullous edema of the urethral orifice because of
calculus at the intravesical portion, ureterocele, tumor compression.
The noninvasive methods are useful. These are radionuclide scintygrpahia, nondirect
angiographia, and ultrasonography. These methods show more distinctly the condition of
the calico-pelvic system and let to choose the optimal treatment. Ultrasonography shows
flattering and dilatation of the calyces and renal pelvis, dysfunction of the urine passages,
edema of the adipose capsule looks as rarefaction about the kidney. It also shows the sizes
of the concrement in the kidney.
The additional methods are thermography and thermovision.
The most patients have got the pyelonephritis as the result of the nephrolithiasis.
Urolithiasis is evident at the x-ray research. The excretory urogram is characterized by the
dilated ureter, renal pelvis and calyces; parenchymal irregularity and delayed excretion
with poor concentration of the medium. The function of the kidney is abrupted due to the
absolute obstruction.
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Differential diagnosis.
The acute pyelonephritis may be confused with the other acute infections, acute
cholecystitis, acute appendicitis, sepsis, etc. Especially when the local signs are moderate
the main differential signs are leukocyturia and bacteriuria. But these signs may appear
after the first day of the illness, the urogram should be taken not only once.
Treatment.
The main scheme includes the diet, bed rest, hydratation, desintoxication, general
strengthening and specific antibacterial treatment.
The bed rest and hospitalization are required. The difficulties of the treatment include
the bacterial resistance to the drugs, change of the bacterial strains, alergisation. The diet
should be sparing. The energetic support provides carbohydrates and plants fats. The
source of proteins may be cheese, hen eggs, then boiled fish and meat. Spices are
forbidden. Vitamins and a lot of fluid are necessary. The salt is limited. Perorate
hydratation includes to 3-l of fluid during a day on equal portions. The parenteral
hydratation means the endovenous infusion of isotonic, Ringer-Lokk’s, glucose,
Polyglycine solutions with vitamins and antibacterial agents. 1,5-2l of the certain solution
may be infused for two times a day. Albumin, plasma, g-globulin are also infused.
Antimicrobial treatment with desintoxicative and general stimulate measures are
effective in case of primary process.
The secondary pyelonephritis requires draining of the kidney, sometimes even the
purulent source removal. Before the urine outflow isn’t restored the antibacterial mediums
are dangerous especially of the strong action. The bacteriemic shock may develop. An
acute primary pyelonephritis is treated massively with the maximal dosage of the
antibacterial mediums in different combinations.
Urine and blood specimens must be obtained immediately for culture. Recognized
pathogens must be tested for antimicrobial sensitivity. Until the results of these tests are
known antimicrobial drugs should be given empirically.
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If the main pathogenesis of the pyelonephritis is damage of the urine outflow treatment
should restore it firstly. Catheterization is performed frequently. “Stent” catheter is used
commonly. It is injected even to pregnant women.
When there isn’t any effect of conservative measures an operative extraction of the
concrement is performed and nephrostoma is applied. To age patients and patients with
critical general state the transcutaneous puncture nephrostoma is performed under the
ultrasonography control.
The choice of the antibacterial specific measures is based on analysis of the
development of the disease, anamnesis, while culture tests are not ready /24-48 hours/.
Pathogen Staphylococcus is the agent from panaricium, furuncle; E.Coli, Proteus, Blue
pus bacillus- Pseudomonas Auruginosa causes pyelonephritis after cholecystitis,
appendicitis, it seldom may be Clebsiella and Enterococci.
A lot of urine culture strains are resistant to Penicillin G, Polymixine, Streptomycin,
Laevomicytine. But they are sensitive to macrolides /Erythromycin, Oleandomycin/; to
Methylcilline, Oxacilline, Carbenicilline; to aminoglycosides /Kanamycine, Monomycine,
Gentamycine/.
Gram-negative pathogens are sensitive to Carbenicilline. The other hemisynthethic
penicillines are non-active. The most effective drugs are aminoglycosides and
cephalosporines.
The clinical effect depends also on the concomitant microflora antimicrobial sensitivity.
The combined therapy is obviously needed because of the association of the pathogens
that have different antimicrobial susceptibility.
