Etiology
Acute pyelonephritis is an infectious inflammatory disease that involves both the parenchyma and the pelvis of the kidney; it may affect one or, on occasion, both kidneys.
Aerobic gram-negative bacteria are the principal causative agents; common strains of E coli are the predominant pathogens. All species of Proteus are especially important because they are potent producers of urease, an enzyme that splits urea and produces highly alkaline urine that favors the precipitation of phosphates to form magnesium ammonium phosphate (struvite) and calcium phosphate (apatite) stones. Klebsiella species are less potent producers of urease but elaborate other substances that favor urinary stone formation.
Gram-positive bacteria other than the enterococ-cus Streptococcus faecalis seldom cause pyelonephritis. Staphylococci may infect the kidney by the hematogenous route and cause bacteriuria and renal abscesses. Obligate anaerobic bacteria rarely cause pyelonephritis.
Pathogenesis
Renal infection usually ascends from the urethra and lower genitourinary tract. Hematogenous infection of the kidney occurs infrequently; lymphatic spread occurs rarely, if ever.
The short urethra in girls and women and its close proximity to the anus allow periurethral pathogenic bacteria easy access to the bladder during sexual intercourse or urethral manipulation. Girls and women with breached local defenses due to biologic, anatomic, or other abnormalities frequently experience introital and periurethral colonization by pathogenic enteric bacteria and are especially prone to infection that ascends from the urethra.
Males are less susceptible to ascending urethral infection because the male urethra is much longer than the female urethra and the meatus is not so near the anus and because the prostate normally secretes antibacterial factors that give some protection against invading pathogens.
Once pathogenic bacteria reach the bladder via the urethra, whether infection becomes established is influenced by the quality of the bladder defenses: the efficacy of voiding and muscle coordination, the antimicrobial properties of the urine, and factors that allow or inhibit bacterial adherence to surface cells.
Once bladder infection is established, whether infection ascends via the ureters and involves the kidneys is influenced by microbial virulence factors, the presence or absence of vesicoureteral reflux, the quality of ureteral peristalsis, and the susceptibility of the renal medulla to infection.

Classification
The primary and secondary pyelonephritis are distinguished.
There is no dysfunction of the urine outflow during the primary pyelonephritis.
The secondary pyelonephritis goes with urostasis.
The secondary pyelonephritis goes with urostasis
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.
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.
Clinical Findings
A.
Symptoms: The usual symptoms of acute_py-elonephritis include abrupt onset of shaking chills, moderate to high fever, a constant ache in the loin
(unilateral or bilateral), and symptoms of cystitis: frequency, nocturia, urgency, and dysuria. Significant malaise and prostration are the rule; nausea, vomiting, and even diarrhea are common. Young children most often complain of poorly localized abdominal discomfort and seldom localize the discomfort specifically to the flank.
B.
Signs: The patient generally appears quite ill. Intermittent chills are associated with fever ranging from 38.5 to 40 °C (101-104 °F) and tachycardia (the pulse rate may range from 90/min to 140/min or faster). Fist percussion over the costovertebral angle overlying the affected kidney usually causes pain. The kidney often cannot be palpated, because of tenderness and overlying muscle spasm.
Abdominal distention may be marked, and rebound tenderness may suggest an intraperitoneal lesion. Auscultation usually reveals a quiet intestine.

C.
Laboratory Findings: The hemogram typically shows significant leukocytosis (polymorphonu-clear neutrophils and band cells); the erythrocyte sedimentation rate is increased. Urinalysis usually shows cloudy fluid with heavy pyuria, bacteriuria, mild proteinuria, and often microscopic or gross hematuria.
Leukocyte casts and glitter cells (large polymorphonuclear neutrophils containing cytoplas-mic particles that exhibit dramatic brownian movement) are occasionally seen. Quantitative urine culture generally grows the responsible pathogen in heavy density (≥100,000 colonies/mL); sensitivity tests are helpful in therapy and of vital importance in the management of complicating bacteremia. Serial blood cultures are indicated, because bacteremia commonly accompanies acute pyelonephritis. In uncomplicated acute pyelonephritis, total renal function generally remains normal, and the serum creatinine level is not elevated.
D.
X-Ray Findings:
A plain film of the abdomen may show some degree of obliteration of the renal outline owing to edema of the kidney and perinephric fat. Suspicious calcifications, must be carefully evaluated, because infected renal stones and calculous obstruction complicating pyelonephritis require special management.
Excretory urograms
Excretory urograms performed during the acute stage of uncomplicated pyelonephritis usually show few abnormalities but are important in surveying for possible complicating factors. The severely infected kidney may appear enlarged, show a decreased nephrogram effect on the initial film, and reveal little or no caliceal radiopaque material. Following appropriate therapy, the urograms return to normal.
Voiding cystograms are best delayed until several weeks after the infection is cleared; otherwise, transient vesicoureteral reflux, often associated with the accompanying cystitis, may be confused with more serious permanent reflux.
E. Radionuclide Imaging: At times, imaging ' the kidneys with gallium-67 helps to determine the site of infection and distinguish between acute pyelonephritis and renal abscess. Despite some false-positive and false-negative images,
Hurwitz et al (1976) claim 86% accuracy in confirming acute pyelonephritis by this method.
Instrumental Examination

