Nephrotic Syndrome (NS)

Volume status is not what the edema suggests - These patients swing between an underfilled intravascular space, from low oncotic pressure, and frank hypervolemia from tubular sodium retention. Follow the weight trend, pulse, and blood pressure rather than the pitting edema, and know the current diuretic dose.

Look at the albumin and the metabolic panel - Serum albumin sits below the normal 3.5 to 4.5 g/dL range and creatinine varies with how much renal function has been lost. Diuresis is hard to achieve once albumin drops under 1.5 g/dL, which is why some of these patients arrive having had albumin infusions.

They are hypercoagulable - Urinary loss of antithrombin III plus increased hepatic synthesis of procoagulants produces DVT, pulmonary embolism, and renal vein thrombosis; a PE can be the first sign of the disease. Keep compression on and get them moving early. Routine primary anticoagulation is not proven, so confirm the plan rather than assume it — and if they are on an anticoagulant, check the current ASRA guidance before any neuraxial technique rather than working from memory.

Renal vein thrombosis - Flank pain, hematuria, a rapid fall in renal function, and worsening proteinuria in a nephrotic patient. Membranous nephropathy is the most common underlying association.

Infection risk is real - Urinary loss of immunoglobulin and alternate complement pathway components, layered on corticosteroids, calcineurin inhibitors, cyclophosphamide, or rituximab, makes encapsulated organisms and peritonitis a genuine threat. Strict asepsis for lines and for any neuraxial technique.

Ask about steroids - Corticosteroids are first-line for idiopathic disease and many patients are relapsing or steroid-dependent. Get the current dose and duration, plus any steroid-related cataract or bone disease.

Edema is not just peripheral - It starts periorbital and dependent, then generalizes with ascites and pleural effusions as weight climbs. A pleural effusion on the preoperative chest film changes the ventilation plan.

Know the antihypertensives - ACE inhibitors and ARBs are widely used in secondary nephrotic syndrome, especially diabetic nephropathy, to cut proteinuria by lowering intraglomerular and systemic pressure. Find out whether the morning dose was held.

Anemia and hypertension once the kidney is failing - Both appear when renal function is impaired. Check a hemoglobin and establish the baseline blood pressure before induction.

Nephrotic-range proteinuria in the third trimester - That is a classic preeclampsia finding rather than new primary renal disease, and it moves the case onto an obstetric track.

Nephrotic syndrome (NS) is massive proteinuria — 3 g or more of protein per 24 hours — from a damaged glomerular filtration barrier, with hypoalbuminemia, edema, and hyperlipidemia following from it. Podocyte foot processes, the slit diaphragm, and the glomerular basement membrane normally exclude large and negatively charged proteins. When that barrier or its negative charge is lost, albumin pours into the urine and makes up about 85% of the protein lost. Falling plasma colloid oncotic pressure drives fluid into the interstitium, and the tubules retain sodium and water on top of it.

Primary causes are minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy; secondary causes include diabetes, lupus, amyloidosis, HIV, malignancy, and drugs. The perioperative trouble comes from what else washes out in the urine: antithrombin III, immunoglobulin, and complement components.