HistoryThis section has been translated automatically.
The chronic form of pyelonephritis was first described by Schlagenhaufer in 1916. In 1944, Osterlin referred to the chronic form of pyelonephritis as "xanthogranuloma" (Suman 2020). Erik Ask Upmark described a parenchymal malformation of the kidney for the first time in his 1929 paper "Juvenile malignant nephrosclerosis and its relation to the disturbance in renal development", which was later named after him as the so-called "Ask-Upmark kidney" (Westenfelder 1985).
DefinitionThis section has been translated automatically.
Pyelonephritis (PN) is a tubulointerstitial nephritis usually caused by a urinary tract infection (Herold 2020). However, PN can also occur without a clearly preceding cystitis (Kasper 2015).
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ClassificationThis section has been translated automatically.
PN can occur as:
1. acute pyelonephritis = APN (usually bacterial abscess).
This can affect only one or both kidneys (Herold 2020).
Acute PN is differentiated between the following types(Keller 2010):
- 1. a. Uncomplicated PN, these
- is acquired on an outpatient basis
- is accompanied by no vomiting
- there are no predisposing factors
- 1. b. Complicated PN
- there are signs of severe systemic inflammation such as nausea, vomiting, circulatory instability etc. (Wagenlehner 2017)
- Risk factors such as diabetes mellitus, gravidity, male gender, urinary bladder catheter, anatomical malformations (Manski 2019), weakening of the immune system (Michel 2016), etc. are present
- Complications are more frequent in the course (Suman 2020)
- 1. c. Emphysematous PN
This is a necrotizing inflammation caused by E. coli in > 70%. In this case, gas accumulation is found in the renal parenchyma, renal pelvic caliceal system and perinephric tissue (Kuhlmann 2015; (Suman 2020; Colgan 2011).
2. chronic pyelonephritis = CPN.
Chronic PN is not uniformly defined (Vahlensieck 2014). Predominantly, the following differentiations are found in the literature:
- 2. a. Chronic focal destructive pyelonephritis (CPN): This is understood to be a persistent or relapsing PN that is always associated with parenchymal damage (Keller 2010).
- 2. b. Xanthogranulomatous pyelonephritis (XPN): XPN occurs predominantly unilaterally. The course is always progressive and leads to granulomatous destruction of both the kidney and renal capsule and surrounding tissues (Kuhlmann 2015).
- 2. c. Ask- Upmark- kidney: Ask- Upmark- kidney is scarring parenchymal damage in childhood after acute pyelonephritishas taken place, resulting in chronic pyelonephritis (Manski 2019).
For more details, see "Chronic pyelonephritis."
Occurrence/EpidemiologyThis section has been translated automatically.
PN is generally more common in women than in men and occurs particularly frequently in pregnant women as acute PN (Michel 2016).
Acute PN: It is one of the common diseases and causes about 250,000 physician visits and about 200,000 hospitalizations per year in the US. Females between the ages of 15 - 29 are most commonly affected, followed by infants and the elderly.
APN also occurs in men, but only very rarely. In these cases, functional or anatomical anomalies are usually present (Kasper 2015 / Colgan 2011),
Studies have demonstrated a familial predisposition to APN. In women with frequent urinary tract infections / pyelonephritis, vaginal and periurethral mucosal cells bind three times more uropathological bacteria than in unaffected women (Kasper 2015).
In patients with acute cystitis, acute pyelonephritis develops in <5% due to ascension of the pathogens (Manski 2019 / Schmelz 2014).
In pregnant women, on the other hand, APN by ascension occurs much more frequently, up to 23 %.
According to Manski (2019), the course may be complicated in the presence of concomitant:
- Anemia (23 %)
- renal dysfunction (7 %)
- respiratory insufficiency (7 %).
PN, in turn, in pregnant women can lead to:
- reduced birth weight
- increased neonatal mortality
- emphysematous PN:
Emphysematous PN occurs very rarely. It preferentially affects older women with diabetes mellitus (Suman 2020).
XPN: XPN is a rare disease with an incidence of 1.4 / 100,000 (Manski 2019). It predominantly affects women in middle age (Kuhlmann 2015).
EtiopathogenesisThis section has been translated automatically.
Acute PN primarily results from ascending infections of a urinary tract infection (Manski 2019).
