Kidney and Ureter Inflammation

Kidney and Ureter Inflammation

Ameet Gupta1 and Krishna Narahari2

1 Urology Department, New Cross Hospital, Wolverhampton, UK

2 Urology Department, University Hospital of Wales, Cardiff, UK


Inflammatory condition of the kidneys and ureter are common place in modern practice. These conditions can present the urologists with patients who are extremely unwell and suffering with life‐threatening sepsis. Prompt assessment of such patient is vital, and basic resuscitation skills need to be coupled with an extensive knowledge of the possible underlying pathologies along with their medical and surgical management options. Although rare in Western countries, chronic infections such as tuberculosis (TB) and parasitic infections should always be part of a differential diagnosis. For trainees in urology, it is important to have a board range of differential diagnoses at your disposal and knowledge of how to investigate these effectively – both on the wards and in an examination setting.

Keywords: pyelonephritis; emphysematous pyelonephritis (EPN); xanthogranulomatous pyelonephritis (XPN); renal abscess; renal tuberculosis; schistosomiasis; glomerulonephritis

12.1 Medical Inflammatory Conditions of the Kidney

There are a number of medical inflammatory conditions of the kidney that the urologist should have a familiarity with because they may present to the acute urology on‐call situation.

The classification of these conditions is dependent upon the site and is broadly divided into glomerulonephritides (inflammation of the glomeruli) and tubulointerstitial [1].

12.1.1 Glomerulonephritides (Table 12.1)

Table 12.1 Summary of glomerulonephritides.

Source: Adapted form [1].

Type Histology Causes Presentation Treatment
Minimal Change Unknown pathogenesis

Nonspecific finding of podocyte foot processes. Otherwise normal
Atopy, HLA‐DR7, Drugs Commonly idiopathic, presents with sever nephrotic syndrome Good response to corticosteroid
Focal segmental glomerulosclerosis (FSGS) Unknown pathogenesis

Nonspecific immune deposits; segmental scars in glomeruli
HIV infection, obesity, heroin use, previous local glomerular injury Primary disease: Idiopathic nephrotic syndrome

Secondary disease: proteinuria
Less responsive to treatment
Focal segmental glomerulonephritis Small‐vessel vasculitis segmental inflammation and necrosis

Variable immune deposits
Primary or secondary small vessel vasculitis; Occurs in systemic disease
Good response to corticosteroid
Membranous glomerulonephritis Podocyte injury due to surface antigen antibodies Glomerulosclerosis secondary to thickening of basement membrane Granular subepithelial IgG immune deposits noted HLA‐DR3, drugs, hepatitis B, heavy metals, malignancy Idiopathic
Common cause in adults
Immunosuppressants and corticosteroids
IgA nephropathy Unknown pathogenesis

Segmental nephritis and increased mesangial matrix and cells

IgA immune complexes seen
Commonly idiopathic, liver disease Wide spectrum of presentation, haematuria (early sign), hypertension Supportive

Poor response to immunosuppressive therapy
Poor evidence for steroid use
After infection Infiltration by neutrophils and macrophages combined with diffuse

Subendothelial immune deposits
Any infection (commonly streptococcal) Haematuria, hypertension, sodium with fluid retention and oliguria Spontaneous resolution
Mesangiocapillary glomerulonephritis Immunoglobulin type:
Circulating immune complexes deposition

Complement type:
Caused by complement abnormalities
Infections, autoimmunity, complement gene mutation Haematuria, proteinuria Treat underlying disease, immunosuppressive therapy
Goodpasture syndrome Autoantibodies to α3 chain of type IV collagen in basement membrane. Linear IgG immune deposits Crescentic nephritis HLA‐DR15 Rapid loss of renal function over days and weeks. Lung haemorrhage Cyclophosphamide, corticosteroids, and plasma exchange therapy
Lupus nephritis Anti‐DNA antibodies. Immune deposits always seen depending on type.
Complement consumption, complement deficiencies Can present with alone with no extrarenal manifestations Prednisolone and cytotoxic therapy

HIV, human immunodeficiency virus; HLA, human leucocyte antigen; IgA, immunoglobulin A; IgG, immunoglobulin G.

Commonly this group of disorders are immunologically mediated and respond to immunosuppressive therapy. Histopathology, via renal biopsy, is required to make the diagnosis [1].

12.1.2 Tubulointerstitial (Table 12.2)

Table 12.2 Causes of acute and chronic tubulointerstitial renal disease [1].

Acute Chronic
Drugs: Penicillin, NSAIDs, Mesalazine, PPI Drugs: Tenofovir, analgesia, lithium, cyclosporine, tacrolimus, drugs causing AIN
Infection: Pyelonephritis, TB, Leptospirosis, Hantavirus Infection: Pyelonephritis
Immune: Autoimmune nephritis, transplant rejection Immune: Sarcoidosis, Sjögren syndrome, SLE, chronic transplant rejection
Toxic: Myeloma light chains, mushrooms (Cortinarius) Toxic: Lead, mushrooms (Cortinarius), Herbal medicines

Metabolic: Excessive phosphate administration, hypokalaemia, hyperoxaluria
Congenital: VUR, inherited, Wilson disease, MSK, sickle‐cell disease, renal dysplasia

AIN, acute interstitial nephritis; MSK, medullary sponge kidney; NSAIDs, nonsteroidal anti‐inflammatory drugs; PPI, proton‐pump inhibitor; SLE, systemic lupus erythematosus; TB, tuberculosis; VUR, vesicoureteral reflux.

This is a disease of the renal tubules. It presents with proteinuria, electrolyte disturbance, and varying degrees of renal failure. Tubulointerstitial disease is further split into acute and chronic [1].

12.2 Acute Surgical Inflammatory Conditions of the Kidney

12.2.1 Pyelonephritis

Pyelonephritis is inflammation of the kidney and renal pelvis. In the presence of no complicating factors (e.g. congenital malformations, instrumentation of the urinary tract, or states of reduced immunity such as diabetes) this condition can be termed uncomplicated pyelonephritis. Aetiology and Risk Factors

Gram‐negative bacteria are common causative organisms of upper urinary tract infections because they are in lower urinary tract infections. Escherichia coli (E. coli) is responsible for the majority of pyelonephritis cases (80%), but other organisms such as Klebsiella pneumoniae, Proteus mirabilis, Streptococcus faecalis, and Pseudomonas should be considered when choosing antibiotic therapy. Factors affecting bacterial virulence are key to infections. See Chapter 20 for more details. Although pyelonephritis can affect any population or age group, there are certain groups of patients at higher risk (Table 12.3).

Table 12.3 Risk factors for pyelonephritis in adults.

  • Female
  • Vesicoureteric reflux (VUR)
  • Urinary tract obstruction
  • Urinary tract calculi
  • Neuropathic bladder
  • Diabetes mellitus
  • Congenital malformations
  • Pregnancy
  • Indwelling catheters
  • Instrumentation of the urinary tract Clinical Presentation

Acute pyelonephritis is a clinical diagnosis. Classically, it presents with symptoms of systemic upset (i.e. pyrexia, nausea, vomiting, anorexia, and lethargy) and more specifically with unilateral loin pain, worse over the renal or costovertebral angle.

Patients might complain of lower urinary tract infection symptoms (L‐UTI): frequency, urgency, dysuria, and offensive smelling urine.

Care must be taken in the initial assessment of patients with sepsis (Table 12.4). Severe sepsis has a reported mortality of 20–42% [4].

Table 12.4 Definitions of used terms for infection [2, 3].

Term Definition
Infection Microbial phenomenon characterised by an inflammatory response to the presence of micro‐organisms or the invasion of normally sterile host tissue by those organisms.
Bacteraemia Presence of viable bacteria in the bloodstream
Septicaemia Presence of infective agents or their toxins in the bloodstream
Systemic inflammatory response syndrome (SIRS) It is the response of the body to a variety of insults or stimuli, which causes widespread inflammation (e.g. infection, burns, trauma, surgery, or pancreatitis)
Two or more of the following are required for SIRS:
Pyrexia (>38.0) or hypothermia (<36.0)
Tachycardia (>90 bpm)
White cell count (>12 000 cells/mm3 or < 4000 cells/mm3, or > 10% immature [band] forms)
Tachypnoea (>20 breaths min−1 or PaCO2 < 4.3 kPa or requirement of mechanical ventilation)
Sepsis Presence of SIRS and a documented source of infection (proven source)
Severe sepsis Sepsis with at least one organ dysfunction, hypoperfusion, or hypotension.
Altered organ perfusion with dysfunction Altered mental state, oliguria, hypoxaemia, or lactic acidosis
Septic shock Severe sepsis with hypotension despite fluid resuscitation (sustained systolic blood pressure <90 mm Hg or > 40 mm Hg drop in one hour from baseline).
Refractory septic shock Septic shock lasting more than one hour despite fluid resuscitation or pharmacological interventions (ionotropic or vasopressor support). Pathophysiology of Sepsis

Inflammation caused by chemical, mechanical, or infective stimuli occurs and precedes healing. This is usually localised to the area of the stimuli; however, activation of inflammatory cascades on a systematic level can give rise to systemic inflammatory response syndrome (SIRS). For example, this can be initiated by the out membrane of gram‐negative organisms, the lipopolysaccharide layer or their endotoxins, or in gram‐positive organisms, the lipoteichoic acid, or peptidoglycan.

These triggers activate receptors on immune cells (neutrophils, macrophages, lymphocytes, and plasma cells) leading to production of pro‐inflammatory cytokines, tumour necrosis factor α (TNF α), interleukins (IL‐2, ‐6, and ‐8) and activation of the kinin, complement, and fibrinolytic system cascades. The cytokines, TNF‐α, and IL lead to the production of prostaglandins, leukotrienes, platelet‐activating factor, and phospholipase A2; these cause endothelial damage, which in turn causes capillary leakage. In addition, the activated neutrophils release nitric oxide, which leads to vasodilation (Figure 12.1). The activation of the coagulation systems leads to microthrombi formation leading to dysfunctional tissue perfusion.

Image described by caption and surrounding text.

Figure 12.1 Effects of tissue damage.

These effects result in widespread microvascular injury, tissue ischaemia, and clinical manifestation of hypotension. Investigation

Initial investigations should include urine analysis with bedside urine dipsticks to check for the pH, white blood cells, nitrites, and red blood cells.

Perform urine microscopy and culture to identify causative organisms and provide antibiotic sensitivities.

Send blood for full blood count (FBC) and urea and electrolytes (UE) as well as inflammatory markers such as C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Blood cultures must be sent for all pyrexial patients before antibiotic use. For those patients who present with septic shock lactate levels must be obtained via arterial blood gas measurement.

X‐ray of the kidneys, ureter, and bladder (KUB) should be carried out to assess for obvious renal stone disease or gas around the kidney (the later finding could suggest emphysematous pyelonephritis [EPN]). Renal tract ultrasound must be performed to rule out renal collecting system obstruction, stone disease, or malformations which may alter further investigations and management. Computed tomography (CT) scans, however, are becoming the standard imaging modality in the acute setting and should be considered if symptoms are >72 hours to exclude abscesses (Figure 12.2) [5].

Image described by caption.

Figure 12.2 Transverse and coronal computed tomography scan showing sever pyelonephritis of the left kidney with significant perinephric fat stranding and increase in renal size, contrasted scan shows patchy uptake of contrast in infected kidney.

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital. Management

Management is determined by how unwell the patient is. Patients who are clinically well can be deemed as mild to moderate but those who require hospital admission can be defined as severe. In hospital settings, sepsis should be treated along an agreed protocol, such as the Surviving Sepsis campaign bundles [2]. In most cases, if the infection is severe enough to require hospitalisation, then management should be as a multidisciplinary approach and must include local high‐dependency unit (HDU) and intensive‐therapy unit (ITU) teams.

Until antibiotic sensitivities can be established, initial management is with broad‐spectrum antibiotic therapy targeted at gram‐negative organisms. Local antibiotic resistance is an important factor in deciding on antibiotic cover for patients. In mild to moderate cases of acute pyelonephritis, oral antibiotics may suffice. However, intravenous antibiotics will be required for severe infections, and once the pyrexia has settled, the intravenous antibiotics can be switched to oral antibiotics. Fluoroquinolone such as ciprofloxacin can be used as a first‐line therapy because most organisms are sensitive to them; however, local antibiotic guidelines should dictate appropriate antibiotic use [5].

12.2.2 Renal Abscess

Previously known as a ‘renal carbuncle’, this rare infection is a collection of pus within the renal parenchyma. Aetiology and Risk Factors

Any condition that reduces host defences or leads to abnormal drainage of the renal collection system predisposes one to renal abscess formation (i.e. diabetes mellitus, nephrolithiasis, or ureteric obstruction) [6].

Before the widespread use of antibiotics, renal abscess were due to haematogenous spread of gram‐positive bacteria such as staphylococci. Today the most common organisms are gram‐negative uro‐pathogens such as E. coli, Klebsiella spp., and Proteus spp. Clinical Presentation

Symptoms are similar to any upper tract urinary infection (i.e. pyrexia, loin pain, and malaise). Symptoms may be acute over days and weeks or become chronic over months, which eludes to the likelihood of abscess formation. Very rarely the abscess may be ‘pointing’ (Figure 12.3).

Image described by caption.

Figure 12.3 Perinephric abscess with significant renal destruction.

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital. Investigation

CT is the gold standard diagnostic investigation, with a renogram to assess kidney functionality. Management

Abscess >5 cm are commonly drained percutaneously or with open surgery. Small abscesses (≤3 cm) are treated with antibiotics and expectant management. Abscesses of 3–5 cm can be treated with either modalities (i.e. drainage or conservatively with reportedly similar results) [68].

12.2.3 Pyonephrosis or Infected Hydronephrosis

Pyonephrosis is the accumulation of pus within the renal collecting system. It is associated with irreversible damage to the renal parenchyma resulting in permanent loss of function. Aetiology and Risk Factors

Risk factors to development of pyonephrosis are attributed to any factor that causes hydronephrosis (e.g. ureteric obstruction by stones or cancer) with subsequent development of infection (i.e. infected obstructed system). Clinical Presentation

Patients present with pyrexia, renal or costovertebral angle tenderness, and are acutely unwell with systemic toxicity. History might be eluding to aetiology and usually symptoms present for a few days or weeks prior to the worsening sepsis. Investigation

Assessment of a patient who is acutely unwell should follow that of acute pyelonephritis. CT scans are the gold standard and will establish the diagnosis and aetiology as well as aid determination of the extent of the disease. CTs can show the presence of air in the system, stone burden, and degree of hydronephrosis, oedema, and thickening of the urinary tract as well as perinephric fat stranding. Isotope scans can assess kidney functionality. If not available, then X‐ray of the KUB could demonstrate air in the collecting system and ultrasound can identify hydronephrosis and echogenic material with in the collecting system, as well as perinephric fat stranding. Management

Initial management should include resuscitation and intravenous broad‐spectrum antibiotics. Urgent decompression of the effected renal collecting system is the priority. Until decompression of the system is achieved, the patient will continue to deteriorate, hence, the need for urgent decompression. This can be achieved by either percutaneous drainage with a nephrostomy insertion or ureteric drainage with a ureteric stent.

12.2.4 Perinephric Abscess

Extension of infection outside the renal parenchyma into Gerota fascia can result in perinephric abscess formation. Usually resultant from rupture of a cortical abscess or an obstructed infected renal system. Rarely, haematogenous spread from a distant infective source (i.e. bowel, gallbladder) can also lead to perinephric abscesses.

Patients who are diabetic and those who are immunocompromised are at a higher risk of developing a perinephric abscess. Patients with presumed acute pyelonephritis who fail to respond to antibiotic management within two to five days or symptoms lasting more than five days, warrant further radiological investigations to rule out a perinephric abscess.

Examination of the flanks may reveal a palpable mass, and there maybe erythema of the overlaying skin. Extension of the hip may elicit severe pain in the back due to psoas spasm and inflammation.

Initial management should include resuscitation and intravenous broad‐spectrum antibiotics followed by urgent percutaneous drainage. In severe cases or in those with persistent or loculated collections, open surgical drainage maybe required. Potentially, although rarely, a nephrectomy is needed, especially if the kidney is non‐functioning.

12.2.5 Emphysematous Pyelonephritis (EPN)

First described in 1898 by Kelly and MacCallum, emphysematous pyelonephritis (EPN) is a rare necrotizing infection of the renal parenchyma or perirenal tissue caused by gas forming uro‐pathogens [9]. Aetiology and Risk Factors

The majority (85%) of patients presenting with EPN have diabetes mellitus with 34% caused by an obstructive uropathy. Other risk factors such include: obstructive uropathy, immunosuppression, alcoholism, drug abuse, and neurogenic bladder; anatomical abnormalities have also been associated [1012].

EPN affects woman more than men 4 : 1 [12]. This is thought to be due to the increased risk of urinary tract infections (UTIs) in women [11, 13, 14].

E. coli is the most common organism followed by Klebsiella, Proteus, and Pseudomonas species; coagulase‐negative Staphylococcus and Group D Streptococcus have also been implicated [11, 12, 15, 16]. Clinical Presentation

EPN is a life‐threatening condition with a high mortality rate. Patients present with pyrexia (75%), renal angle pain and tenderness (70%), haematuria (30%), pyuria (78%), and are profoundly unwell and exhibit signs of severe sepsis with 25% presenting in septic shock [12]. Patients are sometimes treated as pyelonephritis until they fail to respond to management. Nearly 45% present with associated acute kidney injury (AKI). Rarely crepitus may be felt in the region of the renal angle. Investigation

All patients who are acutely unwell must first be resuscitated before specific investigation can be carried out. Initial work up should include a full history and clinical examination. Particular attention should be noted to rule out a new diagnosis of diabetes mellitus or previously known history of the disease. Further investigations follow that of acute pyelonephritis (bloods and urine analysis).

Once the patient is stable, then prompt imaging of the renal collecting system must be undertaken. X‐ray can be used to identify gas pattern shadowing with in region of the renal collecting system, but this can be non‐specific and only accurate in diagnosing EPN in 53% of patients [12]. Ultrasound again can demonstrate gas in or around the renal collecting system and should be considered if no other imaging modalities are available, with an accuracy of about 68% [12].

A CT urogram is the gold standard with a 100% accuracy in diagnosing EPN (Figure 12.4). There are two CT‐based scoring systems (Table 12.5).

Image described by caption.

Figure 12.4 (a–d) Transverse and coronal computed tomography (CT) images showing gas within the renal collecting system (white arrow) consistent with emphysematous pyelonephritis (EPN).

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital.

Table 12.5 Classification of EPN based in CT findings [12, 14].

Wan Classification
Class 1 (severe) Parenchymal destruction with either total absence of fluid content on CT or the presence of streaky gas pattern regardless of the absence of presence of bubbly or loculated gas.
Class 2 (Mild) The presence of renal or perirenal fluid in association with a bubbly or loculated gas pattern or as gas in the collecting system with acuter bacterial nephritis or renal or perirenal fluid containing an abscess.
Huang Classification
Class 1 (Mild) Gas within the renal collecting system only
Class 2 (Mild) Gas in the renal parenchyma with or without extension into extrarenal space
Class 3A (Severe) Perinephric gas or abscess formation
Class 3B (Severe) Perirenal gas or abscess formation
Class 4 (Severe) Bilateral EPN or solitary kidney with EPN

CT, computed tomography; EPN, emphysematous pyelonephritis. Management

Initial management should include resuscitation, intravenous broad‐spectrum antibiotics, and adequate control of blood sugar levels. As the majority of causative organisms are gram‐negative bacteria, antibiotic therapy should target these until specific cultures and sensitivities are available.

