Immune Deposits in Kidneys of AAV Patients Not Tied to Kidney Failure
No link to ultimate outcomes for ANCA vasculitis with renal involvement seen
The buildup of immune molecules in the kidneys of ANCA-associated vasculitis (AAV) patients appears to be linked to some symptoms and signs of kidney disease, but not severe ones, and it cannot predict how kidney disease will progress, a study reported.
No significant differences in end-stage kidney disease was seen between two groups of AAV patients with renal involvement: those with and those without such deposits.
The study “What is the prognosis of ANCA-associated glomerulonephritis with immune deposition?” was published in the journal Renal Failure.
AAV comprises a group of autoimmune conditions marked by inflammation and damage to the smallest blood vessels in the body. Often, inflammation is evident in the kidneys, a condition called glomerulonephritis. When this happens, the kidneys can be less effective at filtering and removing waste products and excess water.
Immune complexes are formed when antibodies bind to their antigens, substances that can trigger an immune response. Part of the body’s normal immune response, immune complexes that build in the blood or internal organs can cause disease.
Some studies have shown that immune complexes tend to accumulate in the kidneys of AAV patients, along with components of the complement system, a group of proteins that work alongside the immune system to mount an immune response. What this buildup means for people with AAV, however, is unclear.
Hematuria, or blood in urine, seen as more severe with immune deposits
A team of researchers in China and the U.S. looked at kidney tissue samples taken in biopsies from 80 patients (51 women and 29 men; median age of 53) with AAV-associated glomerulonephritis, who had been followed for a mean of two years at the nephrology department of a hospital in Chengdu.
Of these 80 people, 72 (90%) had microscopic polyangiitis (MPA), six (7.5%) had granulomatosis with polyangiitis (GPA), and two (2.5%) had eosinophilic granulomatosis with polyangiitis (EGPA). Almost all (91.2%) were positive for ANCAs, the autoantibodies that cause most AAV cases.
A buildup, or deposition, of immune complexes and complement proteins was evident in 38 (47.5%) people. Patients with immune deposition had more severe hematuria than those without immune deposition, with about four times as many red blood cells in their urine (133 vs. 33 red blood cells per high power field under a microscope). They also had lower levels of circulating C3, a complement protein (0.8 vs. 0.93 grams per liter of serum, the clear liquid part of blood).
When researchers took a closer look at the kidneys’ filters, called interstitial tubules, they saw that fewer patients with immune deposition showed signs of tubular atrophy or wasting. Patients with immune deposition also had less tubular fibrosis, or scarring, than those without immune deposition. Usually, both tubular atrophy and fibrosis are tied to a poorer prognosis, the researchers noted.
The presence or absence of immune deposits also did not associate with end-stage kidney disease, marked by chronic kidney disease reaching an advanced state of organ function loss, or with patient mortality. Over the time these patients were followed, five people with and seven without immune deposits progressed to end-stage kidney disease, the study noted.
“Immune deposition may indicate lower complement C3, more severe hematuria and glomerular lesions, milder tubular atrophy, and interstitial fibrosis, but it cannot predict the renal outcome,” the researchers concluded.