I still think we’re often flying by the seat of our pants when it comes to diagnosis, treatment, and long-term implications of tick-borne diseases.
Michelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at: firstname.lastname@example.org.
Yaretzi, a handsome eight-year-old golden retriever, had a pretty typical history for an Island dog when it comes to tick-borne diseases. Lyme-vaccinated as a puppy, he still got infected as a young dog, but we caught it early and treated him. At five, he once again tested positive for Lyme and also for another tick-borne disease, Anaplasmosis. Additional tests indicated he had been exposed, and made antibodies, but was probably not actively infected with organisms.
“We don’t really know what we’re talking about when it comes to these diseases,” I admitted to his owner. Maybe I exaggerate our ignorance. There’s plenty of erudite information published in veterinary journals and textbooks, but I still think we’re often flying by the seat of our pants when it comes to diagnosis, treatment, and long-term implications of tick-borne diseases.
The important thing was by eight years old, Yaretzi was testing negative again and feeling great. Except for one thing. “He drinks an awful lot of water,” his mom said.
Excessive drinking is technically called polydipsia. Excessive urination is polyuria. The two often go together. Medical folks just say “PU/PD.” When owners report polydipsia, the first thing we do is document it, by having them measure their pet’s water for 24 hours. A normal dog drinks between 20 and 70 milliliters per kilogram body weight per day. For a 30-kilo dog like Yaretzi, that’s roughly three to nine cups. Water consumption varies with exercise, salty foods, and hot weather. We don’t consider it true PD until a dog consistently drinks more than 100 milliliters per kilo daily. For Yaretzi, that’s almost 13 cups. Measuring total daily urine output, well, that’s harder to get owners to do. With true polyuria, urine is usually abnormally dilute.
Yaretzi’s daily water consumption measured borderline high. His urine, unusually dilute. His owner, exceptionally dedicated.
The list of possible causes for PU/PD is enormous. We began running tests. We ruled out diabetes and kidney failure. Endocrine tests ruled out underactive thyroid and the adrenal gland disorder called Cushing’s disease. His liver function proved normal with a bile acids test. Urine cultures ruled out bacterial infection. His white blood cell count was consistently low but we found no explanation for this. Yaretzi went to a specialist who repeated some tests, and added others. Ultrasound showed a few small nodules on his spleen, but the specialist thought these benign and unrelated to his PU/PD. More samples were collected to determine serum sodium level and osmolality, urine sodium fractional excretion and osmolality, and a urine protein: creatinine ratio.
Huh? What? Wait! Don’t turn the page! No more big words, I promise. Okay, maybe just a few. Protein-losing nephropathy (PLN) and diabetes insipidus (DI.) You need classes in pathophysiology and endocrinology to fully understand, but since you probably want to get to the beach, here’s the short version.
Kidneys are made up of thousands of tiny units called nephrons that filter the blood. The parts that do the filtering are called the glomeruli. These work like strainers, letting little molecules like electrolytes pass through, while keeping cells, and bigger molecules like proteins, in the blood. Other portions of the nephron then balance electrolytes and pH. When the glomeruli get injured, the holes in the strainer get too big. Stuff that is supposed to stay in the blood, like protein, leaks out into the urine. A little protein in the urine can be normal, which is why special tests beyond standard urinalysis are needed. Yaretzi had an elevated urine protein: creatinine ratio, confirming abnormal protein loss via the kidneys, i.e., PLN. Over time, dogs with PLN become protein-depleted. Usually this is evident on basic blood tests, but Yaretzi’s was apparently in the very early stages, and his blood protein levels still normal.
What causes PLN? Most cases are thought to be the result of chronic inflammation or infection. Here’s your short course in immunology. The immune system makes antibodies against foreign proteins (called antigens.) Antibodies stick to antigens. These antibody-antigen complexes get trapped in the glomerular membranes. The immune system attacks those trapped complexes, inadvertently damaging the glomeruli. This inflammatory condition is called glomerulonephritis (Oops, another big word). Underlying diseases that produce the antigens can be anything from chronic dental disease, to Lyme, to cancer. Another disease that can also damage glomeruli and lead to PLN is called amyloidosis. Definitive diagnosis of the cause of a case of PLN requires kidney biopsy, but we rarely recommend going to these lengths. Instead we treat any underlying problems identified and then just treat the symptoms.
“It sounds counterintuitive,” I said, “but he needs a low protein diet. I’m prescribing a medication that reduces protein loss through the kidneys, and low-dose aspirin to minimize risk of blood clots. Omega-3 fatty acids are also helpful. They’re already in the recommended prescription diet.”
Our last question was whether Yaretzi also had diabetes insipidus (DI), a rare disorder that occurs when the pituitary gland doesn’t make enough antidiuretic hormone (ADH) or when the kidneys themselves are unable to respond properly to ADH. Dogs with diabetes insipidus pass huge quantities of very dilute urine, then drink excessively to compensate. Once the specialist has all the final laboratory results back, we will test for DI by giving Yaretzi a small dose of synthetic ADH. If his kidneys are able to respond, his urine should become more concentrated, and he should drink and pee less, confirming the problem to be inadequate pituitary ADH production. We suspect, however, that the problem is in his kidneys, that whatever is causing his PLN also interferes with his kidneys responding properly to ADH.
A complicated case. We don’t have all the answers yet. Are those past episodes of tick-borne disease exposure implicated? Golden retrievers have a high incidence of cancer. Is there a tumor hiding somewhere? Maybe he has some unidentified genetic abnormality? It’s a puzzle we hope to solve. In the meantime, his mother just keeps filling his bowl with water, and his days with love.