Historically, antibiotic therapy coupled with open nephrectomy or surgical drainage was the treatment of choice. However, advances in the last decade have established image‐guided, percutaneous drainage under local anaesthetic as the intervention of choice for EPN. Figure 12.5 depicts a flow diagram of EPN management.

Flow diagram of EPN management starting from emphysematous pyelonephritis branching to mild and severe EPN. Mild EPN branches to obstructive uropathy. Severe EPN branches to percutaneous of open drainage.

Figure 12.5 Recommendations for treating emphysematous pyelonephritis (EPN).

Source: Adapted from [12].

Once the patient is stable, then a MAG‐3 or dimercaptosuccinic acid (DMSA) can be performed to establish renal functionality. Prognosis

In the past, mortality rates were quoted to be as high as 50%; however, with percutaneous drainage, meticulous medical management, and close support with the intensive care unit, survival rates have increased, with current predicted mortality rates of about 18% [12]. Although, the cause of the majority of cases, the presence of diabetes mellitus or nephrolithiasis play no role in increasing mortality rates, but septic shock was the greatest predictor with >50% attributed mortality.

12.2.6 Xanthogranulomatous pyelonephritis (XPN)

Xanthogranulomatous pyelonephritis (XPN) is a rare acute and chronic kidney infection, leading to destruction of renal tissue and permanent loss of renal function. It is associated with underlying renal stone disease or renal obstruction. Pathophysiology, Aetiology, and Risk Factors

Infections and urinary obstruction lead to engorgement and destruction of the renal parenchyma leading to suppuration, haemorrhage, and necrosis. This leads to abscess formation with deposition of granulomatous tissue with granular histiocytes and ‘foamy’ lipid‐laden macrophages. There is also fibrohistiocytoma‐like or plasma cell granuloma‐like patterns, and possible myofibroblast metaplasia. The affected kidney or section of kidney becomes grossly enlarged.

XPN is more commonly diffused, affecting the entire kidney; however, focal cortical or even segmental forms can occur.

Table 12.6 lists risk factors that can predispose to XPN; however, invariably stones are the culprit. E. coli and Proteus are the more common organisms; however, any of the uro‐pathogens can lead to XPN.

Table 12.6 Risk factors for XPN.

  • Pelviureteric junction (PUJ) obstruction
  • Renal stone disease
  • Chronic interstitial nephritis
  • Bladder or ureteric tumour
  • Duplex renal collecting system
  • Pregnancy
  • Diabetes mellitus
  • Obesity
  • Rheumatoid arthritis
  • Hepatitis C infection and liver cirrhosis Clinical Presentation

Patients present in a similar manner to those with pyonephrosis or acute pyelonephritis. Symptoms include flank or loin pain, pyrexia, haematuria, and systemic upset. On clinical examination, it may be possible to ballot a renal mass on the affected side. Investigation

Urine and blood cultures may be positive for common uro‐pathogens. Blood test may show renal dysfunction, anaemia, or leucocytosis. Inflammatory markers such as CRP and ESR will be elevated.

US imaging of the renal tract may demonstrate a dilated collecting system and an enlarged kidney containing echogenic material. CT scanning may show renal stones within the renal mass. Due to indistinct radiological appearance, XPN is indistinguishable from renal cell carcinoma. However, occasionally the ‘Bear Paw’ sign can be picked up on the cross‐sectional appearance of the kidney. The renal pelvis is contracted, whereas the calyces are dilated, mimicking the toe pads of the bear paw. The role of magnetic resonance imaging (MRI) is not well established in the context of XPN, and so is not routinely used. Radioisotope imaging will demonstrate a poorly or nonfunctioning kidney.

Definitive diagnosis can only be made with tissue analysis. Microscopic examination shows yellow nodules of pus, necrosis, and haemorrhage within the calyces. Management

Most patients will initially be treated with antibiotics until their acute infection has settled. After diagnostic imaging, patients will proceed to a nephrectomy to rule out malignancy after which, the confirmation the diagnosis of XPN is usually made. Intraoperatively, XPN can be technically challenging due to the severe inflammation, which results in obliteration of tissue planes as they become fused together and become difficult to dissect. Complications and Prognosis

Within the literature, there have been cases noted of sinus and fistula formation because of chronic infection. These can be to adjacent organs or structures (i.e. psoas abscess or even cutaneous) but are considered extremely rare [17, 18].

12.3 Chronic Surgical Inflammatory Conditions of the Kidney

12.3.1 Tuberculosis Introduction

Tuberculosis (TB) commonly manifests as a respiratory infection. Extrapulmonary TB can affect any part of the body with the kidney being the most common. Table 12.7 shows other genitourinary manifestation of TB.

Table 12.7 Manifestations of genitourinary TB infection and common routes of infection.

Organ Manifestation
Renal Abscess formation
Fistula formation
Ureteric (secondary to renal TB infection) Fibrosis with stricture formation: leading to obstruction
Ureteric orifice dysfunction: leading to reflux
Bladder (secondary to renal TB infection) Chronic ulcerations (worm‐eaten edges)
Reduced capacity bladder and poor compliance
Prostate (haematogenous spread) Chronic prostatitis
Fistula formation
Urethra or penis (secondary to bladder TB infection) Stricture disease
Penile lesions
Epididymis Pain

TB, tuberculosis. Aetiology and Risk Factors

Tubercle bacilli reach the urinary tract via the bloodstream from a primary focus in the lung or bowel. There can also be tertiary spread from bone lesions. The bloodstream brings the mycobacteria to the kidney where they form multiple minute abscesses in the parenchyma (Figure 12.6), which later invade the tubule, erode into a calix, spread to other calices and the pelvis, and finally progress down the ureter into the bladder. Caseating granulomas are formed, which are Langhans giant cells surrounded by lymphocytes and fibroblasts. With the chronic infection, there is healing by fibrosis and calcification. The fibrous tissue contracts, leading to obstruction of one or more calices. The fibrosis eventually leads to destruction of the renal tissue, resulting in atrophic kidneys, ultimately leading to loss of functionality and autonephrectomy. Ureteric involvement leads to stricture formation at the vesicoureteric junction (VUJ) more commonly, followed by pelviureteric junction (PUJ) and mid‐ureter [1922] (Figure 12.7). Involvement of the ureteric orifice leads to distortion, the ‘golf‐hole’ appearance, and may give rise to reflux.

Diagram displaying a kidney with multiple small abscesses (a), a kidney with a big abscess (b), a kidney with tuberculous abscess (c), a kidney with multiple caliceal lesions (d), and a kidney with tuberculous pyocalix (e).

