<% 'if (Session("Type") <> 1 and Session("Type") <> 5 and Session("Type") <> 28) then Response.Redirect "../Msg.asp?Messaggio1=Restricted access area!!!&Messaggio2=Return to HomePage" 'if Session("UserCount") = "" then Response.Redirect "../Msg.asp?Messaggio1=Error while initialising the quiz!!!&Messaggio2=Return to HomePage" a_capo = chr(13) + chr(10) NumQuestions = 5 RightAnswer1 = "b" RightAnswer2 = "e" RightAnswer3 = "b" RightAnswer4 = "a" RightAnswer5 = "c" currentID = Request("currentID") if currentID = "" then currentID = 1 Answer1 = Request("Question1") if Request("Answer1") <> "" then Answer1 = Request("Answer1") Answer2 = Request("Question2") if Request("Answer2") <> "" then Answer2 = Request("Answer2") Answer3 = Request("Question3") if Request("Answer3") <> "" then Answer3 = Request("Answer3") Answer4 = Request("Question4") if Request("Answer4") <> "" then Answer4 = Request("Answer4") Answer5 = Request("Question5") if Request("Answer5") <> "" then Answer5 = Request("Answer5") if currentID = 11 or currentID = 22 or currentID = 33 or currentID = 44 then Label = "Continue" elseif currentID = 55 then Label = "Continue" else Label = "Evaluate" end if %> Cristiana Rollino - Case study




FLANK PAIN AND FEVER IN A MAN

rollino

by Cristiana Rollino
Department of Nephrology, S.G. Bosco Hospital. Turin. Italy Address correspondence to:

Dr. Cristiana Rollino
Nefrologia
Ospedale S.G. Bosco
P.za Donatore di Sangue 3
10154 Torino
Italy

Tel 390112402287
FAX 390112402458
cristiana.rollino@libero.it

 

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HISTORY
Besides hypertension, since May 2000, no relevant elements were recorded in the patient history (59 years old).
In October 2005 serum creatinine was 1.2 mg/dl, hematuria was found in the urinary sediment and PSA was slightly elevated (7.1 ng/ml).
In November 2005 the patient complained of a fever of up to 40°C with dysuria and left flank pain. He was given paracetamol and levofloxacin but, as the symptoms did not clear up, he presented to the Emergency Department.
Blood pressure was 130/80 mmHg, heart rate 60/min, Oxygen saturation 98%, body temperature 40°C; no other abnormal signs were evident at physical examination; Giordano’s sign was positive on the left.
Serum creatinine was 2.3 mg/dl, leukocytes 18700/mm3, hemoglobin 11.5 g/dl, platelets 135000/mm3, C-Reactive Protein 27 mg/dl, albuminemia 2.8 g/dl. 50 white blood cells/hmf and 50 red blood cells/hmf were found in the patient’s urine.
Blood cultures were negative, urine cultures showed E. coli 106 cfu/ml. Proteinuria was 0.4 g/die.
ECG: normal cardiac rhythm. Chest X-Ray was normal. Renal sonography showed a normal aspect of the renal parenchyma. The bladder had a normal echographic aspect. No pathological images were evident.

References:




