Pyelonephritis

Overview

Infective tubulointerstitial kidney disease — Acute (suppurative) vs Chronic (scarring, repeated episodes) — different mechanism/morphology, shared bacterial etiology.

Acute pyelonephritis

Acute suppurative inflammation, pyogenic bacteria, usually follows LOWER UTI.

Etiopathogenesis: E. coli ~90%, then Enterobacter/Klebsiella/Pseudomonas/Proteus.

2 routes:

1. Ascending (COMMONEST) — colonic organisms contaminate urethra, esp. reproductive-age females (short urethra, hormonal effects, no prostatic antibacterial secretions, intercourse trauma = “honeymoon pyelitis”). ↑Susceptibility: diabetes, pregnancy, obstruction, instrumentation. Bladder multiplication (±asymptomatic bacteriuria) → ascends against flow → pelvis/cortex. VESICOURETERIC REFLUX NOT significant in ACUTE (unlike chronic).
2. Haematogenous — less common, more with obstruction/debility/immunosuppression.

Morphology: Gross — enlarged/swollen, cortical yellow-white abscesses+haemorrhagic rim. Micro — acute interstitial inflammation destroying tubules, neutrophils burst into tubules or form abscesses. GLOMERULI+VESSELS SPARED (key discriminator from GN).

Clinical: acute chills/fever/loin pain/lumbar tenderness/dysuria/frequency. Urine: bacteria, pus cells, PUS CELL CASTS. Culture-guided antibiotics → resolution in most.

Complications (more with diabetes/obstruction):

1. Papillary necrosis — also in analgesic abuse/sickle cell. Necrotic papillae resemble infarction; coagulative necrosis + dense neutrophil zone
2. Pyonephrosis — extensive undrainable abscesses (esp. with obstruction) → multilocular pus sac (“renal carbuncle”)
3. Perinephric abscess — extends through capsule

Chronic pyelonephritis

Chronic tubulointerstitial disease, repeated inflammation+scarring — mechanistically DISTINCT from acute (not just unresolved acute). 2 mechanisms:

1. Reflux nephropathy (MAJOR cause) — vesicoureteric reflux (esp. children, girls — congenital short/absent intravesical ureter segment, not compressed on micturition). ↑Pelvic pressure → forces urine into tubules (intrarenal reflux) → damage+scarring. More with UTI but sterile urine reflux alone can also damage.
2. Obstructive pyelonephritis — outflow obstruction at any level → predisposes infection → recurrent episodes → damage+scarring. Rarely recurrent acute attacks alone.

Morphology: Gross — small contracted (<100g), UNEQUALLY/asymmetrically reduced (distinguishes from other contracted kidney causes), irregular scars, U-SHAPED cortical depressions, calyectasis+dilated pelvis.

Micro:

• Interstitium: chronic infiltrate (lymphocytes/plasma cells/macrophages)+fibrosis. Xanthogranulomatous variant (uncommon): foamy macrophages+giant cells
• Tubules: atrophy+dilatation, colloid casts = “THYROIDISATION” appearance
• Pelvicalyceal system: dilated, chronic inflammation/fibrosis, lymphoid follicles, squamous metaplasia
• Vessels: obliterative endarteritis in scars, ±hypertensive arteriolosclerosis
• Glomeruli: tuft usually intact but PERIGLOMERULAR FIBROSIS; advanced = hyalinisation

Clinical: often insidious — CRF or HTN presentation, or acute recurrent picture (fever/loin pain/dysuria/pyuria/bacteriuria/frequency). Dx: IVP. Longstanding → secondary systemic amyloidosis (same mechanism as bronchiectasis/lung abscess).

Clinical relevance

Glomerulus+vessel sparing in acute pyelonephritis (vs GN’s primary glomerular targeting) = key discriminator, direct mirror image — acute pyelonephritis is interstitial/tubular disease, glomerulus is bystander. Asymmetric contraction of chronic pyelonephritic kidney (vs symmetric in chronic GN/benign nephrosclerosis) = reliable gross discriminator among small-contracted-kidney causes — don’t lump together. Reflux nephropathy mechanism (intrarenal reflux, raised pelvic pressure) explains why scars characteristically involve renal POLES (papillae structurally more reflux-susceptible there) — anatomic distribution follows directly from mechanism. Tubular “thyroidisation” = distinctive testable finding — colloid-cast-filled dilated tubules can genuinely resemble thyroid follicles, correct context essential.

Overview

Pyelonephritis is infective tubulointerstitial disease of the kidney, spanning acute (suppurative) and chronic (scarring, from repeated episodes) forms — genuinely different diseases in mechanism and morphology, unified by shared bacterial etiology.

Acute Pyelonephritis

Acute suppurative inflammation of the kidney from pyogenic bacteria, most often following lower urinary tract infection.

Etiopathogenesis

Organism: E. coli causes ~90% of UTIs; Enterobacter, Klebsiella, Pseudomonas, Proteus follow in decreasing frequency.

Two routes of renal infection:

1. Ascending infection — the commonest route. Colonic organisms contaminate the urethral orifice, especially in reproductive-age females — attributed to their shorter urethra, hormonal effects facilitating bacterial mucosal adherence, absent antibacterial prostatic secretions, and urethral trauma during intercourse (“honeymoon pyelitis”). Susceptibility rises with diabetes mellitus, pregnancy, urinary obstruction, or instrumentation. Bacteria multiply in the bladder (often producing asymptomatic bacteriuria), then ascend against urine flow through the ureters into the renal pelvis and cortex. Notably, vesicoureteric reflux is not a significant factor in acute pyelonephritis (unlike chronic — see below).
2. Haematogenous infection — less common; more frequent with urinary tract obstruction or in debilitated/immunosuppressed patients.