Figure 12.6 The pathogenesis of renal tuberculosis: (a) haematogenous infection produces multiple small abscesses, most of which resolve completely, leaning one or two foci in the papillai. (b) These erode into the lumen of the calix, (c) carrying infection into other calices in which caseation (d) and cavitation (e) take place.

Diagram displaying two urinary tracts with unsuspected tuberculous granulomas in wall of ureter and bladder (left) and ureteric stricture and contracted bladder (right).

Figure 12.7 Healing of the tuberculosis in the ureter leads to a stricture.

The earliest lesions cannot be detected in the kidney until a small tuberculous abscess ruptures into the calix, giving rise to irritating symptoms and pyuria. Untreated, these abscesses enlarge, coalesce, and calcify until the entire kidney may be converted into a calcified mass, previously known as a ‘cement kidney’.

As the mycobacteria spread down the ureter, they cause patches of granuloma in its wall, and on reaching the bladder, similar granulomas form in the vicinity of the ureteric orifice. Sometimes these are so oedematous that they resemble a papillary tumour. Later in the disease, there is ulceration which may become confluent throughout the bladder. Clinical Presentation

Initial symptoms include fever, night sweats, weight loss, lethargy, and failure of treatment for a persistent UTI. Late symptoms can include haematuria and loin pain. Patients may present with lower urinary tract infections that mimic cystitis or prostatitis.

A detailed history should be sought to illustrate previous TB infections or contact with persons infected with TB. A detailed travel history of the patient and their most recent contacts is also important. Investigation

Examination may be unremarkable for these patients. Urine testing usually shows sterile pyuria and negative cultures. If TB is suspected, then three early morning urine samples (EMUs) should be sent for Ziehl‐Neelsen staining to confirm the presence of acid‐fast bacilli. Three samples are needed because the TB bacterium is excreted only intermittently in the urine; hence, multiple samples of urine that have been in the bladder overnight allow for a greater chance of detection. The specimen is cultured on Lowenstein‐Jensen medium; however, cultures can take up to four weeks because the TB bacterium’s doubling time is exceedingly slow (15–20 hours). Therefore, polymerase chain reaction (PCR) testing can also be carried out.

CT urogram and intravenous pyelogram (IVP) could show moth‐eaten calyces, renal calcification, cavitation of the renal parenchyma, hydronephrosis or hydroureter due to stricture, infundibular stenosis, and small shrunken kidney (autonephrectomy) [23] (Figures 12.8 and 12.9). Pelvic calcification may be seen due to vas, seminal vesicle or prostatic involvement.

3 CT scans in different views displaying tuberculosis of left kidney.

Figure 12.8 (a–c) Tuberculosis of left kidney.

Image described by caption.

Figure 12.9 Kidney‐ureter‐bladder (KUB) X‐ray of kidney tuberculosis.

Cystoscopy, retrograde studies, ureterorenoscopy, and biopsy can also be performed to assist in the diagnosis. Renograms can establish kidney functionality. Management

Before the advent of effective anti‐tuberculosis drugs, nephrectomy and cavernotomy was the treatment of choice in such patients. Today, prompt diagnosis and initiation of appropriate antibiotic therapy is the cornerstone of management.

Six months of multidrug anti‐TB regimens are effective for urinary TB infections [24, 25]. Aggressive antibiotic use is to allow achievement of prompt eradication, decrease therapy duration as with individual medication, and the likelihood of drug‐resistance developing.

The regime consists of two months of isoniazid, ethambutol, rifampicin, and pyrazinamide followed by four months isoniazid and rifampicin alone.

Almost half of patients will require a surgical intervention if the disease process is not treated early. Surgical management plays a part in treating complications such as abscess formation and ureteric stricture. Nephrectomy for nonfunctioning kidneys and bladder augmentation or diversion or cystectomy for the small capacity, scarred ‘thimble’ bladder maybe required.

12.3.2 Ureteric TB

During this first few months of treatment, the urinary tract is kept under very close surveillance, by ultrasound supplemented where appropriate by CT urogram, because unnoticed tuberculous lesions heal quickly, and obstruction may develop silently in the ureter and lead to loss of a kidney.

For short strictures with an accessible lumen, good kidney function (>25%) and a good bladder capacity, endourological procedures can be attempted. Alternative complex strictures (e.g. long segment, bilateral, inaccessible lumen, poor kidney function) require more invasive surgical procedures.

Ureteric stents can be attempted with good outcomes [26]. Endoscopic balloon dilation may be attempted; however, it is rarely definitive and repeated procedures are often required [27]. Endoureterotomy incision can be done; however, care must be taken to site of incision, depending on the level of the ureter involved. Lower ureteral strictures are incised in an anteromedial direction, taking care to stay away from the iliac vessels, whereas upper ureteral strictures are incised laterally or posterolaterally. The ureterotomy incision can be made using a cold knife, a cutting electrode, or laser. The incision should be made from the ureteral lumen out to periureteral fat in its full thickness [27].

Short defects of the upper or mid‐ureter can be treated by uretero‐ureterostomy with ureteric anastomosis principles applied (Table 12.8).

Table 12.8 Principles of ureteric anastomosis.

  1. Spatulation of both ends of the ureters for wide anastomosis.
  2. Ends of both ureters should be cleanly cut and viable with good blood supply.
  3. Mucosa‐to‐mucosal anastomosis sutured with absorbable suture over a ureteric stent.
  4. Tension‐free closure with care not to devascularise the ureter.
  5. A drain can be placed.

A stricture at the upper end of the ureter will require a pyeloplasty or ureterocalicostomy (Figure 12.10); however, because the renal destruction is so severe in such cases that usually reconstruction is not possible.

Image described by caption.

Figure 12.10 A tuberculosis stricture of the upper end of the ureter may be relieved by pyeloplasty (a–d) or by ureterocalicostomy (e–g).

At the lower end, it may be necessary to re‐implant the ureter by means of a Boari flap (Figure 12.11) or a Psoas hitch.

Image described by caption.

Figure 12.11 A tuberculosis stricture of the lower end of the ureter may be relieved by reimplantaing the ureter into the bladder with a Boari flap, so long as the bladder is not too contracted. When the bladder is contracted, it may be necessary to add on a piece of bowel.

Obstruction in the middle‐third of the ureter is more difficult to deal with; on the right side, the appendix may lend itself as an ideal substitute for the stenosed segment (Figure 12.12), but on the left side, it may be necessary to bridge the gap with ileum or colon (Figure 12.13).

Image described by caption.

Figure 12.12 A long length of stenosed ureter may be replaced with ileum.

Image described by caption.