The germs are primarily E. coli (70%-95%) followed by Staphylococcus saprophyticus with about 5% and only rarely occur Proteus, Klebsiellen, Enterobacteriaceae and Mycoplasma hominis (Keller 2010). Gram-positive germs are predominantly the result of haematogenous spread, as are fungi, tubercle bacilli, viruses and parasites, which are, however, extremely rarely the cause of PN (Michel 2016).
Another role is played by congenital or acquired vesicoureteral reflux (VUR) in the upper urinary tract. This causes a pendulum urine, from which recurrent pyelonephritides up to terminal renal failure can develop (Manski 2019 / Kuhlmann 2015).
For more details see "Acute pyelonephritis".
However, pyelonephritis can also develop without a clearly preceding cystitis (Kasper 2015).
Chronic PN can be triggered by:
- recurrent episodes of acute PN
- congenital or acquired vesicoureteral reflux
- a neurogenic urinary bladder disorder (Manski 2019)
- analgesic nephropathy
- sickle cell disease (Kasper 2015).
In chronic PN, both urine and renal tissue are bacteriologically negative in a proportion of patients. Immunological and toxic effects of killed parts of the pathogens are thought to maintain the inflammation (Keller 2010).
For more details, see "Chronic pyelonephritis".
In XPN, a complete obstruction in the ureter or a partial obstruction in the area of the renal calices due to e.g. a nephrolithiasis or - far less frequently - due to a (renal) tumor play a role etiologically . An atypical virulence of the pathogens and / or an altered immunological defense system are probably also important (Kuhlmann 2015).
Another cause may be bacterial infections, which are most commonly germs such as E. coli, Proteus mirabilis, Klebsiellen and Staphylokokken (Manski 2019).
Risk factors for XPN include (Suman 2020):
- Diabetes mellitus
- arterial hypertension
- Z. n. kidney transplantation
- Brachydactyly syndrome
PathophysiologyThis section has been translated automatically.
Acute PN: In acute PN, inflammation causes edematous swelling of the kidney(s). Subcapsularly there are pinhead-sized, raised abscesses with hemorrhagic margins, which sometimes confluent. Pus-filled tubules extend as yellow roads from the cortex to the papillae. The mucosa in the renal pelvis covered with exudate shows thickening. Scarring healing is likely, especially in children (Manski 2019).
Emphysematous PN: In emphysematous PN, there is intraparenchymal gas formation in the kidney (Colgan 2011). For more details, see "Acute pyelonephritis".
Chronic PN: In this case, the kidney is reduced in size by bumpy retractions, and the renal pelvis and caliceal system are usually scarred. In bilateral involvement with marked scarring, CPN can lead to chronic renal failure. (Manski 2019).
XPN (Xanthogranulomatous pyelonephritis): In XPN, the renal pelvis is filled with pus (called pyonephrosis). In addition to tissue necrosis, there are also inflammatory yellow-orange foci with small abscesses. The inflammatory process is initially segmentally limited and may later spread diffusely to the entire kidney and the adjacent retroperitoneum or adjacent structures. During this process, the renal parenchyma is gradually replaced by granulomatous tissue (Manski 2019).
For more information, see "Chronic pyelonephritis".
Clinical featuresThis section has been translated automatically.
AcutePN: Acute PN typically shows a sudden onset (Kasper 2015). A triad of:
- Fever (This shows a typical sawtooth pattern. The fever can be mild to very high, with or without chills Kasper 2015).
- palpitating renal pelvis (so-called flank pain) (Herold 2020).
However, these characteristic symptoms may be absent in immunosuppressed patients or hyposensitive patients (e.g., spinal cord injured, diabetic) (Michel 2016).
According to Manski (2019), however, atypical symptoms also occur - especially in children and the elderly - such as:
- abdominal pain
- severe feeling of sickness
ChronicPN: With the exception of acute episodes, chronic PN is asymptomatic. Only in the further course do secondary symptoms develop due to, for example, arterial hypertension, anemia and uremia (Manski 2019).
XPN: In XPN, in addition to the above triad, there is often weight loss, a general feeling of illness and a palpable tumour in the area of one flank (Manski 2019).
DiagnosticsThis section has been translated automatically.
