| disease | Chronic Pyelonephritis |
Acute uncomplicated urinary tract infections usually do not cause kidney scarring or progressive kidney damage, especially in adult patients. Chronic pyelonephritis in adults is typically the result of pyelonephritis that gradually developed during childhood.
bubble_chart Pathogenesis
Acute uncomplicated urinary tract infections usually do not cause renal scarring or progressive kidney damage, especially in adult patients. Chronic pyelonephritis in adult patients is typically the result of a gradual progression from pyelonephritis in childhood. Prospective studies indicate that in the absence of adverse factors such as diabetes, stones, analgesic nephropathy, or urinary tract obstruction, urinary tract infections are a relatively benign pathological process and rarely lead to kidney damage or loss of renal function.
Due to the incomplete development of the kidneys in infants and young children, urinary tract infections in this age group are prone to cause the typical renal scarring of chronic bacterial pyelonephritis. These coarse renal scars often occur at the upper and lower poles of the kidneys. This type of pyelonephritis is referred to as chronic infantile pyelonephritis or chronic atrophic pyelonephritis. Because the renal calyces are pulled by the scars formed by the kidney's excess parenchyma, a dilated calyx can be seen beneath each scarred area. Current evidence suggests that the interplay between urinary tract infections and vesicoureteral reflux plays a key role in the mechanism of renal scarring, and the severity of renal scarring appears to be directly related to the severity of vesicoureteral reflux in pediatric patients. The most severe renal scarring occurs in patients with intrarenal reflux.
bubble_chart Pathological ChangesGrossly, the kidneys are visibly atrophied, with the degree of atrophy depending on the severity and uniformity of the lesions. The surface of the kidneys shows uneven scarring, and the renal capsule appears pale and difficult to peel off. In longitudinal and transverse sections of the kidneys, mild cases retain mostly normal cortex and medulla, while severe cases exhibit widespread destruction of normal renal structure by inflammation and fibrosis, with the renal pelvic mucosa appearing pale and fibrotic.
Microscopic examination reveals extensive infiltration of plasma cells and lymphocytes in the renal parenchyma, varying degrees of tubular degeneration, dilation of some tubules containing proteinaceous secretions, fibrosis and marked hyalinization of affected glomeruli, often with thickened arteriolar and small arterial walls. Apart from scarred and chronic inflammatory areas, patchy acute inflammatory foci are also observed, making the parenchymal scars overlying dilated calyces less typical.
Since the pathological changes of chronic bacterial pyelonephritis and many other non-infectious interstitial nephritides are quite similar, histological examination cannot definitively determine the etiology of chronic pyelonephritis. Routine autopsy findings indicate that the incidence of pathological changes consistent with chronic pyelonephritis is 10-15%. Undoubtedly, the true incidence of chronic bacterial pyelonephritis is significantly lower than this figure.
bubble_chart Clinical Manifestations
(1) Symptoms: Pediatric (occasionally adult) patients may experience acute exacerbations of chronic bacterial pyelonephritis. Fever is only observed during the acute stage of an attack, and patients without acute episodes may be asymptomatic. When chronic pyelonephritis reaches an advanced stage and involves both kidneys, symptoms related to hypertension, anemia, and azotemia may appear.
(2) Signs: Unless there is an acute infection episode, specific signs are difficult to detect. Patients in the advanced stage may exhibit elevated blood pressure.
(3) Laboratory tests: In the absence of acute infection episodes or azotemia, blood tests are usually normal. Urinalysis results depend on the presence of active infection and the severity of renal damage, with pyuria and bacteriuria detectable in only some cases. Significant proteinuria indicates severe disease with glomerular involvement. If bacteriuria is present, urine culture will be positive. Depending on the disease stage, serum creatinine and blood urea nitrogen (BUN) may be normal or elevated.
(4) Imaging: Abdominal plain films may reveal unilateral or bilateral kidney shrinkage with irregular contours. Urinary tract stones may occasionally be observed. Urography can detect characteristic features of chronic pyelonephritis, such as renal pelvis dilation, cortical scarring or atrophy, cortical deformation, poor or delayed contrast visualization. In unilateral atrophic pyelonephritis, the contralateral kidney may show compensatory enlargement. If vesicoureteral reflux is present, ureteral dilation may be seen. Retrograde urography may show similar findings, and retrograde cystourethrography can identify vesicoureteral reflux, particularly more common in pediatric patients.