Figure 12.13 After the appendix has been mobilised on the mesoappendix a.

Alternatively, if the ureter can be mobilised sufficiently, a transureteroureterostomy can be done. However, caution for bilateral ureteric involvement.

For long ureteric strictures, or multiple or whole ureteric involvement, an ileal replacement will be required; alternately autotransplantation is an option, especially if other methods of repair fail or are not feasible.

In the bladder, the healing process may shrink so much that it needs to be enlarged by enterocystoplasty to restore its reservoir function. The traditional solution has been to use the caecum, but this may generate high pressures and threaten the upper tract; many surgeons now prefer a detubularised segment of bowel, even if the patient has to catheterize to empty it. Complications and Prognosis

Complications arise from infection spreading to adjacent genitourinary structures (Table 12.6).

12.3.3 Chronic Pyelonephritis Introduction

Chronic pyelonephritis is the end product of recurrent or continuous inflammation of the kidney. It leads to scaring of renal tissue and permanent loss of renal function. The inflammation can be related to an infective cause such as recurrent UTIs or, as in the case of children, due to a noninfective aetiology such as vesicoureteric reflux (VUR), which leads to more marked scarring. In adults, noninfective causes are those such as high pressure retention of urine due to benign prostatic hyperplasia (BPH) or detrusor‐sphincter dysnergia in spinal cord injury, while infected causes are seen with obstructed infected uropathy (e.g. obstructive stone). Clinical Presentation

Most patients are asymptomatic unless they show signs of recurrent UTI. Due to the insidious nature of the disease, patients may present with symptoms of end‐stage renal failure. Investigations

The diagnosis can be made from radiological appearances and also pathological analysis. Baseline renal function must be performed followed by radiological investigations to confirm the diagnosis. Ultrasound, CT, intravenous urogram (IVU), or radioisotope imaging (DMSA) will show renal scarring, deformed calyces, and thinning of the renal cortex. Scars are typically in the upper or lower poles because these are more prone to reflux. The affected kidney may also look atrophic or shrunken on scanning. Management

Treating the underlying cause may help prevent loss of further renal function. Optimization of renal function is imperative, and a nephrologist is required to monitor these patients. Patients with end‐stage renal failure should be considered for renal transplant or dialysis. In children, prompt assessment of VUR is required. Complications and Prognosis

End‐stage renal failure is the only associated complication if bilateral disease.

12.3.4 Papillary Necrosis

Papillary necrosis (PN) originates from impairment of the vascular supply and from subsequent focal or diffuse ischemic necrosis of the distal segments of the renal pyramids. Common causes of PN include, pyelonephritis, obstructive uropathy, sickle‐cell disease, TB, cirrhosis and chronic alcoholism, analgesics (NSAIDs specifically), renal vein thrombosis, diabetes, and systemic vasculitis (i.e. mnemonic: POSTCARDS). The arterial supply to the renal papilla comes partly from the vasa recta and partly from arteries at the fornix of the calix. Either vessel may become occluded when the papilla becomes oedematous or injected with urine, and the papilla becomes ischaemic and sloughs off. A line of demarcation forms, and the dead papilla may pass down the ureter to cause obstruction or remain in the renal pelvis to act as the nucleus for stone formation. The presence of the ischaemic papilla exacerbates existing inflammation and obstructive changes in the collecting tubules in the medullary rays. The process culminates with healing by epithelializing the papilla; however, there is usually ensuing scarring and atrophy of the kidney.

Patients present acutely with an AKI with deteriorated renal function, gross haematuria, flank pain, and occasionally tissue fragments in the urine.

Treatment is conservative starting with removal of the underlying cause. Broad‐spectrum intravenous antibiotics if infection is present; maintain hydration, glycaemic control, urinary alkalinisation, and cessation of analgesics; and patients with sickle cell disease may require exchange transfusions.

12.4 Other Inflammatory Conditions of the Kidney

12.4.1 Malakoplakia

This is a rare inflammatory condition that can affect any area of the body, but most commonly presents within renal collecting system. It was first described by Michaelis and Gutmann who described extra and intracytoplasmic histiocytes that they termed ‘Michaelis‐Gutmann bodies’ [28].

It can affect any age group but is predominantly seen in patients older than the age of 50. Any form of immunosuppression or recurrent gram‐negative UTIs puts people at greater risk (Table 12.9) [29, 30].

Table 12.9 High‐risk groups for the development of renal malakoplakia.

Immunosuppression Chronic steroid use
Solid organ transplant patients
Chronic systemic diseases
Alcohol abuse
Poorly controlled diabetes
Recurrent urinary tract infection Escherichia coli

Patients present with symptoms of a renal mass or renal failure. There may be a history of recurrent UTIs. Radiological scanning can show an enlarged, nonfunctioning kidney with multiple poorly differentiated lesions which can mimic renal cell carcinoma. Differential diagnosis include XPN, lymphoma, renal cell carcinoma, or renal abscess [29].

Most patients undergo nephrectomy because of the suspicion of malignancy, and at histological analysis, the diagnosis is made. Renal biopsy could be considered to aid in preoperative diagnosis. Some authors have theorised that antibiotic treatment only may suffice if the diagnosis can be made in this way [31, 32].

12.4.2 Hydatid Disease

This rare parasitic infection only affects the kidney in 3–4% of cases [33]. It is caused by ingestion of a dog parasite known as Echinococcus granulosus (a type of tape worm). Dogs are the definitive host other farm animals, and humans act as an intermediate host. Infection in humans is due to contact with dog or animal faeces (Figure 12.14).

Diagram illustrating the life cycle of Echinococcus granulosus with arrows from a sheep to a dog and adult tapeworm, to a child with a dog, to a stomach and liver, to a kidney, then to a cyst with a daughter cyst.

Figure 12.14 Life cycle of Echinococcus granulosus.

Patients can be asymptomatic and the diagnosis can be made incidentally. Others may develop haematuria or chronic loin pain [34]. There is no one definitive test, but eosinophilia is noted in up to 50% of cases. Indirect haemagglutination and enzyme‐linked immunosorbent assays are the most sensitive tests. Immuno‐electrophoresis against arc‐5 antigens is also widely used [3436].

Ultrasound and CT scans will show a thick‐walled, fluid‐filled spherical cysts with calcified walls. Differential diagnosis could be renal cell carcinoma.

