• nonspecific bacterial infection of the kidney
  • can affect parenchyma, pelvis, and calyces
  • most common organism: E. coli
  • urinary tract obstruction may or may not be present

Routes of bacterial invasion

1.     spread from the outside – in

  • contamination of the bladder and ureters may spread to the kidney
  • bladder infection is common in females – short urethra

2.     Bloodstream

  • not very frequent
  • S. aureus
  • pyelonephritis is found sometimes in cases of bacterial endocarditis and as part of bacteremia from boils or carbuncles

3.     Lymphatic

  • not much evidence here, but it is postulated

Contributing factors in pyelonephritis

1.     Urinary tract obstruction

  • alone doesn’t cause pyelonephritis
  • frequency of urinary tract infection is much higher in the presence of obstruction
  • Causes: stones, urethral structures, prostatic hypertrophy, tumors, congenital valves of posterior urethra

2.     Vesicoureteral reflux

  • vesicoureteral valve becomes incompetent (usu. very very competent)
  • Conditions: cystitis
  • congenital abnormality
  • paraplegia
  • more

3.     Calyx-tubular reflux

  • reflux of urine from the calyx to the renal tubules
  • can produce scars identical to chronic pyelonephritis
  • failure of mechanism (valvular) that normally prevents calyx-tubular reflux

4.     instrumentation of the urinary tract

5.     age and sex

6.     vulnerability of the renal medulla to infection

7.     diabetes mellitus

Acute Pyelonephritis

  • Gross
  1. enlarged and bulging
  2. small raised abscesses on surface and throughout the parenchyma
  3. maybe perinephric abscesses
  4. congested pelvic mucosa
  5. calyces widened and papillae blunted
  6. necrosis of the papillae
  1. acute inflammatory cell (neutrophils) infiltration of the interstitium
  2. renal tubule destruction
  3. acute inflammatory cells present within the tubules
  4. pelvis and calyces show acute inflammation
  5. some large areas of the kindey may appear unaffected
  6. abscesses may be seen

Chronic Pyelonephritis

  • Gross
  1. can be bi, uni, or segmental involvement
  2. affected region shows scarring and atrophy
  3. surface shows large shallow scars
  4. some cases – pelvis and calyces and ureter are dilated
  • Micro
  1. chronic inflammation of the calyces and pelvis
  2. interstitial fibrosis
  3. tubular atrophy
  4. chronic inflammation in the parenchyma
  5. hyaline casts (eosinophilic) in the lumen of tubules
  6. glomeruli: periglomerular fibrosis and atrophy of glomerular tuft
  7. maybe some thickening of BV walls (esp if HTN)

Interstitial Nephritis (Types)

Analgesic abuse nephropathy

  • Bilateral chronic interstitial nephritis & renal papillary necrosis in those that have taken large quantities in combination of analgesics over an extended period of time
  • papillary necrosis occurs first
  • cortical tubulointerstitial inflammation and fibrosis later
  • may lead to end stage renal disease

Balkan Nephritis

  • chronic interstitial nephritis
  • common in Yugoslavia and Bulgaria
  • progressed to uremia
  • characterized by chronic interstitial inflammation, interstitial fibrosis and tubular atrophy
  • NEPHROTOXIN is suspected; none identified yet
  • higher incidence of transitional cell carcinoma

Acute Interstitial Nephritis

  • Drug hypersensitivity: sulfonamide, diphenylhydantoin, and methicillin
  • accompanied by fever, rash, eosinophilia, and acute renal failure
  • Renal biopsy
  1. lymphocytes, plasma cells, eosinophils, histiocytes, and neutrophils
  2. edematous interstitial stroma
  • immunologically mediated – rejection, lupus, other GN
  • Radiation nephritis

Tubular Diseases (Types)

Acute Tubular Necrosis

  • excellent recovery if patient can stand initial period of disease because the tubules have a regenerative capicity
  • Associated with a number of diseases
  1. Toxic Acute Tubular Necrosis
  • Poisons: mercury chloride, CCL4, ethylene glycol, phosphorus, and certain insecticides
  • Sulfonamide polymyxin, amphotericin B, barbituates, salicylates
  • Micro:

1.     necrosis of the epithelium of the renal tubules

2.     necrotic debris in the lumen

3.     dystrophic calcification may be seen

4.     tubular basement membranes are generally preserved (it is here that the new epithelial cells may be seen regenerating)

  1. Ischemic Acute Tubular Necrosis
  • common underlying feature is renal vasoconstriction
  • Causes: dehydration, hypovolemia, shock renal arterial vasoconstriction, severe bacterial infections, massive burns w/ hemolysis of RBCs, massive srushing injury which releases massive myoglobin from muscle.
  • Gross:

1.     kidneys swollen

2.     pale cortex and darker medulla w/ accentuated striation

  • Micro:

1.     focal tubular necrosis

2.     tubule dilated w/ flattened cells

3.     brownish or granular redish casts

4.     BM disrupted

5.     tubular epithelium degenerating

6.     interstitial edema

7.     focal tubular regeneration

Other Tubular Changes/Diseases

  • Hydropic change (Osmotic nephrosis)
  • Fatty change
  • Hypokalemic nephropathy
  • Chronic tubular disease
  • Primary functional defects of the tubules
  • Myeloma Kidney