  1. Sobel JD, Kaye D. Urinary Tract Infections. In: Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases - Fourth Edition, edited by Churchill Livingstone Inc., 1995: 662-690.
  2. Scholes D, Hooton TM, Roberts PL, Gupta K, Stapleton AE, Stamm WE. Risk factors associated with acute pyelonephritis in healthy women. Ann Intern Med 2005;142:20-27.
  3. Bass PF, Jarvis JA, Mitchell CK. Urinary tract infections. Prim Care 2003;30:41-61.
  4. Efstathiou SF, Pefanis AV, Tsioulos DI, Zacharos ID, Tsiakou AG, Mitromaras AG, Mastorantonakis SE, Kanavaki SN, Mountokalakis TD. Acute pyelonephritis in adults: prediction of mortality and failure of treatment. Arch Int Med 2003; 163:1206-1212.
  5. Korzets Z, Plotkin E, Bernheim J, Zissin R. The clinical spectrum of acute renal infarction. Isr Med Assoc J 2002;4:781-784.
  6. Kavashima A, Le Roy AJ. Radiologic evaluation of patients with renal infections.
  7. Roberts JA. Management of patients with infectious diseases in an emergency department observation unit. Emerg Med Clin North Am. 2001;19:187-207.
  8. Majd M, Nussbaum Blask AR, Markle BM, Shalaby-Rana E, Pohl HG, Park JS, Chandra R, Rais-Bahrami K, Pandya N, Patel KM, Rushton HG. Acute pyelonephritis: comparison of diagnosis with 99mTc-DMSA, SPECT, spiral CT, MR imaging, and power Doppler US in an experimental pig model. Radiology 2001;218:101-108.
  9. Kalyanakrishnan Ramakrishanan K, Schedi DC. Diagnosis and management of acute pyelonephritis in adults. Am Family Physician 2005;71:933.942.
  10. Warren JW, Abrutyn E, Hebel JR, Johnson JR, Schaeffer AJ, Stamm WE. Guidelines for Antimicrobial Treatment of Uncomplicated Acute Bacterial Cystitis and Acute Pyelonephritis in Women. Clin Infect Dis 1999;29:745-758.
  11. Bergeron MG. Treatment of pyelonephritis in adults. Med North Am 1995;79:619-649.
  12. Behr MA, Drummond R, Libman MD, Delaney JS, Dylewski JS. Fever duration in hospitalized acute pyelonephritis patients. Am J Med 1996;101:277-280.
  13. Lipsky BA. Prostatitis and urinary tract infection in men: what's new, what's true? Am J Med 1999;106:327-334.
  14. Raz R, Sakran W, Chazan B, Colodner R, Kunin C. Long-term follow-up of women hospitalized for acute pyelonephritis. Clin Infec Dis 2003;37:1014-1020.
  15. Jakobsson B, Berg U, Svensson L. Renal scarring after acute pyelonephritis. Arch Dis Child 1994;70:111-115.
  16. Rushton HG, Maid M, Jantausch B, Widermand BL, Belman AB. Pyelonephritis in male infants: how important is the foreskin?, J Urol 1992;147:1327-1332.
  17. Wallin L, Bajc M. Typical technetium dimercaptosuccinic acid distribution patterns in acute pyelonephritis. Acta Paediatr. 1993;82:1061-1065. Infect Dis Clin North Am. 2003;17:433-56.
  18. Fraser IR, Birch D, Fairley KF, John S, Lichtenstein M, Tress B, Kincaid-Smith PS. A prospective study of cortical scarring in acute febrile pyelonephritis in adults: clinical and bacteriological characteristics. Clin Nephrol 1995;43:159- 164.
  19. Cotton SA, Gbadegesin RA, Williams S, Brenchley PE, Webb NJ. Role of TGF-beta1 in renal parenchymal scarring following childhood urinary tract infection. Kidney Int 2002 ;61:61-67.
  20. Gbadegesin RA, Cotton SA, Watson CJ, Brenchley PE, Webb NJ. Association between ICAM-1 Gly-Arg polymorphism and renal parenchymal scarring following childhood urinary tract infection. Int J Immunogenet. 2006 ;33:49-53.
  21. Bates JM, Raffi HM, Prasadan L, Mascarenhas R, Laszik Z, Maeda N, Hultgre SJ, Kumar S. Tamm-Horsfall protein knockout mice are more prone to urinary tract infection: rapid communication. Kidney Int. 2004;65:791-797.
  22. Saemann MD, Weichart T, Horl WH, Zlbinger GJ. Tamm-Horsfall protein: a multilayered defence molecule against urinary tract infection. Eur J Clin Invest 2005 ;35 :227-235.
  23. Pohl HG, Rushton HG, Park JS, Chandra R, Majd M. Adjunctive oral corticosteroids reduce renal scarring: the piglet model of reflux and acute experimental pyelonephritis. J Urol 1999;162:815-820.
  24. Huang A, Palmer LS, Hom D, Andreson AE, Kushner L, Franco I. Ibuprofen combined with antibiotics suppresses renal scarring due to ascending pyelonephritis in rats. J Urol 1999;162:1396- 1398.
  25. Khalil A, Tullus K, Bakhiet M, Burman LG, Jaremko G, Brauner A. Angiotensin II type 1 receptor antagonist (losartan) down-regulates transforming growth factor-beta in experimental acute pyelonephritis. J Urol 2000;164:186-191.
  26. Wing DA. Pyelonephritis. Clin Obstet Gynecol 1998;41:515-526.
  27. Hill JB, Sheffield JS, McIntire DD, Wendel GD. Acute pyelonephritis in pregnancy. Obstet Gynecol 2005;105:18-23.
  28. Birchard KR, Brown MA, Hyslop WB, Firat Z, Semelka RC. MRI of acute abdominal and pelvic pain in pregnant patients. AJR Am J Roentgenol. 2005;184:452-458.
  29. Graham JM, Oshiro BT, Blanco JD, Magee P. Uterine contractions after antibiotic therapy for pyelonephritis in pregnancy. Am J Obstet Gynecol 1993;168:577-580.
  30. Geerlings SE, Meiland R, van Lith EC, Brouwer EC, Gaastra W, Hoepelman AI. Adherence of type 1-fimbriated Escherichia coli to uroepithelial cells: more in diabetic women than in control subjects. Diabetes Care. 2002;25:1405-1409.
  31. Ronald A, Ludwig E. Urinary tract infections in adults with diabetes.Int J Antimicrob Agents. 2001;17:287-292.
  32. Abdul-Halim H, Kehinde EO, Abdeen S, Lashin I, Al-Hunayan AA, Al-Awadi KA. Severe emphysematous pyelonephritis in diabetic patients: diagnosis and aspects of surgical management. Urol Int 2005;75:123-128.
  33. Giral M, Pascuariello G, Karam G, Hourmant M, Cantarovich D, Dantal J, Blancho G, Coupel S, Josien R, Daguin P, Mechineau S, Soulillou JP. Acute graft pyelonephritis and long-term kidney allograft outcome. Kidney Int. 2002;61:1880-1886.
  34. de Castro MC, Saldanha LB, Nahas W, David DS, Arap S, David-Neto E, Sabbaga E, Ianhez LE. Post-transplant neutrophilic interstitial nephritis-an important cause of graft dysfunction. Transpl Int.1998;11 Suppl 1:S144-6.
  35. Audard V, Amor M, Desvaux D, Pastural M, Baron C, Philippe R, Pardon A, Dahmane D, Lang P, Grimbert P. Acute graft pyelonephritis: a potential cause of acute rejection in renal transplant. Transplantation. 2005;80:1128-30.
  36. Shu T, Green JM, Orihuela E. Renal and perirenal abscesses in patients with otherwise anatomically normal urinary tracts. J Urol. 2004;172:148-150.
  37. Siegel JF, Smith A, Moldwin R. Minimally invasive treatment of renal abscess. J Urol 1996; 155:52-55.
<%if currentID = 11 then%> <%end if%>