Medical management uses albendazole, which is an anti‐helminthic agent that causes degenerative changes in the intestinal cells of the worm by binding to the colchicine‐sensitive site of tubulin, thus inhibiting microtubule production, leading to impaired uptake of glucose by the parasites, and depleting their glycogen stores. Medical management is commonly used as an adjunct to surgical resection. Intact removal of lesions is extremely important at nephrectomy as spillage of cyst contents results in a severe anaphylactic reaction. The use of scolicidal agents such as hydrogen‐peroxide before resection is recommended [33, 36]. Puncture‐aspiration‐injection‐reaspiration (PAIR) procedure is a minimally invasive treatment option to remove hydatid cysts. It is a US‐guided percutaneous puncture of the cyst, aspiration of the fluid with instillation of the scolicidal solution for 30 minutes, and followed by reaspiration of the fluid. Percutaneous thermal ablation of the cystic germinal layer by radiofrequency ablation is a new alternative currently being explored [37].

12.4.3 Fungal Infections

Fungal infection occurs in patients who are immunocompromised and those that have been given broad‐spectrum antibiotics. Scanning and urine cultures are the main route of investigation. The main course of treatment is the use of antifungals. Ureteroscopy and removal of fungal balls in the renal collecting system may also be required to facilitate clearance.

12.4.4 Brucellosis

This is a zoonotic disease from infected animals. Human infections comes about from ingestion of contaminated unpasteurized and un‐boiled diary produces. It is rare in the UK but is seen in Mediterranean countries. Although it can affect any part of the body, renal manifestations are very rare [38].

Symptoms are variable and nonspecific, but it can cause calcifying granulomatous changes within the kidney. Treatment is with prolonged courses of tetracycline antibiotics.

12.4.5 Chyluria and Filariasis

In the Far East, chyluria is by no means uncommon. The patient presents with thick urine resembling anchovy sauce but usually without any other symptoms. Rarely, it is a cause of haematuria. The only serious consequence may be the urinary loss of protein, which occasionally leads to significant protein deficiency and loss of weight.

Investigations show a communication between the renal lymphatics and its collecting system (Figure 12.15). The condition is traditionally attributed to the microscopic round worm Wuchereria bancrofti, but it is rarely possible to confirm this diagnosis.

Image described by caption.

Figure 12.15 (a) Combined lymphangiogram (left) and retrograde urogram (right) in a patients with chyluria. (b) Lymphangiogram in chyluria.

W. bancrofti lives in the lymphatics where it sets up an inflammatory response. The tiny worms creep at night into the peripheral blood where they are sucked up by feeding mosquitoes and injected into the next victim (Figure 12.16).

Diagram illustrating the life cycle of Wuchereria bancrofti, with arrows from a man labeled deep lymphatics to a worm, to a blood vessel, to a mosquito, to microfilariae, the to a man labeled superficial lymphatics.

Figure 12.16 The life cycle of Wuchereria bancrofti. Pathophysiology

Pathogenesis is dependent on the immune system and inflammatory responses of the host. After infection, the worms will mature within six to eight months; male and female worms will mate and then release the microfilariae which can be release for up to 10 years.

An asymptomatic phase usually consists of high microfilaremia infection. Usually there is no symptoms of infection due to cytokine IL‐4 suppression of the immune system.

In the inflammatory (acute) phase, the antigens from the female adult worms trigger an inflammatory response. The worms in the lymph channels disrupt the flow of the lymph, causing lymphedema. Symptoms are of fever, chills, opportunistic infections, and painful lymph nodes, lasting for about five to seven days.

Obstructive (chronic) phase is marked by lymph varices, lymph scrotum, hydrocele, chyluria, and elephantiasis. A key feature of this phase is scar formation and thickening of the skin and elephantiasis, which develops gradually with the attack of the lymphatic system. Investigations

The parasite might be seen on a blood smear; however, PCR can detect filarial DNA fragments. Ultrasound detection of the parasites movements and noises can confirm parasitic infection, whereas a lymphogram will demonstrate communications between the kidney and lymphatics. Treatment

In most cases, no treatment is needed. Prevention is key, with avoidance of mosquito bites by nets or repellent.

The medical treatment is diethylcarbamazine (6 mg kg−1 annually or bi‐annually), which eliminates the microfilariae from the blood and kills the adult worms. It acts by inhibiting the microfilarial arachidonic acid metabolism. This makes the microfilaria more susceptible to immune attack. Combination therapy with ivermectin or albendazole plus diethylcarbamazine is more effective than monotherapy.

If the patient is obviously losing protein, the kidney is surgically explored and stripped of all its surrounding fibrotic and oedematous tissue. A preliminary lymphogram using contrast stained with a blue dye may make the dissection more exact. Every lymphatic trunk that is encountered must be meticulously ligated.

12.5 Inflammatory Conditions of the Ureters

12.5.1 Retroperitoneal Fibrosis Introduction

Retroperitoneal fibrosis (RPF) was first described by Ormond in 1948 [39], this condition is defined by fibro‐inflammatory tissue encasing the abdominal aorta and iliac vessels, which can involve the ureters. Its incidence is thought to be 1.38 per 100 000 of the population in the fifth or sixth decade of life; men are twice as commonly affected as women [40]. RPF is part of a disease spectrum known as chronic periaortitis, which is a large vessel arteritis [41]. Long‐term management of this disease is undertaken by rheumatologists and nephrologists, but urological input is required to assist in drainage of the upper tracts. Aetiology and Pathophysiology

RFP can be idiopathic (IRPF) or secondary. Though coined ‘idiopathic’, the likelihood is that it is an autoimmune process called ‘periaortitis’. Commonly associated secondary causes are iatrogenic or traumatic (e.g. surgery, radiotherapy, or chemotherapy), tumour or malignant process (lymphoma being the most common followed by metastatic disease), infection like TB, and drugs such as beta‐blockers, hydralazine, haloperidol, amphetamine, LSD, and even methyl methacrylate cement (used in joint replacement surgery). It can be associated with autoimmune disease such as Crohn disease or Riedell thyroiditis or associated with vascular disease or treatments, abdominal aortic aneurysm, angioplasty, or intravascular stenting.

The most common cause found in more than 60% of patients is periaortitis. Inflammatory response to the leakage of insoluble lipids through the arterial wall from the atheromatous plaque leads to the formation of the fibrous whitish plaque that can extend to the ureters, pelvic organs, and retroperitoneal structures. Histologically there are chronic inflammatory infiltrates made up of macrophages, eosinophils, plasma cells, and lymphocytes; the central plaque is formed of fibrous scar tissue, while the growing periphery is active chronic inflammation. There are myofibroblasts and type 1 collagen within the fibrotic component [42]. Clinical Presentation

Clinical manifestations can be variable. Patients may present earlier on with nonspecific symptoms such as back and abdominal pains, loss of appetite or weight, night sweats, and malaise. If ureteric involvement is present, then patients may have colicky type symptoms. Late presentation is of symptoms of renal failure (acute or chronic) due to ureteric obstruction. New onset hypertension might be the only symptom. Scrotal swelling, hydroceles, and varicoceles can also occur, depending on the extent of the plaque and the vascular and lymphatic segments involved [42]. Investigations

There are no set diagnostic criteria for RPF, and the diagnosis is usually made after exclusion of other diagnoses, such as malignancy, have been ruled out. Multiple imaging modality might be needed to establish diagnosis as well as plan and follow up treatment (Figures 12.17 and 12.18).

Image described by caption.
Image described by caption.

Figure 12.17 Intravenous urogram (IVU), computed tomography (CT) scan, magnetic resonance imaging (MRI) scan, and renogram show retroperitoneal fibrosis (RPF).

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital.

Image described by caption.

Figure 12.18 (a–c) Retroperitoneal fibrosis: the ureters are compressed and drawn medially by a gard white sheet of fibrous tissue around the aorta and inferior vena cava.

Baseline renal function and full blood counts including inflammatory markers. ESR is elevated in the majority of cases. CT and radioisotope scanning (MAG3 or DMSA) will help to determine drainage and function of the kidneys. Retrograde pyelogram can also be used to assess narrowing and obstruction of the ureters.

CT‐guided biopsy of the RPF mass confirms diagnosis; however, a negative result for cancer does not exclude it.

MRI scanning can be used to track progression and remission of the disease. On T2‐weighted sequences hyper‐intensity can correlate with disease activity.

Other imaging modalities used are F‐fluorodeoxyglucose (FDG), positron emission tomography (PET), and CP3 67gallium (Ga) scintigraphy [43]. Management

Aims of treatment are to relieve ureteric obstruction, preserve renal function, and halt or reverse disease progression.

Relief of ureteric obstruction is a priority to preserve renal function. This can either be achieved with percutaneous nephrostomy placement (with or without anterograde stenting) or retrograde double‐J stents [42, 44, 45].

Treatment of the underlying causes is critical, but in the case of IRPF, medical management is now the mainstay of treatment and should be started as soon as possible. In cases refractory to these measures, ureterolysis and omental wrapping of the ureters will be required. Steroids

Glucocorticoids have been used for many years in RPF. They halt disease progression and help preservation of renal function [46, 47]. High doses are typically employed (up to 1.5 mg kg−1) and titrated down once the inflammatory markers normalise. A number of studies have been performed to ascertain the optimum administration, but there is no set regime [44, 48, 49]. What is characteristic of all studies is that relapse is common (25–50%) after doses are titred down, but re‐remission can be attained by reinstatement of high doses [42, 44].

High‐dose long‐term glucocorticoid use is associated with significant morbidity and should be avoided but may be the only route in problematic patients. Steroid‐sparing Drugs

Tamoxifen [50, 51], azathioprine [47, 49], cyclosporine [47], mofetil mycophenolate [47, 5254], and cyclophosphamide [47, 55] have been utilised as possible alternatives to steroid treatment. There is no evidence that combination with glucocorticoids provides any further benefit, but these drugs can be deployed in patients who have recurrent replaces on steroid treatment or who have contraindications to glucocorticoids.

A randomised controlled trial (RCT) comparing tamoxifen to prednisolone found relapse rates were lower in the steroid group (6 vs 39%); additionally, the steroid groups sustaining longer remission times [51]. Hence, recommendations are for glucocorticoid, with or without, concomitant steroid‐sparing agents should be the treatment of choice [42].

Emergent therapies consist of monoclonal antibodies such as infliximab and rituximab have shown promise but require further work [42, 56]. Ureterolysis

This can be done by either open, laparoscopic, or robotic approaches, depending on the surgeon’s experience. The colon is reflected off the ureter first on one side and then the other (Figure 12.19). The plane of cleavage between the ureter and the surrounding sheath of fibrous tissue is dissected away, liberating the ureter (Figure 12.20).

Image described by caption.

Figure 12.19 The colon is mobilised on each side and reflected medially.

Image described by caption.

Figure 12.20 The fibrous tissue is incised to release the ureter.

This is sometimes very difficult because the fibrosis actually penetrates the muscular wall of the ureter, and when the lumen is breached, a nephrostomy is a mandatory precaution if one is not already in position. If the injury is small, it can be left to heal with a stent in situ; however, if extensive ureteric segment is damaged, primary anastomosis, ureteric reimplantation, or even nephrectomy might be required. To prevent a return of the fibrosis, it is safest to wrap each ureter in omentum (Figure 12.21).

Image described by caption.

Figure 12.21 After ureterolysis, each ureter is wrapped in omentum. Prognosis

Whether the ureters have been placed in the peritoneal cavity or wrapped in omentum, it is necessary to follow the patient carefully. Recurrence of the fibrosis is always a possibility, and so is a new manifestation of the fibrosis in the mediastinum or porta hepatis. Fortunately, a very useful index of return of active disease is provided by the sedimentation rate. This, and the blood pressure, should be monitored indefinitely in view of the long‐term risk of atherosclerotic disease. Permanent upper tact decompression may be necessary.

12.5.2 Ureteric Endometriosis

Although this is rare (incidence of 0.01–1%), it is a clinically important diagnosis to make as ureteral endometriosis can lead to silent loss of the kidney due to chronic obstruction [57, 58].

Lesions can be intra‐ or extraluminal causing stricture disease and fibrosis. Retrograde urethrography and CT urogram can be used to assess for obstructive lesions, but biopsy will confirm the diagnosis [59]. Cyclical bleeding is seldom observed, and the response to hormonal manipulation has been disappointing. Healing may be followed by obstructing fibrosis calling for reimplantation.

12.5.3 Amyloidosis

Amyloidosis of the ureter is extremely rare. It should be considered as a differential to a ureteric tumour causing unilateral obstruction. Only a handful of cases have been described in the literature [60, 61]. Local resection and anastomosis has been successfully accomplished where the length of ureter has been short.

12.5.4 Pelvic Lipomatosis

This is a rare, nonmalignant, overgrowth of firm pelvic fat which surrounds and infiltrates the bladder, colon, and ureters. It occurs in males in their thirties and is more common in those of African ancestry. It is associated with cystitis cystica and cystitis glandularis in a third of patients. Compression of the ureters causes progressive hydronephrosis and renal failure [58, 62, 63].

CT scanning is the diagnostic test of choice which will show increased adipose tissue around the bladder and dilatation of the renal collecting system.

There is no definitive treatment, but surgical resection is difficult because the fat infiltrates organs and there is no clean plane of cleavage. Most patients require urinary diversion or percutaneous drainage.

Aug 6, 2020 | Posted by in UROLOGY | Comments Off on Kidney and Ureter Inflammation

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