Anamnestic questions should be asked in particular:
- previous urinary tract infections
- existing pregnancy
- analgesic abuse
- Risks for a complicated course are e.g.:
- diabetes mellitus
- urinary bladder catheter
- Anatomical malformations (Manski 2019)
- weakening of the immune system (Michel 2016)
Physical examination: Typical for acute PN is a palpitating renal bed. In men, a rectal examination should also be performed to exclude concomitant prostatitis in cases of palpitations (Michel 2016).
ImagingThis section has been translated automatically.
Acute PN: Sonography is important to exclude urinary outflow obstruction. The kidneys may appear enlarged, the parenchyma is usually widened and appears less echoic. The wall thickness of the renal pelvis is increased with a cut-off value of 2.0 mm (Michel 2016). If an echo-poor mass is detectable in the area of the kidneys, it is most likely a renal abscess. In this case, a CT should always be performed (Manski 2019).
For more details, see "Acute pyelonephritis".
Chronic PN: The kidneys appear small overall, with focally thin, echogenic cortex (Manski 2019).
XPN: In this case, a kidney can be visualized enlarged and shows an echogenic spatial structure indistinguishable from a ( renal) tumor. Sometimes a nephrolithiasis may be present (Manski 2019). CT is recommended for further clarification (Kuhlmann 2015).
i. v. pyelogram
Acute PN: If sonographically there is a suspicion of urinary outflow obstruction or nephrolithiasis, an i.v. pyelogram could be performed for further diagnosis. Nowadays, however, further diagnosis is usually made by CT (Manski 2019).
For more details see "Acute pyelonephritis".
Chronic PN: In chronic PN, calyx deformities are often seen. These can show different degrees of severity. Plump calyces are found whose necks approach each other. Often there is already a loss of parenchyma (Keller 2010). Especially at the renal poles, the cortex appears thin and the kidneys are small overall (Manski 2019)
XPN: In this case, nephrolithiasis is found in 40 % - 70 %.
Contrast of the affected side is absent in 30 % - 80 % of patients. The renal shadow appears predominantly enlarged (Manski 2019).
Acute PN: In acute PN, CT is indicated if.
- there has been no resolution of fever after 72 h
- in the case of sonographic suspicion of
- an abscess
- an emphysematous PN
- obstruction (Manski 2019)
For more details see " Acute pyelonephritis".
Chronic PN: In this case, changes are found in the CT such as:
- Plumping of the renal calices
- Deformations of the renal calices
- Narrowing of the parenchyma (Herold 2020)
XPN: CT is the method of choice for XPN. Here, a mass with inhomogeneous contrast medium accumulation is seen. Sometimes the presence of renal cell carcinoma cannot be excluded.
Lithiasis is detected much more frequently. Renal function itself is decreased (Manski 2019).
Magnetic resonance imaging
MRI is advantageous over CT in the question of extrarenal spread of PN and evaluation of changes in the renal pelvic caliceal system. It can also be used as an alternative to CT, especially in cases of pre-existing renal insufficiency (Manski 2019).
For more details, see "Chronic pyelonephritis".
Micturition Cystourethrogram (MCU).
An MCU is used to rule out or confirm the following.
- vesicoureteral reflux
- Neurogenic urinary bladder disorder (Manski 2019).
Renal scintigraphy (also known as isotope nephrogram = ING).
This examination method can be used to obtain a side-separated function of the renal tissue.
Chronic PN: ING is the most sensitive method to detect scarring parenchymal destruction (Manski 2019).
LaboratoryThis section has been translated automatically.
In acute PN, the following changes are usually found:
- elevated BSG
- CRP elevated (Manski 2019)
Procalcitonin increased (Michel 2016)
It should also be examined in severe courses for signs of renal failure such as:
- Cystatin C to determine GFR (Manski 2019).
- Electrolytes such as:
- Blood gas analysis (Michel 2016)
In very severe cases and especially if sepsis is suspected, signs of consumption coagulopathy should be monitored (elevation of ESR, anemia, decrease in platelets, Quick, fibrinogen and coagulation factors [Factor V, VIII, XI]).