Question 1) - Which was the most probable diagnosis?
(Only ONE answer is correct)

> a) Cystitis
> b) Acute pyelonephritis
> c) Prostatitis
> d) Renal infarction
> e) Pancreatitis
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The most probable localization of the infection in this case was the urinary tract, because of right flank pain, fever, leukocytosis, dysuria, negative chest X-Ray, absence of other pathologic physical sign. <% newID = 2 else newID = 11 %>



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Sobel (1) refers to acute pyelonephritis (APN) as a clinical syndrome characterized by flank pain and/or tenderness and fever, often associated with dysuria, urgency and frequency. However, as these symptoms can also occur in the absence of infection, for example, in renal infarction or in cases of renal stones, a more rigorous definition of APN would be the above syndrome accompanied by significant bacteriuria and an acute infection of the kidney. APN can present a wide range of clinical manifestations through to septic syndrome.



DIAGNOSIS
The classical clinical diagnosis of APN is based on: flank pain, fever and bacteriuria or pyuria (1). Pain is present in 86% of cases, fever in 77%, and both are present in 95% of cases (2).
Symptoms of cystitis may accompany 83% of cases: dysuria, urge incontinence and sovrapubic pain.
A third of elderly patients does not have fever: in 20% of cases symptoms are gastrointestinal or pulmonary (3).
According to the severity of the infection nausea, vomit and hypotension may be present as well as shock. Efstathiou (4) proposed a predictive score of mortality (Tab. 1).







If <=7: mortality: 2.5 % in men, 0-2.3% in women
If >=11: mortality 100% in men, 91% in women
Tab. 1. Predictive score for mortality in acute pyelonephritis (4)


Differential diagnosis must include renal infarction, which has similar characteristics including fever (5), inflammatory pelvic disease in women, intestinal perforation, Herpes zoster prodromes, cholecystitis, appendicitis and pneumonia in the low inferior lobe.