The phenomenon of the drug synergism is marked when Gentamycine and
Carbenicilline are administered. The blue pus bacilli has a good antimicrobial sensitivity
and isn’t able to be resistant at that case.
The urine culture (Proteus mirabilis or E.Coli for example) is sensitive to the
combination of the Carbenicilline, Ampicilline or Cefalotine with Gentamycine.
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For better effect a high concentration of mediums and the action at the various
pathogenetic mechanism are necessary. That’s why the different groups are administrated:
antibiotics, sulfanilamides, derivatives of the nitrofuranes, nalidixone acid, nitroxoline.
If the clinical response remains poor after 48-72 hours of the therapy, reevaluation is
necessary to assess. The source of the infection may be founded in the prostate frequently.
The iatrogenic genesis is possible especially after the catheterization.
Absence of the clinical response after 5-7 days needs the surgical decapsulation of the
kidney and the urine outflow restoring.
The criterion of the antimicrobial efficiency of the medium is its action at the Proteus
group. That’s why nitrofuranes are indicated (Furadonine, Furazolidone) as well as
derivates of the nalidixone acid, oxyhinoline (5-NOK, Nitroxoline).
Gexamethylentethramine /Urotropine/ is administered intravenous 5-10ml 40% sol.
Glucose 5 days. Dioxidine /chinoxoline’s derivate/ is injected because of the septic status.
10 ml of 1% sol. It is dissolved in 200 ml of the isotonic solution. 0,1% Furagine
(Salafure) is injected intravenous, too. Plasmapheresis is a high efficiency method to treat
the purulent process, sepsis. It detoxicates and decreases bacteriemia for 75-80% per 1-1,5
hour.
If the antimicrobial combined treatment is effective, the pathogen is sensitive and the
clinical response is favorable this treatment for about 1 week and then replaced with an
appropriate oral antimicrobial drugs for the additional 2 weeks.
The development of the resistance by the initially is possible. That’s why the urine
culture research 2 times a week is required. Treatment may be stopped in 2-3 weeks of the
hemogram and urogram normalization. The summary treatment lasts not less than 6
weeks. The premature stopping of the treatment is the cause of the recurrence and the
chronization.
Prevention of Candidamycosis is required while treatment lasts. Nistatine or Levorine
are administered.
The medication should be given to elevate the general resistance of the organism. The
specific remedies are vaccine, anatoxine, g-globulin. Nonspecific remedies are vitamins,
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hormones, enzymes, anticoagulants, blood substitutes, mineral waters, pH correctors,
mineral balance correctors.In case of severe progressing of the process and
septicopyemia, nephrectomy is indicated.
Observation is required for a follow-up period at least one year after the disease and for
five years after the surgical operation.
Acute purulent pyelonephritis /Apostematous pyelonephritis/.
It is the suppuration of the parenchyma of the kidney with formation of the small
multiply purulent focuses /apostems/. The process occurs unilateral and bilateral. The
purulent focuses are direct under the fibrous capsule, 1-3 mm in size and merging
sometimes. These abscesses are situated radially at the renal medulla from the apex of the
renal pyramid to its base at the cortex.
The virulent pathogens may cause its merging with developing of the abscess, carbuncle
or the purulent diffusion of the kidney.
Its clinical course is similar to sepsis. That is hectic fever ranged to 410C, chilling,
sweating, hypotonia, apathy, delusion, liver failure. Palpation shows the constant pain in
the loin. Clinical findings are more distinct while the obstruction.
Diagnosis.
There is no change in the urinalysis initially, then proteinuria, leukocyturia and
bacteriuria appear. The hemogram shows leukocytosis and shift to the left.
A plain film of the abdomen may show the enlarging of the kidney. Excretory urograms
show kidney dysfunction. The renogram shows the abnormalities of vascularisation,
secretion, and excretion. The renograms may be of the obstructive type that evident the
pathologic process in the kidney. Its location may be showed by the scyntygraphia with
computing.
There are the focuses with decreased accumulation of radionuclide at the scanogram.
The primary cause of the disease /calculus of the kidney or ureter/ may be found while
secondary Apostematous pyelonephritis at the X-ray examination.
