The sick kidney: ARF, CRF, and everything in between
DENVER, CO − Renal disease is commonly encountered in veterinary practice. Animals with acute renal disease will require intensive medical care, while those with chronic renal disease typically require long-term care and significant owner compliance, explained David Liss, RVT, VTS (ECC), presenting at the American College of Veterinary Internal Medicine (ACVIM) Forum. With a greater understanding of the types of renal disease, diagnostic tests, and available treatments, veterinary technicians will be better prepared to administer optimal nursing care to patients with renal disease.
Anatomy and physiology
The kidney is located in the retroperitoneal space in the latter two thirds of the abdomen. It has one artery and one vein, so blood supply to each nephron, the individual cellular unit of the kidney, relies on the patency and continuity of flow. Should cardiac output drop suddenly for any reason, the kidney’s perfusion could be highly compromised. Mr. Liss said that this is why monitoring blood pressure under anesthesia is very important. The kidneys are able to independently manage their own blood pressure at a range of blood pressures, with 60-160 mmHg a preferred range. Below 60mmHg the kidneys cannot perfuse themselves adequately and anything above 160mmHg can cause renal damage.
Types of renal disease
Renal insufficiency represents more than 70% loss of nephrons for azotemia to develop, but does not necessarily manifest as a clinical syndrome. Renal failure means a syndrome of either acute or chronic nature, causing uremia, acid/base disturbances, and abnormal fluid balance. Acute renal failure is a sudden decline in glomerular filtration rate (GFR), which is potentially reversible. Chronic renal failure (CRF), which is not reversible, is a slower process of destruction of healthy renal tissue. Acute or chronic renal failure represents a sudden decline in GFR associated with pre-existing renal disease.
Table 1. Various forms of renal disease
Various forms of renal disease
|
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| Disease | Part of the nephron | Acute or chronic |
| Glomerulonephritis |
Glomerulus | Can be acute, usually chronic |
| Acute tubular necrosis | Tubules | Acute |
| Intersitial nephritis | Interstitium | Chronic |
| Amyloidosis | Glomerulus | Chronic |
| Toxicity: ethylene glycol | Tubules | Acute |
| Toxicity: lilies/grapes/raisins | Interstitium | Acute |
| Pyelonephritis | Interstitium +/- tubules | Acute |
| Aminoglycoside toxicity | Tubules | Acute |
Effort is often made to clarify the type of renal failure as diagnosis can be challenging. For example, if a patient has azotemia that is renal in origin, they will have intrinsic renal failure as opposed to a renal failure caused by a vascular or extra-renal event.
Presentation
Animals with renal failure may present with a history of anorexia, weight loss, vomiting, or diarrhea. They may have ingested a known toxin, or may have been potentially exposed to in the home. They may also be polyuric and/or or polydipsic. Initial interventions include a full history and physical exam.
Diagnostics
A full set of laboratory tests should be run including chemistry, CBC, PCV/TS, venous blood gas, and a urinalysis.
Chemistry results may reveal azotemia, which is characterized by an increase in nitrogenous waste products, namely BUN and creatinine. Azotemia can be pre-renal, renal, or post-renal; a urine specific gravity will help differentiate between the three.
Table 2 Classification of azotemia
Types of Azotemia |
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| Type of azotemia |
USG results | Patient condition |
| Pre-renal | Concentrated <1.030 |
Patient is dehydrated or hypovolemic. This results in a decline in GFR as the body preserves fluids for vascular volume. |
| Renal | Isosthenuric 1.007-1.012 | If patient is dehydrated/hypovolemic the kidneys are not doing their job and concentrating urine. Remember that when the animal is dehydrated, urine should be concentrated, meaning more water is retained. The urine is the same USG as plasma, meaning it is being excreted without any water retention. |
| Post-renal | Varies: usually concentrated | Hard to diagnose post-renal azotemia from USG but if any evidence of obstruction is present, this would result in a post-renal azotemia. |
Additional workup options include ultrasound with fine needle aspirate and cytology, leptospirosis titres (acute), ethylene glycol tests (acute), and tick borne disease titres (acute and/or chronic). All patients should also have baseline blood pressures as many of these patients are hypertensive.