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Question 2) - Which examination should next be carried out  to confirm diagnosis?
(Only ONE answer is correct)

> a) CT without contrast medium
> b) CT with contrast medium
> c) Urography
> d) RMN
> e) b or d
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The diagnosis of APN is based on clinical and laboratory parameters. However, in recent years a role of CT for detecting APN lesions in the adult population has emerged (6,7).
Ultrasound is the first examination that should be performed in order to exclude hydronephrosis or renal calculi. The lesions that can be detected in APN are: ureteral wall thickening, dishomogeneous parenchymal areas (hyperechogenic), increase in kidney size or hypotonia of intrarenal  cavities.
However, echography is not sensitive in identifying intarenal infective areas. Besides scientific rigour, the need of a precise radiologic documentation comes from the fact that in the clinical practice urine cultures are not always positive because of previous antibiotic treatment or infections due to Ureaplasma urealyticum or Mycoplasma hominis that are not routinely searched for by laboratories and it is also necessary to exclude intrarenal abscesses.
This is also the opinion of Majd (8).CT has a high sensitivity for detecting areas of APN (8).

CT must be performed with injection of contrast medium. It may reveal areas of hypodensity characterised by a triangular shape that present their base on the renal cortex (Fig. 1, 2). These areas may be multiple and bilateral and are sometimes evident only in later  phases, several hours after constrast medium infusion. Attenuation of density depends on a focal reduction of blood perfusion due to parenchymal edema, intravascular granulocyte aggregation and abnormal renal tubular function with tubular obstruction by granulocytes and altered mechanisms of membrane transport of the contrast media.





Fig. 1. Multiple areas of left acute pyelonephritis.


Fig. 2. Multiple areas of bilateral acute pyelonephritis.

Nuclear Magnetic Resonance (NMR) has a similar sensitivity and specificity and is to be chosen in young women (8).

The patient was submitted to CT, which showed a regular right kidney and an area of hypodensity on the left kidney which is characteristic of inflammation. The prostate was increased in size and presented calcifications.

<%if currentID = 33 then%> <%end if%>

Question 3) - Which relationship do you think can exist between APN and the prostate?
(Only ONE answer is correct)

> a) Prostate hypertrophy leads to APN
> b) APN in men can be preceded by acute prostatitis
> c) Urinary tract infection are always located also in the prostate
> d) APN can be the first manifestation of a prostate cancer
> e) APN always develop after acute prostatitis
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Pyelonephritis is prevalently due to bacteria ascending from urethra and bladder. Infections by hematogenous spread are more frequent in immunodepressed patients and those with chronic diseases. Staphylococci and fungi may arrive from distant sites, skin or bones (9).
In men, prostatitis and protate hypertophy may predispose to bacteriuria (9).
Old and young age, urinary abnormalities or obstruction, diabetes, immunosuppression and pregnancy represent risk factors (Tab. 2).




Physical examination of our patient showed a congested fibroadenomatous prostate. Transrectal prostate sonography showed a prostate size of  42 x 39 x 23 mm. The structure of the gland was very dyshomogeneous with a great calcified area of 26 mm. The adenoma had a diameter of 22 mm. No abscesses or infiltrative areas were evident. The patient was given ciprofloxacin intravenously 800 mg/die for five days, followed by 1 g/day given orally with a subsequent normalization of the infectious parameters and of renal function.




EPIDEMIOLOGY

Women are affected by APN five times more than men, but have less mortality (7.3 vs 16.5 death/1000 cases) (9). Sexual activity plays an important role in favouring infections. Scholes (2) showed a correlation between APN and frequency of sexual intercourse (more than three times per week) and a change of partner over a period of twelve months. Moreover, spermicide use, previous urinary infections, familial urinary infections (particularly the mother), smoking and stress incontinence are significant risk factors for developing APN (2). In 80% of cases Escherichia coli is the etiologic agent. Efstathiou (4) showed that in urine cultures of APN patients Escherichia coli is present in 56.4% of cases, Enterococchi in 10.7%, Staphylococcus species in 8%, Proteus mirabilis in 6%, Enterob. species 5.3% and Pseudomonas aeruginosa 5.3 % (Fig. 3).





Fig. 3. Frequency of microorganisms isolated in urine cultures of APN pazients (4).

