Lyme Nephritis is a serious, immune-mediated complication arising from infection with the bacterium Borrelia burgdorferi, the causative agent of Lyme disease. This condition is a severe, acute, and often fatal form of kidney failure in dogs, particularly in genetically predisposed breeds like Labrador Retrievers and Golden Retrievers. Characterized pathologically as a type of glomerulonephritis, this severe kidney damage occurs in less than two percent of seropositive animals, despite common exposure to the Borrelia bacteria.
The Unique Link Between Lyme Disease and Kidney Damage
The damage to the kidneys in Lyme Nephritis is not caused by the direct invasion of the Borrelia bacteria into the renal tissue. Instead, the mechanism is an immune-driven process resulting from the body’s prolonged response to the infection. The immune system creates antibodies that bind to bacterial antigens, forming large, circulating structures called immune complexes.
These complexes become lodged in the glomeruli, the delicate filtering units within the kidney. The deposition of these immune complexes initiates a severe inflammatory reaction known as membranoproliferative glomerulonephritis. This inflammation damages the filtering membranes, causing them to become excessively permeable and allowing large amounts of protein to leak from the blood into the urine. This process rapidly compromises the kidney’s function.
Identifying the Clinical Signs in Dogs
The clinical presentation of Lyme Nephritis reflects a rapid deterioration of kidney function, rather than the milder signs of Lyme-related arthritis. Owners may first notice vague signs such as profound lethargy, a significant loss of appetite, and noticeable weight loss. These symptoms are often more severe than those seen with typical Lyme disease.
As the condition progresses and kidney function declines, signs related to uremia and fluid imbalance become apparent. Affected dogs commonly exhibit increased thirst (polydipsia) and a corresponding increase in urination (polyuria). In advanced stages, severe protein loss leads to low protein levels in the blood, which can cause fluid to accumulate as edema, often seen as swelling in the limbs or face, or as fluid in the abdomen.
Diagnostic Testing and Disease Confirmation
Diagnosing Lyme Nephritis requires a combination of tests, as a positive Lyme exposure test alone is insufficient to confirm the kidney disease. Initial blood work typically shows elevated levels of blood urea nitrogen (BUN) and creatinine, a state called azotemia, which indicates severely impaired kidney function. A serological test, such as the C6 antibody test, is necessary to confirm exposure to Borrelia burgdorferi.
The most critical diagnostic step is a urinalysis that reveals significant proteinuria, indicating glomerular damage. This proteinuria is quantified using a Urine Protein Creatinine (UPC) ratio, which measures the severity of protein leakage. While a kidney biopsy provides the definitive diagnosis by visualizing the immune complex deposits in the glomeruli, it is often avoided in a critically ill patient due to the associated risks.
Treatment Approaches and Prognosis
Treatment for Lyme Nephritis is a dual approach, targeting both the underlying bacterial trigger and the resulting kidney failure. Antibiotic therapy, typically a four-week course of doxycycline, is administered to eliminate the Borrelia infection. However, the primary focus is on aggressive supportive care to manage the severe consequences of kidney failure.
Hospitalization with intravenous fluid therapy is often necessary to correct dehydration and flush the kidneys. Medications such as anti-nausea drugs and appetite stimulants are used to address systemic illness. To minimize protein loss, specific medications like Angiotensin-Converting Enzyme (ACE) inhibitors are prescribed. Despite intensive care, Lyme Nephritis carries a guarded to poor prognosis, as the immune damage is often irreversible, and many dogs succumb to the disease or its complications within weeks of diagnosis.