Sepsis is suspected with:
- Increase in INR (International Normalized Ratio)
- decrease of the Quick value
- Increase in C-reactive protein or (faster responding) procalcitonin
- decrease in platelets
- Leukocytosis (Michel 2016)
Blood cultures should be taken immediately in severe cases and/or if sepsis is suspected (Herold 2020). In acute PN, these are positive in 10 % - 20 % (Keller 2010), whereas in XPN they are sterile in up to 25 % of cases (Kuhlmann 2015).
If PN caused by mycoses is suspected, fungal cultures should be prepared from:
- possible intraoperative interventions (Schmelz 2006).
In chronic PN, in addition to the above-mentioned changes, there is:
- anaemia (increased in XPN 57 % - 63 % [Sumann 2020])
- reduced renal clearance
- Liver enzymes increased (in 25 % - 50 % in XPN) (Schmelz 2006)
Leukocyturia is always indicative of pyelonephritis (Herold 2020)
- acute PN:
- Pyuria (if this is absent, there is doubt about the diagnosis of PN).
- bacteriuria (in 80 % - 90 % > 10 5 CFU / ml [colony forming units])
- micro- macro haematuria
- Leukocyte cylinder
- mild proteinuria (Keller 2010 / Manski 2019)
For more details see "Acute pyelonephritis
- Cylindruria (Keller 2010)
- typical foam or xanthoma cells (see "Histology") (Manski 2019).
For more details see "Chronic pyelonephritis".
Urine culture is often positive in XPN but is not diagnostic (Manski 2019).
HistologyThis section has been translated automatically.
Acute PN: In the acute form, wedge-shaped abscess streets with striate accumulations of granulocytes are found in the renal parenchyma between the papilla and the cortex (Herold 2020).
Chronic PN: In chronic focal destructive pyelonephritis, wedge-shaped scarring is found leading to retraction of the renal surface. In addition, there are often deformities of the renal calices and possibly necrosis of the papillae (Herold 2020).
XPN: In XPN, in addition to lymphocytes, plasma cells, and neutrophils, the inflamed tissue also contains the typical large macrophages filled with foamy, lipid-containing cytoplasm, also called foam or xanthoma cells. (Manski 2019).
Differential diagnosisThis section has been translated automatically.
- Kidney tumor
- Renal infarction
- Papillary necrosis (Michel 2016)
- basal pneumonia
- acute appendicitis
- acute cholecystitis
- lumbago / lumbar spine syndrome
- (Sigma-) diverticulitis
- renal or perirenal abscess (Herold 2020 / Manski 2019)
- uro- tuberculosis (Kuhlmann 2015)
- chronic recurrent cystitis (Hofstetter 2013)
- Clear cell renal cell carcinoma
- Papillary renal cell carcinoma
- Sarcoid renal cell carcinoma
- Renal tuberculosis
- Angiomyolipoma of the kidney
- Megalocytic interstitial nephritis
- Renal abscesses (Suman 2020)
Complication(s)This section has been translated automatically.
Urosepsis (life-threatening complication; occurs after instrumental procedures in up to 65%).
- Early symptoms of urosepsis are:
- Tachypnea (> 20 breaths/min)
- Tachycardia (> 90 beats / min)
- Hyperthermia (> 38 ° C)
- Hypothermia (< 36 ° C, alternating with febrile episodes) (Schmelz 2006)
- hydronephrosis or pyonephrosis (in case of obstruction)
- paranephritic or intraparenchymal abscess
- pyelonephritic shrinkage (n)
- purulent nephritis
- chronic renal insufficiency
- renal carbuncle
- renal parenchymal damage
- tubular partial dysfunction such as:
Chronic PN may also present with:
- arterial hypertension - found in 30% - 50% of patients (Herold 2020 / Manski 2019)
- chronic renal insufficiency
For more details see "Chronic PN".
In XPN, the following may also occur:
For more details see "Chronic PN".
General therapyThis section has been translated automatically.
Mild to moderate acute PN can usually be treated as an outpatient. The patient should remain on bed rest. In the case of systemic concomitant diseases such as vomiting, circulatory instability, etc. (Wagenlehner 2017), however, inpatient treatment for parenteral antibiotics is recommended. (Wagenlehner 2017), however, inpatient treatment with parenteral antibiotics is recommended (Kuhlmann 2015).
Internal therapyThis section has been translated automatically.