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The primary Apostematous pyelonephritis should be differed from the other infections,
subphrenic abscess, acute cholecystitis, cholangitis, pancreatitis, pleuritis and other.
The Apostematous pyelonephritis has rather the complicated course. Leukocytosis in
blood may reach to 40x109 with shift to the left and appearing of myelocytes. There is
also eosinophilia, monocytopenia, and sharp elevation of the ESR and anemia.
Treatment.
The urgent surgical measures are required.
The subcostal lumbotomia is performed. The kidney is nude and decapsulated. The
purulent focuses are incised. The retroperitoneal space should be drained and free output
of the urine provided by means of the nephrostomia. The surgical drainage should be
present until the urine output becomes free, inflammation disappears and renal function
normalizes.
The postoperative period requires the antibacterial and desintoxicative treatment that is
similar to chronic pyelonephritis.
Nephrectomia is administered because of the total damage of one kidney and preserved
function of another followed with great intoxication. Bilateral pyelonephritis makes
prognosis rather doubtful. Lethality is 15%.
Renal carbuncle.
It is the suppurative-necrotic damage with formation of the bordered infiltrate in the
cortex of the kidney.
Renal cortical carbuncles develop primary as a result of the hematogenous spread of
infection form the distant sites /most often from the respiratory tract, suppurative diseases
of kidney, skin, furunculosis, felon, mastitis, etc./
Mechanism of carbuncle formation is the septic embolism of the renal artery that causes
the septic infarction of the kidney and the development of carbuncle.
Intravenous drug abusers are especially prone to develop the staphylococcal renal
abscesses. Multiply renal abscesses evolve and eventually coalesce to form a multilocular
abscess. The inflammatory focus doesn’t fuse for a time and fill with pus.
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Size of carbuncle varies from some millimeters to 10 cm. It is sited at the apex of the
right kidney in 50% of cases. The most frequent pathogens are Staphylococcus Aureus,
Staphylococcus Albus, E.Coli and Proteus.
It is combined with the Apostematous pyelonephritis in 30-40% of cases. The infiltrated
cortical carbuncle may rupture into the pyelocalycal system /there would occur a
selftreatment/ or onto the perinephric space.
Clinical findings.
It is typified by the abrupt onset of chills, fever, nausea, vomiting, localized
costovertebral pain, positive Pasternatsky’s symptom, kidney’s enlarging frequently. The
infection may spread by the lymphatic vessels to pleura when the carbuncle is sited at the
upper pole of the kidney.
At the early stages when the carbuncle does not communicate with the collecting
system, symptoms of vesical irritability are absent and analysis is normal, although the
patient may be quite septic.
The irritation of the posterior layer of the peritoneum imitates the appendicitis,
diverticulitis, salpingitis, pancreatitis, cholecystitis and others. A painful palpable mass,
erythema and edema of the skin of the overlying loin are late signs.
The hemogram usually shows marked leukocytosis (10-30x109/l) with a shift to the left.
The urinalysis shows no pyuria or bacteriuria and urine culture is negative. The moderate
pyuria appears.
Typical course is rare. The important fact is masking of the disease. It may course like
cardiovascular, nervous, hepatorenal, digestive, respiratory system dysfunction (disease),
liver damage or thromboembolism. That’s why it’s difficult to make the diagnosis when
there is a cortical carbuncle and urinary tract isn’t obstructed.
X-Ray-finding is very important. If the renal outline is visible the plain film may show
the enlarged kidney or a bulge of the external renal contour. With the perinephral edema,
however, often the renal outline is obliterated and the psoas shadow indistinct. The
shadows of the concrements may be sometimes.
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One can see the deformation and narrowing of the renal pelvis, deviation and indistinct
outlines of the calyces on the excretory urograms and pyelograms. Pyelonephritic
changes, urolithiasis may be observed. Delayed pacification may be found. Carbuncle
may be confused with tumor sometimes while the X-ray imaging. The renal Angiography
usually makes the diagnosis.
The isotope scanning will depict a space-occupying lesion. The scintigraphy with
197
Tc-
neohydrine will show the avascular mass lesion. The renal echograms look like distinct
cone-shaped zones of the increased acoustic density situated within renal parenchyma.
