Lupus Nephritis (LN)

Map the organ involvement before anything else - Anesthetic management scales to how much organ dysfunction there is, so start with a CBC, a complete metabolic panel with creatinine and albumin, and a urinalysis with protein quantification. Anemia is present in more than half of SLE patients, and leukopenia, lymphopenia, and thrombocytopenia are all common.

Cardiac evaluation - Baseline ECG and echocardiography. SLE carries a very high risk of atherosclerotic coronary disease, pericarditis with fibrinous exudate is common, myocarditis occurs, and Libman-Sacks sterile verrucous vegetations sit most often on the mitral valve — a source of thromboembolism as well as a murmur.

Pulmonary evaluation - Chest imaging, and pulmonary function testing if symptomatic. Pleuritis with or without effusion is the most common pulmonary manifestation, chronic interstitial lung disease occurs in up to 50%, and pulmonary artery medial hypertrophy with intimal fibrosis produces pulmonary hypertension.

Renal clearance drives the drug plan - Creatinine, eGFR, and quantified proteinuria set the picture. Where GFR is down, favor cisatracurium over renally excreted relaxants and avoid morphine, meperidine, and codeine because of their renally cleared active metabolites.

Electrolytes and the QT - Patients on a calcineurin inhibitor such as voclosporin or tacrolimus develop hyperkalemia and hypomagnesemia, and those disturbances are thought to underlie the QTc prolongation seen with these drugs. Check potassium, magnesium, and a 12-lead before adding another QT-prolonging agent.

Skip the drugs that provoke lupus - Procainamide and hydralazine have the highest incidence of causing drug-induced lupus, and sulfa drugs are well known to flare established SLE. Choose another antihypertensive and another antibiotic.

Treat them as immunocompromised - Induction and maintenance run on glucocorticoids plus mycophenolate mofetil, cyclophosphamide, azathioprine, rituximab, or a calcineurin inhibitor, with Pneumocystis prophylaxis during induction. Strict asepsis for lines and neuraxial procedures, and a low threshold for taking a fever seriously.

Position for fragile bone - Chronic glucocorticoid therapy costs bone density, which is why these patients get a baseline DEXA, and long-term steroids also cause avascular necrosis of joints. Pad carefully and move joints deliberately.

Neurologic baseline - Document one. SLE patients are at high risk for ischemic stroke, focal or generalized seizures occur with disease activity, and calcineurin inhibitors add posterior reversible encephalopathy syndrome, delirium, tremor, and seizure to the differential for a bad wake-up.

Class V is a thrombotic problem - Class V lupus nephritis behaves as a nephrotic syndrome, and thromboembolic complications are common in that class. Antiphospholipid antibodies compound it with thrombotic microangiopathy and Libman-Sacks thromboembolism. Factor that into the DVT prophylaxis plan and into whether neuraxial is worth it.

Blood availability - Beyond anemia of chronic disease, SLE causes Coombs-positive autoimmune hemolytic anemia and microangiopathic hemolysis, which can make crossmatching slow. Send the type and screen early.

Protect what renal function is left - No NSAIDs, no aminoglycosides, and weigh IV contrast carefully. Most patients are already on an ACE inhibitor or ARB for proteinuria and hypertension plus a statin, so confirm the morning doses.

Lupus nephritis (LN) is renal involvement in systemic lupus erythematosus (SLE) — a type III hypersensitivity reaction in which anti-double-stranded DNA immune complexes deposit in the mesangium, subendothelial, and subepithelial spaces of the glomerulus, activate complement, and recruit inflammatory cells. It typically appears about three to five years after SLE onset, mostly in patients 20 to 40 years old, and is graded by biopsy into six classes that drive both prognosis and treatment. Proliferative classes III and IV carry the worst outlook; class V behaves as a nephrotic syndrome.

Perioperatively the kidney is only part of the story. The same disease brings pericarditis, Libman-Sacks valvular vegetations, accelerated coronary atherosclerosis, pleuritis and interstitial lung disease, cytopenias, and antiphospholipid antibodies.