Analgesia: Metamizole, for example, is suitable as an analgesic (with simultaneous antipyretic effect).
Dosage recommendation: Metamizol 1 g - max. 4 g / d (Frölich 2003; Kuhlmann 2015).
Antibiosis: A urine culture should be obtained before starting antibiosis and antibiosis should be adjusted if necessary after receipt (Manski 2019).
1. a. Uncomplicated acute PN in pre-menopausal women: In this case, antibiotic treatment can usually be given orally. The pathogen spectrum corresponds approximately to that of uncomplicated cystitis.
- Medications of first choice for uncomplicated acute cystitis are e.g.: Ciprofloxacin: Dosage recommendation: 500 mg 2 x / d for 7 - 10 days. Dose adjustment required from a GFR of < 60 ml / min / 1.73 m² KOF.
- Fluoroquinolones such as levofloxacin: dosage recommendation: 500 mg 1 x / d for 7 - 10 days. Dose adjustment required from a GFR of < 50 ml / min / 1.73 m² KOF (Manski 2019 / Herold 2020).
- Cefpodoxin- Proxetil: dosage recommendation: 200 mg 2 x / d over 10 days (Wagenlehner 2017). Dose adjustment is required from a creatinine- clearance < 50 ml (Frölich 2003).
1. b. Severe course of acute PN: In a severe course with accompanying systemic symptoms, inpatient treatment is required, as antibiotics should initially be administered parenterally (Wagenlehner 2017). The 1st choice agents recommended are:
- Ceftriaxone (3rd generation): Dosage recommendation: 50 mg / kg bw / d as a single dose i. v. (Manski 2019). Dose adjustment in renal insufficiency is NOT required (Frölich 2003).
- Cefepime (4th generation): dosage recommendation: 50 mg / kg bw / d every 8 - 12 hours i. v. . Dose adjustment is required from a creatinine clearance < 50 ml (Frölich 2003) (Manski 2019).
- Ceftazidime (3rd generation): dosage recommendation: 50 mg / kg bw / d every 8 hours i. v. Dose adjustment is required from a creatinine- clearance < 50 ml (Frölich 2003) (Manski 2019).
As soon as fever is removed, it can be switched to oral medication, e.g.:
The duration of therapy should be 14 days in total, up to 21 days in severe courses (Michel 2016).
Pregnant patients see "Acute pyelonephritis".
Mycotic pyelonephritis: In PN caused by mycosis, systemic antifungals should be used for treatment such as:
- Amphotericin B: After a test dose of 1 mg / 100 ml over a period of 30 min, the initial dose of 0.1 mg / kg bw / d can be increased daily up to 1 mg - 5 mg / kg bw / d. The single doses should be applied every 4 h. The maximum dose is 4 g. This should not be exceeded in at least 6 weeks (Schmelz 2006).
- 5- Flucytosine: Dosage recommendation: Single doses of 100 mg - 150 mg / kg bw / d should be administered every 4 - 6 h (Schmelz 2006).
- Fluconazole: After i.v. administration of the antimycotics, treatment with fluconazole (e.g. triazole) should follow for 10 - 30 days. Recommended dosage: 50 mg - 400 mg / d orally. This can sanitize 94 % - 95 % of urogenital mycoses or candiduria (Schmelz 2006).
- Transplant kidney: Pyelonephritis of a transplant kidney can lead to a significant deterioration of graft function, which only partially regresses even after successful treatment (Kuhlmann 2015).
- Follow-up: On the 4th day of therapy and about 7 days after the end of antibiotic treatment, urine cultures should be checked for progression (Hegele 2015) .
- 2. a. Chronic focal destructive pyelonephritis: In chronic PN, risk factors (vesicoureteral reflux, analgesic nephropathy, neurogenic bladder dysfunction, etc.) should be eliminated or treated as much as possible (Michel 2016).
Any new-onset urinary tract infection should be promptly treated with targeted antibiotics. In the case of constant recurrences, a low-dose long-term antibiotic treatment may be necessary with e.g.
The duration of treatment should be 3 - 6 months (Manski 2019).
2. b. XPN: Patients with segmental or focal involvement of the kidney may be treated initially with antibiotic treatment plus percutaneous drainage. If this does not lead to healing, a (partial) nephrectomy is required (see "Surgical therapy") (Suman 2020).