In elderly patients, Escherichia coli is less frequently responsible for urinary infections (60%) (9), since bladder catheters and frequent instrumentation select different microorganisms (9) and above all gram-negative bacteria such as Proteus, Pseudomonas, Klebsiella and Serratia.



TREATMENT OF ACUTE PYELONEPHRITIS
Guidelines on APN treatment were published in 1999 (10).
Less severe cases can be treated at home
with oral fluoroquinolone (ciprofloxacin 1-1.5 g/day, pefloxacin 800 mg/day, ofloxacin 600 mg/day), or, if the sensitivity of the bacteria is known, trimethoprim/sulfamethoxazole (TMP/SMX 320/1600 mg/day). A single parenteral dose (ceftriaxone 2 g, gentamicin 3-5 mg/Kg or a fluoroquinolone -es. ciprofloxacin 400 mg-) can be administered before oral therapy.
If the bacteria is gram-positive, amoxicillin or amoxicillin/clavulanic acid can be given. In more severe cases that require hospitalisation parenteral  fluoroquinolone or aminoglycoside associated or not with ampicillin, or with an extended spectrum cephalosporin associated or not with an aminoglycoside, should be given.
For  gram-positive cocci ampicillin/sulbactam (or amoxicillin/clavulanic acid) with or without aminoglycoside should be considered. 
When a clinical improvement is obtained, treatment can be continued orally (fluoroquinolone or trimethoprim/sulfamethoxazole (for gram-positive bacteria, amoxicillin or amoxicillin/clavulanic acid).
Treatment should last for at least 10 days. A treatment of 14-21 days is suggested for less severe cases.
A short length treatment (three days) determines a clinical relapse in 50% of patients (11).
Fever normally disappears within 72 hours from the beginning of treatment;  13% of patients still has fever at 72 hours, 26% at 48 hours (12). Hence treatment should not be modified before 72 hours (12).
The most common reasons of treatment failure are resistant microorganisms or renal calculi.
Men with no urinary obstruction or prostatitis have a good response to a 14-day treatment. Men with recurrent infections require a 6-week treatment. Men with acute prostatitis require a 4-week treatment with doxycycline, trimethoprim-sulfamethoxazole or fluoroquinolone. In cases of chronic prostatitis treatment should be continued for 12 weeks (13).

<%if currentID = 44 then%> <% newID = 5 else newID = 44 %> <%end if%>

Question 4) - Which is the most indicated treatment option in severe acute pyelonephritis?
(Only ONE answer is correct)

> a) Parenteral fluoroquinolone or aminoglycoside associated or not with ampicillin, or extend spectrum cephalosporine associated or not with aminoglycoside
> b) Aminoglycoside associated with vancomycin
> c) Imipenem
> d) Vancomycin associated with Trimethoprim/Sulfamethoxazole
> e) Amoxicillin/clavulanic acid associated with Trimethoprim/Sulfamethoxazole
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LONG-TERM EVOLUTION

The long-term evolution of APN is not yet known, even if the possibile development of cortical scars, hypertension and renal failure suggest the need for periodical controls in these patients (14).
In children, scars develop in 59% of cases at 2 months and 37 % at 2 years (15) (in a series of patients 25% of whom had vesicoureteral reflux), in 43% of cases after 4-40 months (16), in 52% after 5-8 months (17) and, in an adult population, in 77% of cases after 3-12 months (18).
It is possible that a genetic predisposition could favour scar formation. Several genetic factors have been advocated as possibly responsible for this evolution, such as
polymorphism of the interleukin-1 and 6 gene (19), the adhesion molecule gene (20), the TGFß gene (19) and uromodulin. The Tamm-Horsfall protein, besides its antimicrobic action (Tamm-Horsfall protein knock-out mice are prone to urinary infections -21-), is also believed to have strong immunoregulatory activity (22).
Experimental assays of prevention of scar formation have been attempted and good results have been obtained by administrating during the acute phase of disease corticosteroids in pigs (23), NSAD in rats (24) and losartan in mice (25). No studies of this kind exist in man.
Raz studied the long-term evolution of women with APN (14). Sixty-three women were submitted to renal scintigraphy with 99mTc-DMSA after 10-20 years from APN. In 46% of these patients, the Authors found cortical scars. Among the women who had cortical scars, 17.2% presented macroalbuminuria (>300 mg/day) and 13.7% had a glomerular filtration rate  <75 ml/min.

