Abstract
The field of feline nephrology and urology has experienced exponential growth over the past several years. Advanced treatment for both chronic and acute disease is no longer limited to a select few institutions, but is available worldwide. The number of veterinary hemodialysis units is at an all-time high, and individuals specially trained in endoscopic, radiologic and surgical urologic interventions are emerging in all parts of the world.
Fluid therapy for kidney disease: ‘just enough, but not too much’ should be the goal
Along with the rapid advancement of knowledge and technical skill in this field, there is an increasing demand from the public for access to these treatments. Therefore, it is our responsibility as veterinarians not only to provide our clients with access to these treatments, but to obtain the knowledge necessary to advise clients of the benefits, risks and suitability of our patients as candidates for these treatments.
As new treatments emerge, we must also critically re-evaluate long-standing treatment practices for kidney disease that are challenged by recent evidence presented in both the human and veterinary literature. Intravenous fluid therapy has long been considered the cornerstone of treatment for acute kidney injury (AKI). However, misconceptions abound regarding the role of fluid therapy in improving kidney function, particularly glomerular filtration rate (GFR). No evidence exists in the human or animal literature supporting the notion that aggressive intravenous fluid therapy can promote the rate of excretion of uremic solutes beyond that which can be achieved by restoration of normal physiologic perfusion parameters. Nonetheless, it is common practice to prescribe high intravenous fluid rates with the goal of promoting a uremic solute diuresis. Oftentimes, veterinarians attribute a modest decline in serum or plasma creatinine concentrations to an improved GFR, when a more likely cause of the ‘improvement’ is a dilutional effect from fluid accumulation and overload. A large body of evidence exists in the human literature that documents the negative effect of aggressive fluid therapy and subsequent fluid overload on not only survival, but length of hospital stay and secondary endpoints such as oxygenation status.
While it would be inappropriate for the pendulum to swing to withholding necessary fluid therapy, a happy medium of ‘just enough, but not too much,’ based on careful and repeated physical examination of the patient in conjunction with critical evaluation of objective patient data, should be our goal.
In recent years, the definitions of AKI have evolved to recognize that even modest increases in serum or plasma creatinine concentrations represent significant kidney damage. Even if overt azotemia is not present, these frequently overlooked increases have been associated with greater morbidity and mortality in many human and veterinary studies. While creatinine is not an ideal measurement of kidney function, it is the most readily available and frequently used biomarker. Therefore, this association is of great clinical importance.
In a two-part article by Kelly Monaghan and colleagues in this issue of JFMS the current understanding of AKI in cats is extensively reviewed.1,2 Katrien Debruyn and colleagues review the use and interpretation of renal ultrasonography in the entire gamut of feline kidney disease. 3 These articles will certainly help prepare the clinician for addressing this critical area of feline medicine.
Nephrology, Urology, and Dialysis Unit, Animal Medical Center, New York