Carbuncle should be distinguished of the infections, renal tumors, purulent tumor cyst,
tuberculosis of the kidney, acute cholecystitis, subphrenic abscess, and pancreatitis.
Treatment includes the urgent surgical measures.
Lumbotomia is performed. Then decapsulation of the kidney and cone-shaped excision
of the carbuncle are done. Incision, curettage and draining of the kidney or enucleating of
the carbuncle with its incision may be performed too.
The cone excision is organ preserving surgical operation. The cross-shaped incision is
made up to the health tissues just after decapsulation (nuding) of the kidney and revision
of its surface. It shouldn’t be deeper than 0,5 cm. Then the assistant pulls out the internal
angles by means of miniature acute hooks. The surgeon with ophthalmic scalpel removes
gradually by circular incisions the necrotic masses. But the surgeon gets it out from the
surface and next from the deep tissues, orientating to the color of the tissues and bleeding
range. Moderate venous diffusion evident the demarcating of necrosis zone from the
health tissues. The cone-shaped hollow cavity forms after the extraction. Moderate tight
tamponade with gauze favors the hemostasis and outflow of the vulnus secretion.
The postoperative period requires the antimicrobial treatment with considering of the
urine culture and renal tissue culture. The multiple carbuncle or the great damage of the
kidney requires nephrectomy in case when the other kidney is normal.
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Abscesses of the kidney.
These are the result of purulent melting of its parenchyma and forming of cavity filled
with pus. The granular torus borders the purulent focus apart the healthy tissues. Abscess
may spread at the perinephrium. Abscess is the frequent complication of the urolithiasis.
Methastase abscesses are also possible as a result of hematogenous spread. The source
may be the destructive pneumonia and the septic endocarditis. The abscesses are bilateral
and multiply usually.
Clinical findings look typically to the acute pyelonephritis. The bilateral process goes
like sepsis, hepatorenal failure. The solid encapsulated abscess doesn’t change urinalysis.
Leukocytosis with shift to the left, ESR elevation is observed in spite urodynamic is
normal. Hyperleykocytosis, critical anemia, dysproteinemia are observed when the urine
outflow is abnormal. Urinalysis may be normal or moderate proteinuria, microhematuria,
and bacteriuria. The sudden appearance of the heavy pyuria and bacteriuria may herald
the rupture of the previously noncommunicating abscess into the collecting system.
The plain film (urogram) shows the psoas shadow absence, the external renal outline juts
out at the abscesses location.
The excretory urogram shows the limit of the kidneys mobility while breathing,
deformation or amputation of the calyces, compressing of the renal pelvis. After abscesses
rupture the contrast medium may get into its cavity and additional shadow may be seen at
the retorpyelogram. The scyntigrame points the deficiency of the radionuclide
accumulation at the place of abscess. CT-Scans shows the hollow cavity with amount
liquid. Ultrasonography shows the hollow cavity with liquid (pus) inside.
Treatment mostly is surgical. Decapsulation of the kidney with the broad incision of the
abscess and draining of it both the retroperitoneal spaces are performed. The
postoperative period requires the antibacterial and desintoxicative therapy.
Without surgical measures 75% of cases are lethal.
Emphysematous pyelonephritis.
It is an acute inflammative process caused by pathogens those are able to make necrotic
inflammation and gas-producing (Pseudomonas). They are able to decompose glucose to
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gas and acid. They occur with a high frequency at aged women suffering on the diabetes
mellitus. Process is unilateral mostly.
The disease demonstrates with the renal failure and intoxication. It is associated with the
thrombosis of the renal arteries and papillary necrosis. Clinical signs may be similar to
bacteriemic shock. The local symptoms are non significant or absent. There will be a
sharp pain in loin in case of the obstruction of the ureter.
Renal failure leads to azotemia, circulatory insufficiency. Uncontrollable vomiting leads
to dehydration, acidosis, electrolytic disbalance, hepatorenal insufficiency, serous or
fibrous peritonitis. The urine is sharply acidophylic. There usually are proteinuria,
leukocyturia, bacteriuria, and microhematuria.