There can be seen the bullous edema of the urethral orifice because of calculus at the intravesical portion, ureterocele, tumor compression.
Chromocystoscopia shows the range even sometimes the cause of the functional loss of the urine outflow.
Differential Diagnosis
Because of the location and nature of the pain, pancreatitis at times may be confused with acute pyelonephritis. Elevated serum amylase and normal results of urinalysis help to confirm a diagnosis of pancreatitis and rule out pyelonephritis.
Basal pneumonia is a febrile illness that causes pain in the subcostal area. The pleuritic nature of the pain and the chest x-ray usually allow differentiation.
Acute intraabdominal disease, including such conditions as acute appendicitis, cholecystitis, and di-verticulitis, must at times be distinguished from acute pyelonephritis. Although the signs and symptoms may be confusing initially, the normal urinalysis associated with primary gastrointestinal disease and other laboratory tests should make the differential diagnosis uncomplicated.
In women, the onset of acute pelvic inflammatory disease (PID) at times must be distinguished from acute pyelonephritis. Characteristic physical findings and negative urine cultures should make differentiation fairly easy.
In male patients with febrile genitourinary tract infection, the main differential diagnosis consists of acute pyelonephritis, acute prostatitis, and acute epididymoorchitis. Characteristic physical findings and symptoms in prostatitis and epididymitis should make this differentiation easy.
Acute pyelonephritis must be distinguished from renal abscess and perinephric abscess. Radiographic studies often are necessary to confirm the specific diagnosis.
A.
Specific Measures: When the infection is severe or complicating factors are present, hospitaliza-tion may be required. 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. Although clinicians differ in their choice of antimicrobial agents, our preference is to administer an aminoglycoside (amikacin, gentamicin, or tobramycin) plus ampicillin intravenously in full dosage. If the pathogen is sensitive and the clinical response is favorable, this treatment is continued for about 1 week and then replaced with an appropriate oral antimicrobial drug for an additional 2 weeks. Complicating factors, eg, obstructive uropathy or infected stones, must be recognized early and dealt with effectively if complications are to be avoided.
B.
General Measures: Complete bed rest is advised until symptoms subside.
Medication should be given for pain, fever, and nausea. It is important to give fluids intravenously and orally to ensure adequate hydration and maintenance of adequate urinary output.

C.
Failure of Response: If the clinical response remains poor after 48-72 hours of therapy, reevalua-tion is necessary to assess for possible complicating factors (eg, obstructive uropathy) or the use of inappropriate drugs. Excretory urography is required; if this is contraindicated, retrograde urography must be done. Unless treated quickly and effectively, obstructive uropathy complicating acute pyelonephritis can lead to bacteremia and irreversible renal damage.
D.
Follow-Up Care: Clinical improvement does not always imply cure of the infection. In about one-third of patients, symptoms improve despite persistence of the bacterial pathogen. Therefore, repeat urine cultures are important during and after therapy for a follow-up period of at least 6 months.
Prognosis When identified promptly and treated appropriately in a patient who has no underlying complicating factors, acute pyelonephritis carries a good prognosis for cure without sequels. The likelihood of serious sequels and a less favorable prognosis varies with the severity of complicating factors and the patient's age at the onset.
(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.
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 8 th 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. 2 nd and 3 rd 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.
Diagnosis is rather difficult. The enlarged uterine hinders the palpation. The right kidney damage should be differed from the acute appendicitis and cholecystitis.
Ultrasonography (shows dilatation of the calyces and renal pelvis, dysfunction of the urine passages, edema of the adipose capsule looks as rarefaction about the kidney)
X-ray imaging is inadmissible exclusive rare occasions.
Chromocystoscopia
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.
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 1 st trimester. Wider choice of antibiotics is at the 2 nd and 3 rd 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 2 nd month in dosage 50-100mg per day. Nalidixone acid is admissible after the 4 th month of pregnancy (2g per day for 2-3 weeks). But its administration must be stopped before delivery.