Operative therapieThis section has been translated automatically.
1. c. Emphysematous PN: Emphysematous PN can initially be treated with percutaneous drainage. This should be followed by nephrectomy (Kasper 2015).
For more details see "Acute pyelonephritis".
2. a. Chronic focal destructive pyelonephritis: If the PN is unilateral involvement and renal function is absent, nephrectomy may be appropriate if hypertension is uncontrollable or to prevent further urinary tract infections (Manski 2019)
2. b. XPN: Patients with segmental or focal involvement of the kidney may be treated initially with antibiotic treatment plus percutaneous drainage. If this does not result in healing, (partial) nephrectomy is required. (Suman 2020)
In cases of diffuse or advanced XPN, partial or complete nephrectomy is initially indicated. To avoid sepsis, these patients should receive antibiotics preoperatively and postoperatively (Suman 2020). For this purpose, swabs should be taken intraoperatively and the antibiosis adjusted if necessary after obtaining the antibiogram (Manski 2019).
The surgical procedure itself can be difficult with regard to existing adhesions. Laparoscopic surgery is therefore not recommended (Kuhlmann 2015), especially as it has been shown that the conversion rate from laparoscopic to open surgery is approximately 50% ((Suman 2020).
Cases of bilateral XPN also require nephrectomy followed by dialysis (Suman 2020).
Progression/forecastThis section has been translated automatically.
The mortality of pyelonephritis is 0.4 / 100,000, which corresponds to about 320 cases per year in Germany (Michel 2016).
The emphysematous PN shows a significantly higher mortality of 43 % (Manski 2019).
In XPN, unilateral cases have a good prognosis, whereas bilateral cases are often lethal (Suman 2020).
Patients on a waiting list for kidney transplantation show infectious diseases as (co-)cause of ESRD in up to 15%-25%.
LiteratureThis section has been translated automatically.
- Colgan R et al (2011) Diagnosis and Treatment of Acute Pyelonephritis in Women. Am Fam Physician 1; 85 (5) 519 - 526
- Frölich J C et al (2003) Practical medicinal therapy. Springer Verlag 961, 965, 969
- Hegele A et al (2015) Urology: intensive course for continuing education. Thieme Verlag 161 - 162
- Herold G et al (2020) Internal medicine. Herold Publishers 617 - 622
- Hofstetter A G et al (2013) Urology for the practice. Springer Publishers 110 - 111
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 861 - 868
- Kasper D L et al (2015) Harrison's internal medicine. Georg Thieme Publishers 1051 - 1057
- Keil J (2008) Exam preparation urology. Thieme Verlag 5. 1. 5.
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- Kuhlmann U et al. (2015) Nephrology: pathophysiology - clinic - renal replacement procedures. Thieme Verlag 544 - 545, 560 - 561
- Manski D (2019) The urology textbook. Dirk Manski Publishers 243 - 250
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- Pallwein- Prettner L et al (2011) Xanthogranulomatous pyelonephritis: diagnostic value of MRI. Rofo 2011; 183 - FO_PO39 DOI: 10.1055/s-0031-1279658
- Schmelz H U et al (2006) Facharztwissen Urologie: differentiated diagnosis and therapy. Springer Verlag 122 - 143
- Suman K J et al (2020) Pyelonephritis Xanthogranulomatous. [Updated 2020 Dec 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557399/
- Vahlensieck W (2014) Pyelonephritis and renal abscess. In: Schmelz HU., Sparwasser C., Weidner W. (eds) Facharztwissen Urologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-44942-0_2
- Wagenlehner F et al. (2017) Interdisciplinary S3 guideline epidemiology, diagnosis, therapy, prevention and management of uncomplicated, bacterial, community-acquired urinary tract infections in adult patients update 2017. AWMF register no. 043/044.
- Westenfelder M. (1985) The Ask Upmark kidney, misinterpreted end-stage pyelonephritis (two fully documented cases). In: Kaufmann J. (eds) Proceedings of the German Society of Urology. Negotiation report of the German Society of Urology, vol 36. Springer, Berlin, Heidelberg 454 - 458. https://doi.org/10.1007/978-3-642-82538-5_114
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