The diagnosis is based on the X-ray findings and the culture of the urine (finding out the
gas-producing bacteria). The plain film shows the scoliosis to the affected kidney side and
absence of the outline of the psoas muscle. The gas that is cumulating at the perinephral
area is a pathognomonic sign. To persuade the localized gas collection isn’t intestinal one,
CT scanning is recommended.
The excretory urograms may show delayed visualization or nonfunctional related to
destructive uropathy. The calyces would be compressed when parenchyma is infiltrated.
Differential diagnosis should be made with other infections, acute pyelonephritis,
appendicitis, cholecystitis, pancreatitis, perforated ulcer of the stomach or duodenum.
Treatment is mostly surgical. The association of the emphysematous pyelonephritis and
infarction or necrosis of the kidney requires nephrectomy. It’s a choice operation. 70-80%
of patients recovers then. The bilateral damage requires the bilateral nephrectomy with the
followed-programmed hemodialysis. Prognosis is encouraged then.
The early surgical treatment is preferred last years. Lumbotomia with incision and
removal of the whole perinephral fat, decapsulation with necrotic focuses of the kidney
and nephrostoma are performed. A broad draining of the retroperitoneal space is
necessary in case of abnormal function of the kidney.
Lethality is 40% when the conservative treatment is used only.
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Papillary necrosis is a destructive process at the renal medulla due to ischemic necrosis
of the papillary tip or entire pyramid. Diabetes mellitus, continued angiospasm,
thrombosis, atherosclerosis, injure of the kidneys, shock, over-indulgence in analgesics,
nephrolithiasis, anemia are favoring factors. The urinary tract infection is the obligate
condition of the disease development. The alergisation plays a certain role, too.
Primary and secondary (attending to pyelonephritis) papillary necrosis is differed.
The venous stasis is one of the causes of the papillary necrosis. Complete or partial
occlusion of the renal vein may lead to infarction of the renal medulla.
3 forms of the papillary necrosis are differed.
1)
Infectious form (with obligate previous pyelonephritis);
2)
Angiospastic form (as the result of the blood discirculation at the renal
medulla on basement of the arteriosclerotic change in vessels, thrombosis, embolism.
3)
Vasocompressive or the ischemic form as a result of interstitial edema and
sclerosis that cause the compression of the papillary arteries.
The pelvicorenal refluxes that are attended to renal pelvis hypertension and
calicopelvical diskynesia play an important role.
Dysfunction of the urinary output (obstruction) and obturation of the ureter leads to
papillary necrosis. Besides, the urinary tract obstruction causes the fibrosclerotic
degeneration about the urinary organs by means of infection spreading to the fat tissue as
well as toxic action of urine by itself upon this tissue. As a result the additional reasons to
urostasis, lymphostasis, arterial and venous hyperemia appear. These facts may cause the
papillary necrosis.
By Y.Pitel (1970) the pathogenesis of the papillary necrosis is: necrosis of the papillae
leads to necrotic inflammation of the papillae (necrotic papillitis) leads to the formation of
the venous-calyces fistula leads to fornical bleeding at the base of the acute pyelonephritis
or the acute relapse of the chronic pyelonephritis leads to the progressive fibrosis of calyx
leads to the secondary scarring of the kidney.
Papillary necrosis may be fornical, papillary and total (it spreads all over the medulla of
the kidney).
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Clinical findings. An acute course occurs rarely. 75% patients have chronic process. The
most frequent sign is the gross hematuria in consequence of exfoliation of the necrotizes
papilla. The affected tissue necrotizes because of the suppurative inflammation in one
case or papillae abruption and passing through the urinary tract. If its diameter is larger
than the ureter an occlusion develops.
The clinic depends on continuation and range of the obstruction, activity of the
inflammatory process. The typical sign is passing out of necrotic fragments of the renal
medulla with urine output.
At times the negative shadows that are representing retained papillae are visible. During
the late phases of papillary necrosis, irregular or triangular calcified bodies with
radiolucent centers (the papillae) are the diagnostic findings. In the earliest stages of
interstitial nephritis, before papillary slough, urograms often don’t detect caliceal
abnormalities. The calyces are erosive, but their narrowing is absent. The changes are
nonsignificant. They develop while exfoliation or destruction of the papillae. The
reiteration of the excretory urogram is required when the papillary necrosis is suspected.