Morphology

Gross: enlarged, swollen kidney bulging on section; cortical surface shows small yellow-white abscesses with a haemorrhagic rim.

Micro: extensive acute interstitial inflammation destroying tubules — neutrophils infiltrate the interstitium and burst into tubules, or form focal neutrophilic abscesses. Glomeruli and blood vessels are characteristically spared — a useful discriminator from glomerular disease.

Clinical Features

Acute onset: chills, fever, loin pain, lumbar tenderness, dysuria, urinary frequency. Urine: bacteria, pus cells, pus cell casts. Culture-guided antibiotics eradicate infection in most patients.

Complications (More Common with Diabetes or Obstruction)

1. Papillary necrosis (necrotising papillitis) — more classically associated with analgesic abuse nephropathy and sickle cell disease, but can complicate acute pyelonephritis; may be uni- or bilateral. Grossly, sharply-defined yellow/grey-white necrotic papillae with a congested border, resembling infarction; microscopically, coagulative necrosis (as in renal infarcts) separated from viable tissue by a dense neutrophil zone.
2. Pyonephrosis — extensive, undrainable abscesses (particularly with obstruction) transform the kidney into a multilocular pus-filled sac (“renal carbuncle”).
3. Perinephric abscess — extension through the renal capsule into perinephric tissue.

Chronic Pyelonephritis

A chronic tubulointerstitial disease from repeated inflammation and scarring — mechanistically distinct from acute pyelonephritis, not simply “acute pyelonephritis that didn’t resolve.” Two mechanisms:

1. Reflux nephropathy — the major cause. Vesicoureteric reflux (especially in children, particularly girls) from congenital absence/shortening of the intravesical ureteric segment, so the ureter isn’t compressed during micturition. Reflux raises renal pelvic pressure, forcing urine into renal tubules (“intrarenal reflux”), damaging the kidney and producing scars — more common with UTI (symptomatic or not), but sterile urine reflux alone can also cause damage.
2. Obstructive pyelonephritis — outflow obstruction at any level predisposes to infection; recurrent obstruction-plus-infection episodes cause damage and scarring. Rarely, recurrent acute pyelonephritis attacks alone produce this picture.

Morphology

Gross: small, contracted kidneys (<100 g), characteristically unequally/asymmetrically reduced (distinguishing it from other causes of contracted kidney, which shrink more uniformly); irregularly scarred surface with adherent capsule; scars produce characteristic U-shaped cortical depressions; calyceal blunting/dilatation (calyectasis) and dilated pelvis.

Micro:

• Interstitium: chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages) with marked fibrosis. An uncommon variant, xanthogranulomatous pyelonephritis, shows foamy macrophages admixed with other inflammatory cells and giant cells.
• Tubules: atrophy and dilatation; dilated tubules filled with eosinophilic colloid casts produce a “thyroidisation” appearance (resembling thyroid follicles).
• Pelvicalyceal system: dilated, with chronic inflammation/fibrosis of the walls; lymphoid follicles with germinal centres; epithelial squamous metaplasia.
• Vessels: obliterative endarteritis in scarred areas, ± hypertensive hyaline arteriolosclerosis.
• Glomeruli: tuft usually intact within scarred areas, but with periglomerular fibrosis; advanced disease shows glomerular hyalinisation.

Clinical Features

Often insidious — presenting with chronic renal failure or hypertension, or sometimes with acute recurrent pyelonephritis features (fever, loin pain, dysuria, pyuria, bacteriuria, frequency). Diagnosed by intravenous pyelography (IVP). Longstanding disease can develop secondary systemic amyloidosis (the same chronic-inflammation-driven mechanism seen in Bronchiectasis and Lung Abscess).

Clinical Relevance

• The sparing of glomeruli and vessels in acute pyelonephritis, versus glomerulonephritis’s primary glomerular targeting, is a key discriminator worth holding in direct contrast — acute pyelonephritis is fundamentally an interstitial/tubular disease with the glomerulus as an innocent bystander, the mirror image of the primary GN entities.
• The asymmetric, unequal contraction of chronic pyelonephritic kidneys (versus the more symmetric contraction of chronic GN or benign nephrosclerosis) is a genuinely reliable gross discriminator between the major causes of a small contracted kidney — worth learning as a specific distinguishing feature rather than lumping all “small kidney” causes together.
• Reflux nephropathy’s mechanism (intrarenal reflux forcing urine into tubules under raised pelvic pressure) explains why the resulting scars characteristically involve the renal poles, where papillae are structurally more susceptible to reflux — the anatomic distribution of scarring is a direct consequence of the underlying mechanism, not random.
• Tubular “thyroidisation” is a distinctive, specific, testable histologic finding worth remembering by name — a chronic pyelonephritic kidney’s dilated colloid-cast-filled tubules can genuinely resemble thyroid follicles on cursory microscopy, making the correct histologic context essential to avoid misinterpretation.

• Ascending vs haematogenous infection routes to acute pyelonephritis
• Reflux nephropathy vs obstructive pyelonephritis: two mechanisms converging on chronic scarring
• Acute vs chronic pyelonephritis compared: morphology, mechanism, and clinical course