Can a dog recover from renal failure?
There are some significant differences between acute and chronic kidney failure. While many instances of acute kidney failure can be reversed if treated early and aggressively, chronic kidney failure can only be managed with consistent veterinary care.
Note: The advice provided in this post is intended for informational purposes and does not constitute medical advice regarding pets. For an accurate diagnosis of your pets condition, please make an appointment with your vet.
Treatment & Prognosis for Renal Failure in Dogs
Your veterinarian will perform diagnostic blood and urine tests to detect the presence of any abnormalities. While a diagnosis of renal disease or failure can usually be made based on physical examination, in addition to the blood and urine tests. Other tests may also be performed to check for underlying causes for renal disease and/or to discover which stage of renal disease your dog is experiencing.
Severity of symptoms will determine appropriate treatments, which may include IV fluids, though if the disease is extremely severe your pooch may not respond to treatment. Aggressive treatments may include hospitalization for fluid therapy, dialysis or a kidney transplant.
Keep in mind that chronic renal disease cannot be cured. Prognosis is associated with severity of disease. As your dog progresses through stages of renal disease, survival time is likely to grow shorter.
The treatments are intended to reduce the work the kidneys are required to perform, to replace substances such as potassium and to reduce accumulating wastes. Your dog’s initial response to conservative therapy may be relatively slow — it may take weeks or months to see progress. Your vet may also suggest changes in diet to improve your pet’s quality of life and potentially limit the progression of disease, leading to a longer lifespan.
THERAPEUTIC GOAL: Treat Acidemia
Feed a diet that produces a neutral pH, which prescription renal diets are designed to achieve (but not a feature of some urolithiasis diets). Use alkali therapy (Table 5) for patients with persistent acidemia despite appropriate diet. The goal is to maintain a bicarbonate (TCO2) level between 18 and 25 mmol/L.
While potassium citrate provides some potassium supplementation, which is beneficial to hypokalemic patients, it may exacerbate hyperkalemia in patients with normal or mildly increased serum potassium concentrations. In addition, angiotensin-converting enzyme inhibitor (ACE) inhibitor therapy may also result in mild to moderate hyperkalemia. Use potassium supplementation cautiously in patients receiving such medications, and avoid use in hyperkalemic patients.
Hypokalemia is more commonly seen in cats than in dogs. Severe hyperkalemia may be life threatening, and is more often associated with oliguric or anuric acute kidney injury, rather than CKD.
Patients with end-stage CKD and marked reduction in GFR may also demonstrate hyperkalemia, regardless of degree of urine output. By inhibiting the production of angiotensin II, which causes urinary potassium excretion, ACE inhibitor drugs may also produce mild to moderate hyperkalemia as a side effect.
Dr. Becker Discusses Chronic Kidney Failure in Pets
Chronic kidney disease (CKD) is an irreversible and progressive deterioration of renal function, resulting from a decreased number of functional nephrons. Unfortunately, the compensatory mechanisms that respond to nephron loss (glomerular hypertension, hyperfiltration) help facilitate progression of CKD, potentially contributing to it more so than the original injury (Table 1).
Patients of any age may develop CKD, but the greatest incidence is in geriatric patients. However, congenital renal diseases, including dysplasia and various glomerulopathies, may produce CKD at very early ages. Once diagnosed, CKD typically remains a life-long condition.
Editor’s Note: This article was originally published in November/December 2012. Please use this content for reference or educational purposes, but note that it is not being actively vetted after publication. For the most recent peer-reviewed content, see our issue archive.
Early signs of CKD may be mild, even inapparent to the pet owner. Because isosthenuria and azotemia do not develop until 66% and 75% nephron loss, respectively, most renal function has been lost by onset of clinical signs.
During a physical examination in patients with suspected or confirmed CKD, pay particular attention to body condition scoring, cardiovascular status, evidence of dehydration, and renal palpation.
A thorough diagnostic evaluation (Table 2) can confirm the diagnosis of CKD. These tests may identify underlying causes, ongoing renal injury, and consequences of CKD, providing information about prognosis and treatment goals.
Glomerular filtration rate (GFR) is the gold standard measurement of renal function; however, its measurement is rarely indicated in patients with CKD. Creatinine and, to a lesser extent, BUN are correlated with GFR, but, as noted earlier, GFR must be reduced by 75% before azotemia is seen. However, measurement of GFR (typically through iohexol or creatinine clearance testing) may confirm reduced renal function in isosthenuric patients.
A tiered stratification system has been proposed by the International Renal Interest Society (IRIS) to help provide guidelines for clinical management of CKD. Staging is based on serum creatinine values, with substages identified for blood pressure and proteinuria (Table 3).
Treatment goals and recommendations are specific to IRIS CKD stage. Since prerenal contributions will often increase the degree of azotemia to the next stage, normal renal perfusion (adequate patient hydration and effective circulating volume) should be restored before determining the patient’s stage of CKD.
Including the IRIS CKD stage in the medical record relays important information about the severity of CKD. For example, if a dog has a creatinine of 2.5 mg/dL, urine protein:creatinine (UPC) ratio of 1, and arterial blood pressure of 155 mm Hg, its IRIS CKD stage would be considered IRIS 3 P AP 1, or:
Treatment of CKD should be individually tailored to each patient. Although not all interventions have been evaluated by clinical trials, some evidence-based information supports their role in management of CKD. IRIS CKD stage management guidelines are listed in Table 4; medications to help achieve treatment goals are listed in Table 5.
As stated earlier, IRIS CKD staging should be applied to patients only after exclusion of pre- and postrenal contributions.
Uremic toxins, many of which are byproducts of protein metabolism, are solutes that accumulate due to decreased renal clearance, causing detrimental effects. Urea and creatinine are not significant uremic toxins; however, they serve as surrogate markers, providing some information on renal function and degree of uremic toxin retention.
As CKD is irreversible, decreased GFR caused by intrinsic renal dysfunction cannot be improved. Hypovolemic or dehydrated patients will have decreased renal perfusion, causing prerenal reduction in GFR, which is complicated if patients cannot voluntarily maintain hydration.
Measures should be taken to prophylactically maintain hydration in patients that cannot do so on their own (urine output exceeds fluid intake).