Ureteral catheterization
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.
Etiology
Renal cortical abscesses develop primarily as a result of hematogenous spread of Staphylococcus aureus infections at distant sites (most often the skin). At times, foci of primary renal infections caused mainly by gram-negative bacteria (coliform organisms) coalesce in the renal medulla to form abscesses. In the past, most renal abscesses were caused by staphylococci; recently, coliform bacteria have become the predominant pathogens in renal abscesses. Renal abscesses caused by obligate anaerobic bacteria are rare.
An abscess (carbuncle) caused by S aureus develops from hematogenous spread of the organism from a primary skin lesion. Intravenous drug abusers are especially prone to develop staphylococcal renal abscesses. Multiple focal abscesses evolve and eventually coalesce to form a multilocular abscess. Untreated cortical abscesses may rupture into the pyelocaliceal system or into the perinephric space (perinephric abscess). Urinary tract infection occurs only if the abscess communicates with the pyelocaliceal system.
The more common type, renal medullary abscess, evolves from acute or chronic foci of pyelonephritis, often associated with ureteral obstruction or calculous disease (calculous pyonephrosis). The infecting pathogens usually are gram-negative rods. Timmons and Perlmutter (1976) believe that gram-negative bacillary abscesses in children may be a complication of vesicoureteral reflux, with the pathogens invading the collecting tubules. In adults, the kidney usually is damaged by chronic suppurative pyelonephritis that may culminate in one or more abscesses. Medullary abscesses may also rupture into the perinephric space. Onethird of affected patients are diabetics.
Clinical Findings
A.
Symptoms: Staphylococcal renal abscess is typified by an abrupt onset of chills, fever, and localized costovertebral pain. In the early stages, when the

abscess does not communicate with the collecting system, symptoms of vesical irritability are absent and urinalysis is normal, although the patient may appear quite septic. The clinical picture often mimics that of acute pyelonephritis.
In most patients with medullary abscesses due to gram-negative rods, there is a history of persistent or recurrent bouts of urinary tract infection, often associated with urolithiasis, obstructive uropathy, or renal surgery.
B.
Signs: In acute cases, localizing signs are flank tenderness, possibly a palpable mass, and erythema and edema of the skin of the overlying loin. At times, however, abscesses associated with both acute and chronic infections present as febrile illnesses with few localizing signs.
C.
Laboratory Findings: The hemogram usually shows marked leukocytosis with a shift to the left. With cortical abscesses that do not communicate with the collecting system, urinalysis shows no pyuria or bacteriuria, and urine culture is negative. Medullary abscesses generally are associated with heavy pyuria, bacteriuria, and positive urine cultures. The sudden appearance of heavy pyuria and bacteriuria may herald the rupture of a previously noncommunicating abscess into the collecting system. Blood cultures may be positive.
Depending upon the extent of renal involvement and associated renal abnormalities, the serum creatinine and urea nitrogen values may be normal or elevated. Since patients with renal abscesses often are diabetic, glycosuria and hyperglycemia may be found.
D.
X-Ray Findings: If the renal outline is visible, the plain film may show an enlarged kidney or a bulge of the external renal contour. With perinephric edema, however, often the renal outline is obliterated and the psoas shadow indistinct.
Unless the abscess has ruptured into the perinephric space or is quite large, scoliosis generally is not observed. Renal stones may be noted. When cortical abscesses are small, the excretory urogram may appear normal; most often, however, a space-occupying lesion (the abscess) is delineated. Pyelonephritic changes, hydronephrosis, and urolithiasis also may be observed. Delayed opacification or even a nonfunctioning kidney may be found.
Renal angiography usually makes the diagnosis. The abscess fails to opacify; its walls are irregular. Surrounding vessels are displaced, and hypervascularity is common. The most important sign is excessive capsular vessels overlying the abscess.
E.
Ultrasonography:
Renal echograms generally distinguish simple cysts (no internal echoes) from solid masses (many internal echoes) but often fail to distinguish renal abscesses from malignant lesions, particularly necrotic, cystic renal cell carcinomas.
Percutaneous needle aspiration of the mass under ultrasonic guidance may confirm the diagnosis.