Treatment − acute
Treatment of the ARF patient is very labour intensive, and involves administering fluids via a peripheral IV catheter, continuous patient monitoring, nutrition, and prompt treatment of sequelae. Any intravascular volume deficits should be addressed immediately using fluid boluses. After volume replacement hydration, maintenance and urine production should be addressed. A central line may be an option for CVP monitoring. The animal should have regular blood pressure monitoring, and a urinary catheter to monitor urine output. Potential volume overload can be detected with an increase in weight after hydration, elevated blood pressures, CVPs, or decreased urine output. Urine output should be 1-2ml/kg/hr on maintenance fluids. If the patient is polyuric, fluids should be increased to meet demand, and if anuric, fluids slowed to prevent iatrogenic fluid overload. Broad spectrum antibiotics should be initiated to prevent a potential infectious process. Life-threatening electrolyte disturbances (hyperkalemia and hypocalcemia) should be addressed with insulin or glucose, and/or parenteral calcium. If the patient is hypokalemic, potassium should be added to the fluids.
Early nutrition is also important in the renal failure patient. Acid-base abnormalities, typically metabolic acidosis, will often resolve or improve with fluid therapy. Sodium bicarbonate therapy is only reserved for life threatening acidemia. These patients should receive stress ulcer prophylaxis, including an H2 blocker and/or a proton pump inhibitor (omeprazole or pantoprazole). Because emesis can be caused by uremia, a centrally acting anti-emetic may be necessary. Metoclopramide, maropitant or ondansetron/dolasetron are efficient in managing emesis in these patients. Hyperphosphatemia can cause nausea, so phosphorus binders (aluminum hydroxide) should be given if the patient can tolerate enteral medication. If the patient is anemic, blood transfusion may be necessary. Renal function should be assessed with fluid therapy; if the patient decompensates into oliguria or anuria, dialysis should be considered, and the patient should be monitored for fluid overload as well. This can manifest as chemosis, peripheral edema, tachypnea, hypoxemia, and/or pulmonary edema. Constant auscultation of the lungs may help prevent the development of wet lungs.
Treatment − chronic
Patients hospitalized for chronic renal failure should receive the same level of monitoring as an acute renal failure patient with the addition of monitoring for anemia. Some patients compensate well for anemia, but others may require a transfusion. Mr. Liss stressed that the decision to transfuse is not always easy and should not be based solely on the PCV values. These patients may also have GI blood loss as uremia affects platelet function and predisposes to gastric ulceration. Chronic renal failure patients are typically hypokalemic and should receive potassium supplementation. The philosophy of treatment with chronic cases is to treat the acute crisis and then focus on long-term management. Nutritional support may be necessary in the form of an E-tube, PEG tube or other longer term feeding device. Low protein and phosphorus diets truly slow progression of the disease and enhance survival. Hypertension should be managed typically with calcium channel blockers, and proteinuria managed with ACE inhibitors.
Prognosis
For chronic renal failure, prognosis depends on the severity of the disease. With mild-moderate disease (creatinine <3-5 mg/dL) survival is 1-3 years. Proteinuria and hypertension are negative survival indicators. With ARF, mortality is about 60%; two-thirds of the patients that survive ARF will have some degree of chronic renal failure.
In summary, renal disease affects dogs and cats alike, both of which can have a
myriad of symptoms. Understanding the mechanism behind the disease and its sequelae
can have a profound influence on patient outcome. Technicians should be
familiar with
the kidney and its function, common renal diseases, and the nursing
interventions that
should be implemented. Renal disease also can have a prolonged
course and
technicians are vital to ensuring effective client communication and compliance. CVT
