Disease – Primary Membranous Glomerulonephritis
Primary membranous nephropathy (pMN) is a chronic disease of the renal glomeruli that results in impairment of the renal functions. The disease bears an autoimmune etiology. It is instigated by the autoantibodies that are directed against glycoprotein phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain containing protein 7A (THSD7A). These antibodies react against the podocytes surrounding the renal glomeruli causing them significant damage. The result is leakage of the proteins in the urine (proteinuria).
Primary membranous nephropathy (pMN) is a leading cause if nephrotic syndrome in the adults. Peak incidence is seen in white-skinned males over 40 years of age. In women however, lupus nephritis is always suspected and considered with pMN. Primary membranous nephropathy is very rare in children.
Primary membranous nephropathy has to be differentiated from secondary pMN which is seen usually after infections, drug therapy and toxins. Anyhow, early diagnosis and prompt treatment improves disease prognosis with respect to nephrotic syndrome and hypertonicity.
Diagnosis of pMN follows a routine protocol for kidney puncture, histological and electron microscopic examination of the kidney tissue. However, serological testing has helped make the process faster and less irritating for the patient. The characteristic antibodies against PLA2R and THSD7A can be found in the patients with pMN and are strong indicators for the disease. Especially those against PLA2R are found in about 80% of the cases.
Methods to detect the antibodies:
Methods to detect these antibodies include
IFA allows for a semi quantitative determination of the antibodies whereas ELISA and ChLIA allow reliable quantification. The antibody titers hold a high predictive value and they can also be used to monitor therapy success or risk of relapse as these usually vary in accordance with the clinical picture.
The anti-THSD7A IFA is an excellent supplement to the serological testing for anti-PLA2R. Even in patients negative for PLA2R antibodies, additional screening is done for anti-THSD7A to rule out any possibility of the disease.