CT Scans
F. CT Scans: Experience has been limited in the utilization of CT scans for the diagnosis of renal abscess. The attenuation coefficient value (CT number) varies considerably with the amount of liquid pus or solid debris within the abscess, and abscesses cannot be differentiated from hemorrhagic cysts or solid neoplasms with certainty. Percutaneous needle aspiration of the mass under CT control may confirm the diagnosis.
G.
Isotope Scanning: The rectilinear scan will depict a space-occupying lesion. With the use of technetium and iodine compounds, the Anger camera will show an avascular mass lesion. These findings also are compatible with simple cyst. Gallium-67 localizes in inflammatory tissue; an abscess will therefore "light up" on dynamic scanning.
Gallium scanning may demonstrate an abscess even when excretory urograms are normal.
Differential Diagnosis
In acute pyelonephritis, symptoms and signs may be similar to those of abscess; however, no space-occupying lesion is shown on the urogram, and a gallium scan will not show an abscess.
When symptoms of vesical irritability are absent and urinalysis is normal, renal abscess may be confused with acute cholecystitis. The presence of a palpable and tender gallbladder may make the diagnosis. Radiographic visualization of the gallbladder and kidneys should be definitive.
Acute appendicitis may be confused with renal abscess, because renal pain often radiates to the lower abdominal quadrant. The findings on physical examination, laboratory studies, and radiographic studies should allow differentiation.
At times, renal cell carcinoma may be confused with renal abscess, especially when there is fever related to tumor necrosis. Radiographic studies and scans usually will allow differentiation; however, percutaneous needle aspiration may be required in some cases.
Complications
Complications of renal abscess include both bacteremia with generalized sepsis and rupture of the abscess into the perinephrium.
Staphylococcal abscesses should be treated with a penicillin resistant to 3lactamase. In the early stages, antibiotics alone may cure the abscess. When the abscess is caused by gram-negative rod infection, therapy should consist of an aminoglycoside alone or in combination with a cephalosporin or other agent.

Aminoglycosides are important in therapy because they are concentrated in renal parenchyma and thus may obviate the need for surgical drainage.
NEPHROSTOMY
Drainage by percutaneous means or surgical incision may be necessary.
Relief of complicating urinary obstruction is mandatory. Nephrectomy and partial nephrectomy are required less often today than in the past.
Prognosis
The outlook is good provided the diagnosis is made promptly and effective therapy is instituted immediately.
Etiology
Perinephric abscesses lie between the renal capsule and the perirenal
(Gerota's) fascia. Most result from rupture of an intrarenal abscess into the perinephric space; the causative organisms are usually coliform bacteria and
Pseudomonas, less often staphylococci and obligate anaerobes.
Pathogenesis & Pathology
Staphylococcal perinephric abscesses probably originate from rupture of a small renal cortical abscess or, less commonly, from a renal carbuncle. The primary renal lesion may heal, although the perinephric abscess progresses.
Usually, however, perinephric cellulitis and abscess complicate severe renal parenchymal infection caused by gram-negative bacteria in association with calcufous pyonephrosis or infected hydronephrosis. It is presumed that spontaneous extravasation of infected material occurs. In this instance, pus and bacteria usually are found in the urine.
Perinephric abscesses may become quite large. When advanced, they tend to point over the iliac crest (Petifs triangle) posterolaterally.
Clinical Findings
A.
Symptoms: The most common symptoms of perinephric abscess include chills, fever, unilateral flank pain, and abdominal pain. Malaise and prostration occur variably. Only about one-third of patients complain of dysuria.
B.
Signs: Fever tends to be low-grade unless generalized sepsis evolves.
There is usually marked tenderness over the affected kidney and costovertebral angle. A large mass may be felt or percussed in the flank. Abdominal tenderness accompanied by variable rebound tenderness may be elicited. The diaphragm on the affected side may be elevated and fixed. Ipsilateral pleural effusion is common.
Scoliosis with the concavity to the affected side usually is seen; this results from spasm of the psoas muscle, which also causes the patient to lie with the ipsilateral leg flexed on the abdomen. Erythema and edeina of the overlying skin may be