Different stages of the process show different findings. A concrement shadow triangle
shaped with radiolucent center, small shadows of the calcificates at the papilla and calyx
area sloughed, outlines of the papilla and fornicles, fornicopapillar fistula, cavity within
the counter of the renal pyramid connected with the calyx, amputation of the calyces
because of their edema, multiply defects of filling of the renal pelvis, calyces, etc.
Treatment. It is pathogenetic and symptomatic.
Catheterization of the ureter and renal pelvis is indicated in case of occlusion of the
upper portion of the urinary tract. The conservative treatment of the papillary necrosis is
similar to the acute pyelonephritis.
Operation should be for the organ preserving. That is removal of the necrotic mass,
restoring of the urine output by means of nephrostomia. Resection of the kidney is
performed because of the profuse hematuria. In case of the accompanying acute
pyelonephritis the decapsulation is administered. Nephrectomia is reasonable just in case
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of total necrosis of the kidney medulla with the acute purulent pyelonephritis and
satisfactive function of another kidney.
The great complication is the bacteriemic shock. The lethality is 70-90%. The gramnegative bacteriemia occurs in 2/3, gram-positive bacteriemia is in 1/ of patients.
The rapid and massive coming of bacteria and their endotoxines in blood is the
mechanism that causes a complex interaction between the fibrinolitic, coagulation and kin
systems and their effects upon the microcirculation and hemostasis.
Bacteriemic shock develops right after the massive invasion that is the result of urinary
tract occlusion, surgical intervention at the kidneys or in some hour’s even days. Four
forms of bacteriemic shock are differed according to A.Pitel:
1)
Smooth form appears on first day manifests with chilling, fever and moderate
decreasing of the arterial pressure.
2)
Early form develops in the first hours or during the first day. Fever and
collapse are the initial signs.
3)
Distanced form develops after the intermedial stage. Typically infection
previously fixes at the lungs (pneumonia), kidneys (pyelonephritis), epididimitis.
4)
Late form develops in the terminal stage of sepsis.
3 phases are differed according to Lopatkin: early (warm), manifested and terminal
(irreversible).
Laboratory findings.
The leukocytes are usually elevated with the shift to the left. The disseminated
intravascular coagulation is characterized by thrombocytopenia, presence of circulating
fibrin split products. Initially the hematocrite may be increased as a result of loss of
plasma into the interstitial tissue.
Because of the renal blood flow is diminished the specific gravity of urine is increased
and the ratio of serum urea nitrogen to serum creatinine may exceed the normal
extremely. Early sign of shock diminishes the diuresis to 25-30 ml/hour. The systolic
pressure decreases to 80-90 mm Hg at the peak of shock. Anuria develops then.
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Hemoculture is found at the peak of fever. Urinary and blood cultures are similar as a
rule.
Treatment is goaded to manage collapse and infection.
Since shock is a result of the endotoxines action therapy is based on antishock measures.
A decapsulation and nephrostomia are required in spite the critical state of the patient.
Massive antimicrobial therapy without restoring of the urine output is inadmissible.
If the pathogen is not yet been identified the treatment must not await the results of the
culture and sensitivity test. The best drug combination should be administered in maximal
therapeutic dosage. In complex with antibiotics the uroseptics should be administered.
There are the nitrofuranes derivates, Nitroxoline, nalidixone acid. Measures to improve
circulating blood volume and perfusion of vital organs are parenteral fluids
(Rheopolyglycine, Hemodes, Aminocaprone acid solution), corticosteroids (Prednisolone,
Hydrocortisone, Dexamethazone), vasoactive agents (Epinephrine, Mesatone, Ephedrine).
The support of vital organs (heart, lungs, kidney) is required as well as correction of
fluid and electrolyte balance and treatment of disseminated intravascular coagulation.
Heparin 30000-60000 OD per day is administered. Mannitol (200-300ml of 15%sol.)
Furosemide are indicated. Venoruton (500mg twice per day, Pentoxyphillinum (100mg
twice per day), Dyperidamole, Xanthinole nicotinate are going in complex therapy. To
improve nitrate metabolism Testosterone propionate (2ml 5%sol. Every other day) or
Rethabolil (1ml 5%sol. Every 10 days are administered.
