Chronic Renal Failure

Chapter 136 Chronic Renal Failure



Catherine E. Langston, DVM, DACVIM



KEY POINTS



• Chronic renal disease or failure (CRF) is one of the most common reasons for older cats to be presented to the veterinarian, but is also commonly seen in dogs and in young animals.

• Many drugs and therapies are available for management of CRF, but there is no cure. The goal of therapy is to slow progression and to improve the pet’s sense of well-being (quality of life).

• Dietary therapy decreases the number of uremic crises and decreases mortality. All pets with CRF should be encouraged to eat a renal diet if there are no contraindications (such as dietary allergies).

• As uremia progresses and the number of uremic complications increases, the number of medications to control complications increases. The nursing care involved may require a substantial time commitment from the owner.


INTRODUCTION


Chronic renal failure (CRF) is a common disease in cats and dogs. Because each nephron works as a unit, if the glomerulus is damaged irreversibly, the associated tubule will degenerate and vice versa. As nephrons are lost, the remaining nephrons hypertrophy. Although initially adaptive, glomerular hypertension damages the nephron, leading to further nephron loss. After a certain amount of damage has been sustained, renal failure may be progressive despite resolution of the initiating cause. As the renal damage progresses, azotemia develops, and eventually signs of uremia appear.



ETIOLOGY


The chronic lymphoplasmacytic interstitial nephritis that we see commonly, especially in older cats, is probably not a single entity, but the end result of any kind of renal insult. Differential diagnoses for CRF include tubulointerstitial nephritis, renal dysplasia (young animals), polycystic kidney disease (Persians, other longhair cats, less frequent in domestic shorthair cats), chronic pyelonephritis, nephrolithiasis or ureterolithiasis, infarction, lymphoma, glomerulonephritis, amyloidosis, and incomplete resolution of acute renal failure.1



EPIDEMIOLOGY


CRF can affect cats of any age but is more common in older cats. The incidence approaches 15% in cats over 15 years of age. Symptomatic cats tend to be older than asymptomatic cats (mean age 12.5 to 14.5 years versus 8.3 years).2 Although CRF occurs less commonly in dogs, the incidence also increases with age.



CLINICAL PRESENTATION



Asymptomatic


In some patients, mild and asymptomatic azotemia is discovered incidentally, perhaps in conjunction with geriatric or dental screening. The asymptomatic pet with very mild elevations in blood urea nitrogen (BUN) or creatinine, that is maintaining body weight and appropriate hydration, may not need treatment other than diet, although routine monitoring is indicated.



Symptomatic


Mild clinical sings may be present for months to years (especially polyuria, polydipsia, and weight loss) before examination. In pets presented for evaluation because of early signs of renal failure, outpatient management is usually sufficient without the need for a hospital stay. A markedly dehydrated pet with severe uremic syndrome that has decompensated will likely need hospitalization for intensive therapy, including intravenous (IV) fluid administration. Once the uremic crisis is controlled, however, continued treatment at home will help delay another crisis.


Common signs include polyuria and polydipsia, weight loss, anorexia, vomiting, lethargy or depression, halitosis, dysphagia or oral discomfort, and weakness. Common physical examination findings include thin body, dehydration, abnormal kidney size or shape, heart murmur, oral ulceration, gingivitis, halitosis, hypothermia, and pale mucous membranes. Severely affected animals may suffer from altered consciousness, seizures, or bleeding problems, or be moribund.



DIAGNOSIS


The combination of historical and physical examination findings frequently leads to a clinical suspicion of CRF. Diagnostic evaluation can confirm the diagnosis, occasionally indicate the underlying cause, and detect uremic complications.



Laboratory Testing


Common laboratory abnormalities include azotemia, hyperphosphatemia, hypokalemia, metabolic acidosis, and hypercalcemia or hypocalcemia, although the ionized calcium level usually is normal.


Lack of erythropoietin, a hematopoietic hormone, leads to a nonregenerative anemia. Chronic inflammation or iron deficiency from chronic gastrointestinal (GI) blood loss may contribute. Some animals have an acute anemia (that may be partially regenerative) from acute blood loss from GI ulceration. The platelet count is usually normal, although platelet function may be impaired with uremia. A buccal mucosal bleeding time may be prolonged, but coagulation panel (prothrombin time and partial thromboplastin time) results are expected to be normal.


