PN is a renal disorder affecting tubules, intrestitium, and renal pelvis and is one of the most common diseases of the kidney. The term urinary tract infection (UTI) implies involvement of either the bladder (cystitis) or the kidney and their collecting system (pyelonephritis), or both. UTIs are extremely common disorders.
It occurs in two forms:
1. Acute PN is acute pyogenic infection.
2. Chronic PN is a more complex disorder: bacterial infection plays a dominant role, but other factors (vesicoureteral reflux, obstruction) are involved in its pathogenesis.
· The dominant etiologic agents are the gram-negative bacilli that are normal inhabitants of the intestinal tract: E.coli (Proteus, Klebsiella and Enterobacter), Str. fecalis etc.
· In most patients with UTI, the infecting organisms are derived from the patient’s own fecal flora. This is thus a form of endogenous infection.
· There are two routs by which bacteria can reach the kidneys:
a) Through the bloodstream (hematogenous).
b) From the lower urinary tract (ascending infection).
· Although obstruction is an important predisposing factor in the pathogenesis of ascending infection, it is incompetence of the vesicoureteral orifice that allows bacteria to ascend the ureter into the pelvis.
· The hallmarks of acute PN are patchy interstitial suppurative inflammation and tubular necrosis.
· Macroscopically, the kidneys show variable numbers of small, yellowish white cortical abscesses, which are usually spherical, under 2 mm in diameter, and are sometimes surrounded by a zone of hyperemia; the cortical abscesses are often most prominent on the sub-capsular surface, after the capsule has been stripped away. In the medulla the abscesses tend to be in the form of yellowish white linear streaks that converge on the papilla. The pelvicalyceal mucosa is hyperemic or covered with a fibrinopurulent exudate.
· Histologically: the neutrophilic infiltration is limited to the interstitial tissue. Some tubules destroyed: abscesses formed; other tubules filled by puss cells. Glomeruli usually unaffected.
· Clinical features. Classically, acute pyelonephritis has an acute onset with chills, fever, loin pain, lumbar tenderness, dysuria and frequency of micturition. Urine will show bacteria, pus cells and pus cell casts in the urinary sediment.
· Three complications of acute PN are encountered in special circumstances.
- Papillary necrosis is seen mainly in diabetics and in those with urinary tract obstruction. Papillary necrosis is usually bilateral, but may be unilateral.
- Pyonephrosis is seen when there is total or almost complete obstruction, particularly when it is high in the urinary tract (pelvis filled with puss).
- Perinephric abscess implies extension of suppurative inflammation through the renal capsule into the perinephric tissue.
· At the acute phase of PN, healing occurs. The neutrophilic infiltration is replaced by macrophages, plasma cells, and (later) lymphocytes. The inflammatory foci are eventually replaced by scars. The pyelonephritic scar is almost always associated with inflammation, fibrosis, and deformation of the underlying calyx and pelvis.
· Uncomplicated acute PN usually follows a benign course, and the symptoms disappear within a few days after the institution of appropriate antibiotic therapy. In the presence of unrelieved urinary obstruction, diabetes mellitus acute PN may be more serious, leading to repeated septicemic episodes.
Chronic Pyelonephritis (CPN)
Chronic PN is a chronic tubulointerstitial renal disorder in which chronic tubulointerstitial inflammation and renal scarring are associated with pathologic involvement of the calyces and pelvis.
Two types of chronic pyelonephritis are described:
· Reflux nephropathy. Reflux of urine from the bladder into one or both the ureters during micturition is the major cause of chronic pyelonephritis. Vesicoureteric reflux is particularly common in children, especially in girls, due to congenital absence or shortening of the intravesical portion of the ureter so that ureter is not compressed during the act of micturition. Reflux results in increase in pressure in the renal pelvis so that the urine is forced into renal tubules, which are eventually followed by damage to the kidney and scar formation.
· Obstructive pyelonephritis. Obstruction to the outflow of urine at different levels predisposes the kidney to infection. Recurrent episodes of such obstruction and infection result in renal damage and scarring.
· Gross examination. The kidneys are usually small and contracted (weighing less than 100 gm) showing unequal reduction; if bilateral, the involvement is asymmetric. The surface of the kidney is irregularly scarred; the capsule can be stripped off with difficulty due to adherence to scars. There is generally dilatation of pelvis and blunted calyces. This contrasts with chronic glomerulonephritis, in which the kidneys are diffusely and symmetrically scarred.
· The microscopic changes involve predominantly tubules and interstitium.
· The tubules show atrophy in some areas and hypertrophy in others, or dilatation. Dilated tubules may be filled with colloid crystals, producing thyroidisation of tubules (thyroid-like).
· Interstitium. There is chronic interstitial inflammatory reaction, chiefly composed of lymphocytes, plasma cells and macrophages with pronounced interstitial fibrosis. Xanthogranulomatous pyelonephritis is an uncommon variant characterised by collection of foamy macrophages admixed with other inflammatory cells and giant cells.
· Pelvicalyceal system. The renal pelvis and calyces are dilated. And show marked chronic inflammation and fibrosis.
· Blood vessels. Blood vessels entrapped in the scarred areas show obliterative endarteritis.
· Glomeruli. There is often periglomerular fibrosis. In advanced cases, there may be hyalinisation of glomeruli.
· Clinical features. Chronic pyelonephritis often has an insidious onset. The patients present with clinical picture of chronic renal failure or with symptoms of hypertension.
· Chronic obstructive PN may be insidious in onset or may present the clinical manifestations of acute recurrent PN with back pain, fever, frequent pyuria, and bacteriuria.
Infections of the lower urinary tract
· Infections in the lower urinary tract are predisposed by obstruction and stasis.
· Lower urinary tract infection is usually due to Gram-negative coliform bacilli, e.g. E. coli and Proteus, which are normally in the large bowel; because they have a short urethra, women are particularly prone to developing ascending infections.
· In men, lower urinary tract infection is usually associated with structural abnormalities of the lower urinary tract and stasis due to obstruction.
· Diabetes mellitus also predisposes to infection.
· The pelvicalyceal system is dark reddish brown as a result of acute inflammation of the usually smooth creamy mucosal lining due to bacterial infection.
· The kidney is also congested and some small scattered abscesses are present in the cortex and medulla (acute pyelonephritis).
· Obstruction of the drainage of urine from the kidney causes hydronephrosis.
· Obstruction, one of the most important consequences of disease of the lower urinary tract, may occur at any place in the tract: renal pelvis (calculi, tumors), pelviureteric junction (stricture, calculi, extrinsic compression), ureter (calculi, extrinsic compression -pregnancy, tumor, fibrosis), bladder (tumor, calculi); urethra (prostatic hyperplasia or carcinoma, urethral valves, urethral stricture).
· If obstruction occurs in the urethra, the bladder develops dilatation and secondary hypertrophy of muscle in its wall. This predisposes to development of out pouching of the bladder mucosa (diverticulae).
· If obstruction occurs in a ureter, there is dilatation of the ureter (megaureter), with progressive dilatation of the renal pelvicalyceal system, termed hydronephrosis. Fluid entering the collecting ducts cannot empty into the renal pelvis and there is intrarenal resorption of fluid. At this stage, if the obstruction is relieved, renal, function returns to normal. However, if obstruction persists, there is atrophy of renal tubules, glomerular hyalinization, and fibrosis. As an end-stage, the renal parenchyma becomes severely atrophic and renal function is permanently impaired.
· Urinary tract obstruction also predisposes to infection and stone formation.