History and exam

Key diagnostic factors

common

presence of risk factors

Hx of autoimmune diseases, hepatitis B or C, syphilis, malignancy, and use of medications such as non-steroidal anti-inflammatory drugs (NSAIDs), gold, penicillamine, lithium, or captopril.

oedema

Typically generalised, including the lower extremities and peri-orbital regions.

elevated BP

Can be due to increased salt retention and volume overload, or due to renal dysfunction with decreased glomerular filtration rate.

Other diagnostic factors

common

incidental proteinuria or abnormal renal function

Patients may present after being referred with the incidental finding of proteinuria or abnormal renal function.

xanthelasma

Commonly seen owing to resulting hypercholesterolaemia.

foamy urine

May be caused by increased protein in the urine.

uncommon

fatigue/malaise

Non-specific symptom that may indicate an underlying secondary cause.

anorexia

Non-specific symptom that may indicate an underlying secondary cause.

Muehrcke's lines

White lines of the nails due to hypoalbuminaemia.

Risk factors

strong

male sex

Male to female ratio is 2:1.[2]​​​

age >40 years

Primary MN is more common after 40 years of age.[3]​​ The mean age at diagnosis is between 50 to 60 years.[2]​​​

HLA-DR3

Associated with a higher risk of MN.[11]

autoimmune disease

About 10% to 20% of patients with lupus nephritis have MN.​[12] Sjogren's syndrome, rheumatoid arthritis, and mixed connective tissue disease are examples of other autoimmune diseases that are associated with secondary MN.​​[1]

hepatitis B and C

Circulating antigen-antibody complexes can deposit in the sub-epithelial space, leading to MN. These infections can also lead to membranoproliferative glomerulonephritis.[13]​​[14]​​

syphilis

Now a rare cause, but circulating antigen-antibody complexes can be deposited in the sub-epithelial space, leading to MN.

solid organ carcinoma

Lung and colorectal (most common) carcinomas may lead to tumour antigen deposition on the sub-epithelial surface and complement activation.​[15]

medications

Uses of non-steroidal anti-inflammatory drugs (NSAIDs), gold, penicillamine, lithium, and captopril have been implicated as causes.​​[1][16]​ The mechanism associated with drug-induced MN is not clear. Proteinuria generally develops within the first 6 to 12 months of drug treatment, but can occur as late as 3 to 4 years. Discontinuation of the drug leads to resolution of the proteinuria in virtually all cases.​​​​​​​​​

weak

sarcoidosis

In one study, MN was the most frequent glomerular disease occurring in sarcoidosis.[17]​​​

post-renal transplantation

Both recurrent and de novo MN have been reported after renal transplantation.​​[18]

Use of this content is subject to our disclaimer