(5) Cystoscopy: During active infection, cystoscopy often reveals signs of cystitis. Abnormal shape or position of the ureteral orifice may suggest valve dysfunction and vesicoureteral reflux. After thorough bladder irrigation with sterile fluid, insertion of a ureteral catheter to collect urine from the upper urinary tract for culture can localize the infection site.
(1) Special Treatment:
① Drug Therapy: Patients of all age groups with evidence of chronic pyelonephritis require timely diagnosis, careful treatment, and prevention of recurrent infections. To eradicate urinary tract infections, drug sensitivity tests should be conducted to select appropriate antibiotics. For severe new contraction infections (especially in infants and young children), long-term and continuous antibiotic treatment is necessary.
② Surgical Treatment: Surgical intervention is required to correct anatomical defects (particularly urinary tract obstruction) and remove stones in patients. Bladder-ureteral reflux, which affects drug efficacy to varying degrees, also necessitates surgical treatment.
(2) General Treatment: To minimize progressive kidney damage and functional loss, close follow-up of patients is essential. Strict control of urinary tract infections, timely detection, and management of complications are required. Hypertension caused by unilateral atrophic pyelonephritis may be regulated by renin. After careful evaluation, such patients may undergo nephrectomy if indications are present.
The prognosis of chronic pyelonephritis is determined by factors such as the age at onset, anatomical defects, severity of kidney disease, and the efficacy of urinary tract infection treatment. Chronic pyelonephritis generally does not progress to chronic renal failure requiring dialysis or kidney transplantation, except in cases of inadequately treated chronic pyelonephritis in infants and young children.
To prevent the occurrence of renal scarring and progressive kidney damage from chronic bacterial pyelonephritis, it is necessary to detect urinary tract infections in infants and young children early, carefully prevent and treat all urinary tract infections in both infants and adults, and promptly identify and surgically correct any adverse factors that may hinder medical treatment.
In chronic bacterial pyelonephritis, most renal scarring and kidney damage occur during early childhood; therefore, the majority of severe complications of urinary tract infections are associated with pediatric pyelonephritis. Despite recurrent episodes of pyelonephritis, adult patients with normal renal and urinary tract development rarely develop renal scarring or functional loss. However, adults with kidney infections complicated by diabetes, urinary stones, or urinary tract obstruction are at risk of progressive renal damage and functional loss.
Patients with chronic pyelonephritis are prone to bacteremia, hypertension, and kidney stones, especially infected stones. Certain factors that promote the progression of bacterial pyelonephritis from childhood to chronic renal insufficiency in adulthood include: ① recurrent or persistent infections due to incomplete treatment; ② renal hypoplasia or malformations; ③ progressive immune-mediated damage; ④ hypertensive kidney damage; ⑤ severe vesicoureteral reflux-induced renal injury; and ⑥ the presence of infected kidney stones, particularly those caused by urease-producing bacteria.
In the absence of symptoms of acute pyelonephritis (fever and lumbago), it is often difficult to differentiate between upper and lower urinary tract infections. Patients with chronic pyelonephritis typically exhibit renal scarring on excretory urography, whereas those with lower urinary tract infections have normal kidneys. However, urine cultures from patients with renal scarring sometimes show no bacterial growth and only present symptoms of lower urinary tract infections. Conversely, patients with normal excretory urography may occasionally exhibit fever, lumbago, or other symptoms of upper urinary tract infections. Therefore, unless invasive tests are performed, distinguishing between lower urinary tract infections (female urethral syndrome and cystitis, male bacterial prostatitis and cystitis) and upper urinary tract infections can be quite challenging at this stage.
Chronic pyelonephritis must also be differentiated from other causes of chronic tubulointerstitial kidney diseases, particularly analgesic nephropathy. When making the distinction, the possibility of renal subcutaneous nodules should also be considered. The presence of mycobacteria in urine smears and cultures, along with typical manifestations of renal subcutaneous nodules on urography, can aid in differentiation. For patients with urographic findings suggestive of chronic pyelonephritis, further investigations such as renal scintigraphy, angiography, or CT scans may sometimes be necessary to differentiate it from renal tumors.
