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Hydronephrosis / hydroureter

ISSN 2398-2950

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Introduction

  • Cause: obstruction at level of renal pelvis (hydronephrosis) or ureter (hydroureter with possible hydronephrosis)   →   causes rapid deterioration of function of the affected kidney.
  • Signs: pyelonephritis, acute or chronic renal failure, may be no clinical signs if unilateral.
  • Diagnosis: contrast radiography, ultrasound.
  • Treatment: symptomatic for infection, ureteronephrectomy in advanced cases.
  • Prognosis: if treated early enough, renal function may still be intact   →   ureteral function may return to normal.

Presenting signs

  • Asymptomatic.
  • Sublumbar abdominal pain.
  • Hematuria +/- pyuria.
  • Anuria, eg if both ureters ligated.

Acute presentation

Special risks

Pathogenesis

Etiology

  • Urolithiasis Urolithiasis.
  • Iatrogenic: ligation of ureter during ovariohysterectomy, complication after surgical correction of ectopic ureter, complication after neoureterostomy for renal transplantation.
  • Renal Kidney: neoplasia, ureteral Ureter: neoplasia, bladder Bladder: neoplasia, or peri-ureteral neoplasia.
  • Trauma.
  • Ectopic ureter Ureter: ectopic.
  • Intraluminal blood clot within renal pelvis or ureter.
  • Congenital ureteral stricture, or stricture post-injection/trauma/urolithiasis.
  • Retroperitoneal fibrosis.
  • Ureterocele.

Pathophysiology

  • Obstruction at level of the renal pelvis or ureter   →   obstruction of normal urine flow   →   back pressure on kidney and ureter   →   dilation of renal pelvis and ureter proximal of obstruction   →   initially reversible decrease in functional glomerular filtration rate   →   followed by structural damage to the affected kidney and irreversible tubule damage. Post-renal failure if both kidneys affected.
  • Stasis of urine   →   predisposes to urinary tract infection Feline lower urinary tract disease (FLUTD) and urolithiasis Urolithiasis (especially struvite).
  • Increased renin production by acutely obstructed kidney   →   hypertension Hypertension (not in chronic cases).
  • Damage to interstitial cells   →   reduced erythropoietin production   →   anemia (chronic cases).

Timecourse

  • If unilaterally affected: complete failure of the kidney once complete obstruction has been present for 4 weeks.
  • If bilaterally affected: metabolic acidosis and hyperkalemia due to post renal failure   →   cat will die if untreated within days.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers