Acute and chronic pyelonephritis

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Acute and chronic pyelonephritis

Acute pyelonephritis

Definition: Bacterial infection of the renal parenchyma and pelvis. It is a suppurative inflammation of the kidney.
Etiology
  • E. coli causes about 80-85% of cases. Other causes are Klebsiella, Proteus, Enterobacter, Pseudomonas, and Enterococcus. Staphylococcus aureus is typical of hematogenous spread.
  • Proteus splits urea, which makes the urine alkaline and promotes struvite stones.
Routes of infection
  • Ascending (most common): Bacteria move from the urethra to the bladder, then up the ureter to the kidney. Vesicoureteral reflux and intrarenal reflux help this happen.
  • Hematogenous: This is uncommon. It occurs with septicemia or endocarditis, and with S. aureus or Candida.
Risk factors
  • Female sex (short urethra), pregnancy, and sexual activity.
  • Urinary obstruction: stones, BPH, strictures, tumors.
  • Vesicoureteral reflux and neurogenic bladder.
  • Catheterization or instrumentation.
  • Diabetes mellitus and immunosuppression.
Pathology
  • The kidney is enlarged and swollen. Yellow-white abscesses may be visible on the surface and the cut surface.
  • Histology shows patchy neutrophilic infiltrates in the interstitium and tubules. Neutrophil casts (WBC casts) form in the tubules.
  • Complications are:
    • Papillary necrosis, seen in diabetes, obstruction, sickle cell disease, and analgesic abuse.
    • Pyonephrosis, which is pus in an obstructed collecting system.
    • Perinephric abscess.
    • Emphysematous pyelonephritis, a gas-forming infection in diabetics.
    • Gram-negative sepsis.
Clinical features
  • Fever with chills, flank pain, and costovertebral angle tenderness.
  • Nausea and vomiting, plus dysuria, frequency, and urgency.
  • Leukocytosis.
  • Urinalysis: pyuria, bacteriuria, hematuria, and WBC casts, which point to a renal source.
Diagnosis
  • Urine culture (at least 10^5 CFU/mL classically) and blood cultures.
  • Imaging is not needed in uncomplicated cases. Use ultrasound or CT if there is no response by 48-72 hours, if there is sepsis, a stone, or suspected obstruction, or if the patient is diabetic or male.
Management
  • Mild, outpatient, uncomplicated:
    • A fluoroquinolone for 5-7 days, if local resistance is low.
    • Or oral beta-lactams or TMP-SMX for 10-14 days, guided by culture.
    • Many guidelines give a single initial IV dose of ceftriaxone.
  • Severe, vomiting, or sepsis: Admit and give IV therapy. Options are ceftriaxone, a fluoroquinolone, an aminoglycoside, or a carbapenem if ESBL is suspected. Switch to oral once afebrile for 24-48 hours, and treat for 7-14 days in total.
  • Pregnancy: Admit and give IV beta-lactams. Avoid fluoroquinolones.
  • Obstruction or abscess: Drain by ureteral stent, nephrostomy, or percutaneous drainage.
  • Treat the underlying cause, such as a stone or diabetes.

Chronic pyelonephritis

Definition: Chronic tubulointerstitial inflammation with coarse renal scarring that involves the calyces and pelvis. It is a common cause of end-stage renal disease.
Two forms
  1. Reflux nephropathy (more common):
    • It starts in early childhood with vesicoureteral reflux and recurrent UTIs.
    • Intrarenal reflux scars the kidney, usually at the upper and lower poles.
    • It can be unilateral or bilateral.
  2. Chronic obstructive pyelonephritis:
    • Obstruction (stones, BPH, strictures, congenital anomalies) causes recurrent infection and diffuse scarring.
    • It can be unilateral or bilateral.
Pathology
  • Gross: The kidneys are irregularly scarred, with coarse, asymmetric cortical scars that overlie blunted, deformed calyces. The scars are U-shaped depressions over dilated calyces. The pelvis is thickened.
  • Histology:
    • Chronic interstitial inflammation and fibrosis.
    • Atrophic tubules, some dilated and filled with eosinophilic colloid casts ("thyroidization").
    • Periglomerular fibrosis and eventual glomerulosclerosis.
    • Thickened arterioles from hypertension.
  • Secondary FSGS can develop from nephron loss and hyperfiltration. This causes proteinuria, sometimes in the nephrotic range.
Clinical features
  • Often silent. It may present with:
    • Hypertension.
    • Recurrent UTIs or flank pain.
    • Slowly progressive CKD with a tubular concentrating defect (polyuria, nocturia), metabolic acidosis, and salt wasting.
  • Proteinuria is mild to moderate.
Diagnosis
  • Imaging is key. Ultrasound or CT shows asymmetric small kidneys with cortical scars and calyceal blunting.
  • A DMSA scan is the best test for detecting scars.
  • A voiding cystourethrogram (VCUG) is used in children to look for reflux.
Management
  • Treat and prevent infection, correct reflux or obstruction, and control hypertension (ACE inhibitor or ARB).
  • Use renal protective measures and manage CKD, with dialysis or transplant for ESRD.

Related entity: xanthogranulomatous pyelonephritis

  • A rare, severe chronic form, usually from long-standing obstruction by a staghorn calculus with Proteus infection.
  • Lipid-laden (foamy) macrophages replace the parenchyma, so the kidney looks like a yellow mass that can mimic renal cell carcinoma.
  • Treatment is usually nephrectomy.

Key comparison

FeatureAcuteChronic
ProcessSuppurative neutrophilic infectionChronic interstitial inflammation and scarring
Typical patientAdult woman, any ageChild with reflux, or adult with obstruction
PresentationFever, flank pain, pyuriaSilent, hypertension, CKD
Key findingWBC castsCoarse scars with blunted calyces, thyroidization
OutcomeUsually resolves with treatmentProgressive loss of renal function
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