Poorly concentrated urine (urine specific gravity <1.035 in cats, <1.030 in dogs) with azotemia in the absence of urinary obstruction defines CRF. Active urine sedimentation (white blood cells, red blood cells, bacteria) may indicate urinary tract infection as a cause or consequence of CRF. A positive urine culture result may indicate pyelonephritis, although a negative urine culture result does not eliminate pyelonephritis as a cause of CRF. Routine urine culture is recommended even in the absence of lower urinary tract signs or active urine sedimentation because cats with CRF may have silent urinary tract infections. The urine protein-to-creatinine ratio is usually normal (<0.5) in cats with CRF, and varies in dogs depending on the inciting cause. Microalbuminuria indicates renal damage but is not specific for cause, whether primary or secondary. The role of microalbuminuria in monitoring or treating CRF is not yet established.



Imaging


Abdominal radiographs may show abnormal kidney size or shape. Approximately 33% of cats with CRF have small kidneys, 33% have normal-sized kidneys, and 33% have large kidneys.3 Nephroliths or ureteroliths may be readily apparent, although renal function may be normal. It is also common for obstructing ureteroliths that are causing clinically significant renal damage to be smaller than the resolution limits of radiography.


Abdominal ultrasonography frequently reveals diminished renal architecture due to replacement of renal tissue with fibrosis. Other changes that may be readily identified include renal mineralization or nephroliths (although these may be missed on ultrasonography), hydronephrosis, polycystic kidney disease, and perinephric pseudocysts.



Other Diagnostic Modalities


Hypertension occurs in 20% to 30% of dogs and cats with CRF.4,5 Artifactually high blood pressure (“white coat hypertension”) may be minimized by measuring blood pressure before physical examination or other procedures and selecting a calm environment, with the owner present during measurement. Renal biopsy is indicated primarily for renomegaly to evaluate for lymphoma, feline infectious peritonitis, and early glomerulonephritis. Uremia increases the risk of bleeding due to platelet dysfunction. Measurement of glomerular filtration rate rarely is used when azotemia is present, although with the advent of clinically practical methods of measuring glomerular filtration rate (i.e., plasma iohexol clearance, plasma exogenous creatinine clearance), this test is being used more commonly to diagnose early renal disease. Parathyroid hormone concentration may be elevated if renal secondary hyperparathyroidism is present.



TREATMENT


Many drugs and therapies are available for treatment of CRF. The goal of therapy is to slow progression, to minimize hospitalization time, and to improve the pet’s sense of well-being (quality of life).



Hospitalized Patient


Decompensated cats (e.g., dehydrated, anorexic, vomiting) may benefit from hospitalization.



Fluid Therapy


Although subcutaneous fluid therapy is appropriate for outpatient treatment, the large volume of fluid required by animals in a uremic crisis mandates the intravenous route. A balanced polyionic fluid (i.e., lactated Ringer’s solution, Plasmalyte) is generally appropriate. The fluid deficit is calculated (% dehydration × body weight [kg] = volume of deficit in liters) and generally is replaced over 12 to 36 hours, although some situations may necessitate more rapid replacement (i.e., hemodynamic instability or collapse, uncertain urine production capability) or slower replacement (i.e., cardiac disease). In addition to replacing the fluid deficit, a maintenance rate (66 ml/kg q24h) of fluid administration should be added. If polyuria is dramatic or if there are significant other losses (such as vomiting), the fluid rate will have to be adjusted upward accordingly. If the patient is hydrated, give maintenance fluids plus 5% body weight per 24 hours to promote diuresis.


Once the prerenal component of the azotemia has resolved, the serum creatinine concentration will usually decrease by at least 1 mg/dl per day (monitored generally q48h). When the creatinine concentration reaches a baseline value (i.e., no longer decreasing despite IV fluid therapy), fluids should be tapered in preparation for patient discharge. Aggressive diuresis should be tapered gradually over about 2 to 3 days.

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  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Chronic Renal Failure

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