Membranous Nephropathy (MN)

Thromboembolism is the headline - Loss of antithrombin III in the urine makes MN patients hypercoagulable, and deep vein thrombosis, pulmonary embolism, and renal vein thrombosis all occur. Many are already on a vitamin K antagonist or a direct oral anticoagulant. Confirm the agent, the last dose, and the INR, then apply your institution's current neuraxial timing guidance — do not work from memory on this one.

Volume assessment cuts both ways - These patients are edematous with ascites and pleural effusions, yet the diuretics that control that leave them intravascularly depleted. Track weight, pulse, and blood pressure rather than the edema itself, and expect a soft pressure at induction on a diuretic plus an ACE inhibitor or ARB.

Low albumin - Serum albumin is typically below 3.5 g/dL. Below about 1.5 g/dL, diuresis fails without albumin replacement, which is a clue you are dealing with severe disease rather than mild nephrosis.

Look at the chest - Listen for crackles and get a chest film. Pleural effusions and ascites travel with the anasarca and determine how flat the patient will tolerate lying and how much reserve there is on induction.

Renal function and drug choice - Acute kidney injury with an elevated creatinine is part of the MN presentation. Get creatinine and eGFR, avoid NSAIDs and aminoglycosides, weigh IV contrast, and where GFR is reduced favor cisatracurium and skip morphine, meperidine, and codeine.

Cardiovascular exam - Nephrotic hyperlipidemia and hypertension compromise cardiovascular health, so examine the carotids and the peripheral pulses and look for signs of heart failure. Most patients are on a statin along with the ACE inhibitor or ARB.

Treat them as immunocompromised - Immunosuppressive therapy is the Ponticelli regimen of alternating monthly corticosteroids and cyclophosphamide, or a calcineurin inhibitor such as cyclosporine or tacrolimus, or rituximab. All raise infection risk, and long-term steroids add cataract, metabolic syndrome, and avascular necrosis of joints.

Hunt for the secondary cause - About a quarter of MN is secondary, and the underlying disease often drives the anesthetic more than the kidney does: class V lupus nephritis is the most common cause, followed by hepatitis B and C, HIV, syphilis, NSAIDs, heavy metals, and solid tumors of lung, colon, stomach, and prostate.

Recognize renal vein thrombosis - Flank pain with hematuria, worsening proteinuria, and a rapid fall in renal function. CT angiography is close to 100% sensitive and specific; in a transplanted kidney it presents within 48 hours as sudden anuria and graft tenderness.

Membranous nephropathy (MN) is an immune-complex disease in which IgG — most often anti-PLA2R antibody in primary disease — deposits subepithelially between the glomerular basement membrane and the podocytes. Complement activation and the C5b-9 membrane attack complex damage the podocyte cytoskeleton, slit diaphragm integrity fails, and the anionic charge barrier is lost. The result is nephrotic-range proteinuria over 3.5 g/day with hypoalbuminemia, edema, hyperlipidemia, and hypertension. It is the most common cause of primary nephrotic syndrome in white adults, peaking between 50 and 60 years of age.

The part that matters at the board is what the protein loss does. Urinary loss of antithrombin III makes these patients hypercoagulable, and MN is the nephrotic lesion most often associated with renal vein thrombosis as well as an independent risk factor for thromboembolic events generally.