Gestation pyelonephritis.
(Pyelonephritis of pregnancy).
The inflammatory process develops while pregnancy, delivery and puerperal period.
Most frequently it is observed in pregnant (48%) more rare in puerperal (35%) women. It
develops while 1 pregnancy 2 trimester often. There are women 18-25 years old. That is
explained by a not complete adaptation to immunologic, hormone changes of the
pregnancy. It is supposed not to be a primary disease but activation of latent
pyelonephritis.
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Urinoculture finds out E.Coli, Staphylococcus albicans, Clebsiella in pregnant women.
Association of the Proteus and Blue pus bacilli is observed in puerperal women. The
primary source of the infection may be any purulent inflammatory place (furunculosis,
dental caries, inflammatory diseases of the genital organs).
The pathogenetic sign is bacteriuria. It is observed in 7% only. Urodynamic dysfunction
favors the pyelonephritis development. Pathogenesis may be explained with mechanical,
neurohumoral and endocrine factors. The enlarged uterus compresses the pelvic portion of
the ureters causing ureteropyeloectasia while pregnancy. Urostasis at the upper portion
develops because of decreasing of the ureteral muscles and pelvises of the kidney tension.
The moderate hypotonia and hypokinesia of the calicopelvic of the both kidneys and
ureters are observed on 8th week.
Changes of the upper portion of the urinary tract may be explained by weakening of the
sympathetic nervous system tonus. Dysfunction of the urinary output because of the
urinary pathway atonia is a condition for pathogen activation. Vesicoureteral and
pelvicorenal refluxes favor spreading of the infection into the interstitial tissue of the renal
parenchyma (medulla of the kidney).
Acute pyelonephritis of pregnancy. Primary acute process acute rarely. This is an active
phase of the chronic process frequently. The prepueral women have attacks of the acute
pyelonephritis at the 4-, 6-, 12- day of the puerperal period (these are days of the
postpartum complications: endometritis, metrophlebitis).
Clinical findings.
Clinical findings have the own peculiarities according to the different terms of
pregnancy. They also depend on the range of the urinary output damage. A sharp pain in
loin that irradiates to the lower portions of the abdomen, genitals are at the 1 trimester. 2nd
and 3rd trimesters are characterized with a moderate pain because of the dilatation of the
upper urinary tract and intrarenal pressure decreasing.
An acute purulent pyelonephritis develops more frequently in pregnant and postpueral
women. There is a high lethality rate caused by an acute purulent pyelonephritis.
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Diagnosis is rather difficult. The enlarged uterine hinders the palpation. The right kidney
damage should be differed from the acute appendicitis and cholecystitis.
X-ray imaging is inadmissible exclusive rare occasions. The endoscopy investigation
isn’t recommended too. In case of the suspicion of purulent process the complete clinical
research is required including Chromocystoscopia, radionuclide renography, scanning,
excretory urography, ultrasonography. The delayed excretion of the indigocarmine while
Chromocystoscopia is attended to peculiar urodynamic due to pregnant uterus.
Treatment.
The inflammatory process develops while pregnancy, delivery and puerperal period.
Most frequently it is observed in pregnant (48%) more rare in puerperal (35%) women. It
develops while 1 pregnancy 2 trimester often. There are women 18-25 years old. That is
explained by a not complete adaptation to immunologic, hormone changes of the
pregnancy. It is supposed not to be a primary disease but activation of latent
pyelonephritis.
Caesar’s incision by retroperitoneal access is performed because of an acute
inflammation at the last days of pregnancy.
Antibiotics shouldn’t be harmful to fetus. The natural and semisynthetic penicillines are
recommended at the 1st trimester. Wider choice of antibiotics is at the 2nd and 3rd
trimesters because placenta has its barrier function then.
The puerperal women may transfer drugs to child with milk.
Treatment should be continuous. Nitrofuranes are admissible after 2nd month in dosage
50-100mg per day. Nalidixone acid is admissible after the 4th month of pregnancy (2g per
day for 2-3 weeks). But its administration must be stopped before delivery.
The acute purulent pyelonephritis in pregnant women requires the obligate surgical
measures. Its scope depends on form of the disease. It is necessary anyway until the
delivery.
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