COMPLICATED PYELONEPHRITIS

The term “complicated pyelonephritis” refers to APN arising in a clinical context which makes them more dangerous (pregnancy, diabetes, old age and renal abnormalities), or to APN where a worsening of the clinical picture or greater extension of the infection is observed.


Pregnancy

APN in pregnancy may turn out to be very risky: urine cultures of pregnant patients should be regularly monitored.
It appears more frequently during the 2° trimester (26). It associates with nulliparity and young age (26).
It is most often due to Escherichia coli (70%) and gram-positive microorganisms, among which ß-hemolytic Streptococci (10%) (27).
NMR is safe and precise in differentiating APN from other pathologic conditions, such as ovarian and uterine torsion, appendicitis, abdominal abscesses and ovarian cysts (28).
Pregnant women with APN should be hospitalized.
The treatment of choice is amoxicillin or amoxicillin-clavulanic acid. Fluoroquinolones should not be used in pregnancy because of their theratogenicity (3).
Eighty-six percent of pregnant women with APN has uterine contractions in the first hour of antibiotic administration and 50% of them continues to have them up to 5 hours after (29).
Recurrencies occur in 25% of cases: monthly controls of urine cultures should be done (26).



Diabetes

Diabetic patients are predisposed to urinary infections because of mechanisms not yet perfectly known. Geerlings (30) reported an increased vaginal colonization by Escherichia coli in diabetic women. Colonization could be due to a greater adhesion of Escherichia coli to the uroepithelial cells by means of fimbriae or to cytokine excretion and an altered inflammatory response.
APN is 5-10 times more frequent in diabetic than in non-diabetic patients of both sexes (31).
Responsible microorganisms are Klebsiella, Enterobacter, Clostridium or Candida.
Treatment is the same as in non-diabetic subjects (31).
Diabetic patients are more prone to develop emphysematous APN, papillary necrosis and a metastatic localization of the infection (3).
Emphysematous APN is a severe infection of the renal parenchyma and of the surrounding tissues with gas formation (32). Organ function is often severely compromised. When possible nephrectomy is the most appropriate choice(32).


Renal transplantation

APN is frequent in patients with renal transplantation (13% of patients in the series of Giral -33-). Histologic studies have shown interstitial nephritis with polymorphonuclear infiltration in 5% of 220 patients and 63% with fever (34). Infection may be transferred by the donor or during surgery. Ascending bacteria is favoured by instrumental procedures, such as bladder catheterism, stent positioning, cystoscopy or by the preexistence of vesicoureteral reflux, new bladder and vesical neck pathology. Moreover, it is favoured by immunosuppression and infection by Cytomegalovirus, as documented by Giral in a series of 1387 patients (33), among whom Cytomegalovirus infection was the only risk factor for APN at a multivariate analysis.

A generally favourable outcome has been reported (33). However, early APN (in the first 3 months after renal transplantation) represents a negative factor, independently from rejection episodes. The Authors conclude that there is no true evidence to demonstrate that bacterial infections may trigger acute or chronic rejection, as previously hypothesized (35).




Abscesses


Fig. 4. Renal abscess at CT examination.

The evolution of APN into an abscess is possible (Fig. 4). There is little literature about this pathology.
Shu (36) studied the evolution of 26 patients with renal and perirenal abscesses. Eighteen were treated with percutaneous drainage; 66.7% had a positive culture of the collected fluid. No case needed nephrectomy or positioning of nephrostomy. Ten months later all patients but one had complete radiographic resolution.
It is believed that antibiotic treatment can solve about 100% of abscesses with a diameter that is <3 cm and 92% of those with a diameter between 3 and 5 cm (37). In this study abscesses greater than 5 cm required percutaneous drainage in 33% of cases and a surgical one in 37% of cases (37).
Perirenal abscesses may be due to intestinal gram-negative bacteria and sometimes to gram-positive cocci. In 25% of cases several species coexist and rarely fungi, especially Candida spp.  (37).

<%if currentID = 55 then%> <%end if%>

Question 5) - The diagnosis of a renal abscess can be done:
(Only ONE answer is correct)

> a) Clinically
> b) With laboratory data (leukocytes and CRP)
> c) With CT
> d) With renal scintigraphy
> e) With ultrasound examination
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