evident. Minimal edema is best demonstrated by having the patient lie on a rough toweLfor a few minutes.
C.
Laboratory Findings: Leukocytosis is usual but may be mild; a shift to the left is commonly seen. The erythrocyte sedimentation rate usually is elevated; anemia may be present. Pyuria and bacteriuria are found commonly but not routinely. Blood cultures may be positive. Unless bilateral renal disease is present, the serum creatinine and blood urea nitrogen values generally are normal.
Plain film (stoun in the left kidney)
D.
X-Ray Findings: A plain film of the abdomen typically shows evidence of a flank mass. Surrounding edema often results in obliteration of the renal and psoas shadows on the affected side. Scoliosis with the concavity to the affected side is common. The presence of a calcified body in this area suggests an abscess resulting from calculous pyonephrosis. Occasionally, a localized collection of gas caused by infection with gas-forming (coliform) organisms may be observed in the perirenal area.
Excretory urogram
Excretory urograms may show delayed visualization or nonfunction related to obstructive uropathy or parenchymal disease. Changes suggesting a spaceoccupying lesion (eg, carbuncle) may be noted; however, evidence of advanced hydronephrosis or calculous pyonephrosis is seen most commonly. Lack of mobility of the kidney with change in position of the patient or with respiration strongly suggests acute or chronic perinephritis. The entire kidney or only one pole may be displaced laterally by the abscess.
A barium enema may show displacement of the bowel anteriorly, laterally, or medially. Paralytic ileus may be observed on plain films of the abdomen or on upper gastrointestinal series. Chest films may demonstrate an elevated diaphragm on the ipsilateral side; fluoroscopy often shows fixation on respiration. Some free pleural fluid and platelike atelectasis may be observed.
When the findings of excretory urography are equivocal, the performance of retrograde urograms may be helpful.
Gallium-67 localizes in inflammatory tissue; hence, the diagnosis often may be confirmed by use of the scintillation camera.
Echograms, CT scans, and renal angiograms may assist in diagnosis, especially when combined with percutaneous needle aspiration.
Differential Diagnosis
Acute renal infections cause many of the symptoms that accompany perinephric abscess: fever, localized pain, and tenderness. In acute pyelonephritis, the urine uniformly shows evidence of infection; in perinephric abscess, the urine may or may not show evidence of infection. X-ray studies and scans, however, should facilitate differentiation of these 2 conditions.

Infected hydronephrosis may cause fever and localized pain and tenderness and may account for the presence of a flank mass. Again, x-ray studies and scans should make the differentiation.
Paranephric abscess is a collection of pus external to the perirenal fascia and often is secondary to inflammatory disease of the spine (eg, tuberculosis). Many of the signs of perinephric abscess may be seen on a plain x-ray film, but the finding of a lesion in bone in the low thoracic area should suggest the correct diagnosis.
Urograms are normal.
Complications
Unless the correct diagnosis is made promptly and effective therapy is initiated early, the mortality rate from generalized sepsis is quite high. Rarely, the perinephric abscess may point just above the iliac crest posterolaterally or extend downward into the iliac fossa and inguinal region. It is most unusual for the phlegmon to extend within the perirenal fascia across the midline to involve the opposite side of the body.
The abscess may produce considerable ureteral compression, giving rise to hydronephrosis. Even after drainage of the abscess, ureteral stenosis from periureteritis may evolve during the healing process. preventing perinephric abscess. Appropriate therapy of urinary tract infection and removal of calculi and other obstructive conditions are of highest priority.
Prevention
Early, effective treatment of urinary tract disease is the only means of
Generally, treatment is similar to treatment for renal abscesses, except that surgical drainage usually is required for perinephric abscesses but may not be required for intrarenal abscesses. Intensive antimicrobial therapy, based upon culture and sensitivity testing of the pathogen isolated from urine, blood, or pus obtained by needle aspiration of the lesion, is mandatory. Unless adequate percutaneous drainage can be established, surgical drainage usually is needed.
Because of underlying renal disease, nephrectomy may be required, either acutely or subsequent to initial control of the abscess. When nephrectomy is not required— indeed, even if the kidney itself is normal—excretory urography should be performed about 3 montns after therapy is completed to make certain that late complications (eg, ureteral stenosis) are not missed.
Prognosis
Perinephric abscess often is fatal when diagnosis and appropriate therapy are delayed. A high index of suspicion and improved methods of diagnosis and treatment should offer a better prognosis than the 44% mortality rate observed by
Thorley, Jones, and San-ford (1974).