Print Topic



Pyelonephritis in Small Animals


Kidney infection (pyelonephritis) is usually due to ascending bacteria, although hematogenous spread is possible. The organisms and predisposing causes are similar to those of bacterial cystitis. Renoliths and ureteroliths, which impede the normal flow of urine out of the renal pelvis, may be contributory. Animals at risk of pyelonephritis are the very young, the very old, the immunosuppressed, or those with inadequate urine-concentrating ability. In many instances, an underlying cause is not identified. Virulence factors associated with specific bacterial strains play a role in allowing colonization of the urothelium, especially with pyelonephritis caused by Escherichia coli. The fact that pyelonephritis is usually ascending and bilateral suggests that these virulence factors are more important than previously recognized.

Animals with acute pyelonephritis may exhibit kidney or flank pain, fever, malaise, and sometimes vomiting, polyuria, and polydipsia. Urinalysis shows proteinuria, pyuria, bacteriuria, and/or hematuria. WBC casts may be present in fresh urine sediment. The urine culture is usually positive; the CBC may show leukocytosis with a left shift. The biochemical profile may be normal or show azotemia (prerenal or renal) and/or hyperglobulinemia. The animal may be in kidney failure. Chronic pyelonephritis is more difficult to recognize, because clinical signs may be subtle or absent. Polyuria and polydipsia are frequent. In many cases, the disease goes unrecognized until kidney failure occurs. Although abnormalities in the urinalysis are present, they are often less dramatic than with acute kidney infection. A single urine culture can be negative if bacterial numbers are low. Other useful diagnostic tests include abdominal ultrasonography and IV pyelography. Both studies may show dilation of one or both renal pelvises secondary to inflammation and partial obstruction. Asymmetric renal size and architectural changes with renal pelvic dilatation is highly suggestive of chronic pyelonephritis. In some cases, nephropyelocentesis via ultrasonographic guidance is useful to obtain a sample of urine from the dilated renal pelvis for analysis and culture.

Pyelonephritis should be treated aggressively with broad-spectrum antibiotics, based on urine culture and antimicrobial susceptibility testing, for 4–8 wk. The infection may respond to the same antibiotics recommended for cystitis, but more frequent administration (eg, amoxicillin tid rather than bid) and/or higher dosages are indicated. A fluoroquinolone or a combination of a fluoroquinolone with a β-lactam antibiotic is often effective. Dosages should be the same as for other soft-tissue infections. Animals that are febrile, anorectic, dehydrated, or azotemic should be hospitalized to provide IV antibiotics and fluid therapy. Fluid therapy may prevent acute pyelonephritis from progressing to azotemic acute kidney injury and will improve renal perfusion and uremic signs in animals already experiencing uremia. Animals with acute pyelonephritis may recover normal renal function, depending on the amount of damage that occurred before treatment. In cases of chronic pyelonephritis with a severely hydronephrotic, nonfunctional kidney, a nephrectomy may be the treatment of choice once the animal has been stabilized. This will remove the source of infection and hopefully save the opposite kidney. IV pyelography and/or renal scintigraphy are useful to assess the relative function of each kidney. If both kidneys are severely affected, medical management alone is the only alternative. Recovery to chronic, stable renal failure is possible in many cases.

The urine should be cultured during the first 5–7 days of therapy to assess antibiotic efficacy. A urinalysis and culture should be repeated 3–7 days after therapy, and then monthly for 3 consecutive months. If all of these cultures are negative, the interval between urine cultures may be gradually lengthened. Animals with pyelonephritis are at high risk of persistence or recurrence of infection and for secondary infections at other sites (eg, bacterial endocarditis and discospondylitis).

Last full review/revision September 2015 by Scott A. Brown, VMD, PhD, DACVIM

Copyright     © 2009-2015 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, N.J., U.S.A.    Privacy    Terms of Use    Permissions