Acute pyelonephritis is a multifocal acute infection of renal parenchyma and pelvicalyceal system. The diagnosis of acute pyelonephritis is typically based on the presenting complaints of patients, physical examination and laboratory parameters. Imaging is reserved for patients who are not responding to treatment and in complicated cases.
Epidemiology
Adults (F>M) and elderly males are more commonly affected compared to the paediatric population. Sexually active women and men above the age of 60 years (secondary to prostatic hyperplasia) are most commonly affected.
Clinical features
Clinical spectrum includes frequency, urgency of urine, dysuria, flank pain, fever, chills, malaise, nausea, vomiting, anorexia and abdominal pain. Gross haematuria and dysuria are commonly seen in female patients. Elderly patients may show altered mental status, deterioration and damage to other organ systems.
On physical examination, costovertebral and renal angle tenderness is seen. Pain is variable in intensity and is commonly unilateral however bilateral discomfort may be present. Sometimes, suprapubic tenderness may be seen secondary to cystitis.
Children (less than 2 years) present with feeding difficulty, failure to thrive, vomiting and fever.
Lab parameters
Urine analysis shows proteinuria, pus cells, red blood cells and presence of nitrite and white blood cell on a urine test strip. Urine culture and antimicrobial susceptibility testing help in management of complicated and unresponsive cases. Blood analysis reveals raised white blood cell count, ESR and C-reactive protein.
Pathology
Acute pyelonephritis occurs most commonly secondary to ascending lower urinary tract infections (UTIs). Rarely, another cause can be haematogenous bacteraemia.
Ascending UTI occurs by spread of bacterial pathogens from the urinary bladder to kidneys through the ureters.
Haematogenous spread of infection occurs from skin or dental sepsis, endocarditis, osteomyelitis, pulmonary tuberculosis (TB) and intravenous drug abusers.
Urinary tract obstruction, vesicoureteral reflux, bladder outlet obstruction, pregnancy, urinary tract instrumentation, preexisting renal disease, diabetes mellitus and immunosuppression (AIDS, corticosteroid therapy, chemotherapy to treat cancer, kidney transplant) are the predisposing factors for pyelonephritis.
Gram-negative organisms such as Escherichia coli (>80%), Proteus, Klebsiella and Enterobacter are the common causative organisms. Fungi, mycobacteria and viruses may rarely act as causative agents.
In acute pyelonephritis, kidneys become oedematous with multiple inflammatory foci which may develop to microabscesses. Microscopic examination reveals tubular or interstitial necrosis, fibrosis and mononuclear cell infiltrate.
With treatment, these foci of inflammation usually resolve completely. However, in presence of predisposing factors or inadequate treatment, the infection may progress to result in focal or diffuse nephritis. It may further develop to renal and perirenal abscess.
Acute pyelonephritis can be uncomplicated or complicated. Uncomplicated cases are those in which there is no recurrence and no permanent damage to the renal function. Complicated pyelonephritis includes patients with recurrence, predisposing factors development of abscess or emphysematous changes.
Imaging
Majority of these infections respond rapidly to antibiotics without any sequelae. However, some of them can have marked inflammation with focal or diffuse damage. Imaging is required in these severe, complicated cases and in children. The aim of imaging is to assess the severity of infection and to identify any underlying structural abnormality which may predispose to infection.
Intravenous pyelography (IVP): The role of IVP in acute pyelonephritis has decreased rapidly due to low positivity rate compared to the new modalities. IVP may show renal enlargement, minimal dilatation or attenuation of the calyces, decreased, delayed and persistent nephrogram.
Ultrasound (USG): On grey scale imaging, kidneys appear normal most of the time. The positive findings include decreased renal echogenicity, loss of corticomedullary differentiation, decreased visualization of renal sinus fat and posterior acoustic enhancement distally. There may also be appreciable thickening of the pelvicalyceal system, perinephric fluid and increased echogenicity of the adjacent perinephric fat.
In complicated cases, ill-defined hypoechoic areas with posterior acoustic enhancement may be seen which can represent abscesses/necrosis. Haemorrhagic necrosis presents as areas with increased parenchymal echogenicity.
On colour and power Doppler, there is reduced segmental or diffuse parenchymal flow due to arteriolar vasoconstriction and interstitial oedema.
In pregnant patients, USG is the modality of choice.
Contrast-enhanced ultrasound (CEUS): CEUS has capacity to provide a real-time imaging with advantages of safety, simplicity, compliance and absence of ionizing radiations. Normally in early arterial phase (20 and 40 seconds after injection), corticomedullary differentiation is well made out. Following in the next 45–120 seconds, there is gradual loss of this differentiation with development of homogeneous contrast enhancement of cortex and medulla.
In CEUS, patients with acute pyelonephritis show wedge-shaped hypoenhancing areas. Accuracy of CEUS is inferior in the diffuse pyelonephritis as there is no comparable adjacent normal parenchyma. In contrary, diagnostic accuracy is significant in and in focal/multifocal lesions due to intervening normal parenchyma.
Plain CT: Kidneys may appear enlarged and show perinephric fat stranding. These findings are not considered diagnostic.
Contrast-enhanced CT (CECT): CT urography (CTU) is the modality of choice. The sensitivity and specificity of CT is 86.8% and 87.5%, respectively, while that of USG is 74.3% and 6.7%, respectively.
Protocol for CT urography:
Single-bolus injection technique and split bolus injection technique are used for CTU. The former technique is commonly followed.
Single-bolus injection technique is a three-phase CTU protocol. An initial unenhanced phase is followed by administration of nonionic contrast material (100–150 mL of 300 mg/mL iodine concentration at a rate of 2–4 mL/second). Acquisition of the second phase is done after a delay of 90–100 seconds known as the nephrographic phase. The third phase is excretory phase and is acquired after 12–15 minutes following contrast injection. Sometimes a four-phase protocol is followed which consists of two excretory phases at 5 minutes and 7.5 minutes.
The alternative split bolus technique consists of two-phase CTU protocol. The first unenhanced phase is acquired and the first bolus of nonionic contrast (30 CC) is administered intravenously on CT table. Then the patient is removed from the gantry and is encouraged to walk for 10–15 minutes. Patient is again placed on the CT table in prone-position and a second bolus contrast (100 cc) is administered. Second enhanced phase is acquired after a delay of 100 seconds of administration of the second bolus. Thus, in second phase the nephrogenic and excretory phases are acquired simultaneously.
In acute pyelonephritis, CTU demonstrates diffuse or ill-defined multiple wedge-shaped areas of reduced renal parenchymal perfusion with or without renal enlargement (Fig. 10.12.2.1.1). These perfusion deficits can be detected in corticomedullary phase, however best seen on nephrogenic phase.
The characteristic striated nephrogram (Fig. 10.12.2.1.2) consists of alternated hyper- and hypoattenuating radial bands extending from the renal papilla to cortex with delayed excretion of contrast. There is also reduced contrast concentration in the renal tubules secondary to tubular obstruction by inflammatory cells, debris, ischaemia, and interstitial oedema leading to hypoattenuating bands.
Other inflammatory changes such as perinephric fluid, fat stranding and thickening of Gerota’s fascia are detectable. Sometimes, thickening of the pelvicalyceal system and increased enhancement may be appreciable.
Even after 3–6 hours if kidneys are imaged for some reason, striated nephrogram can be still seen due to delayed transition of contrast.
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