Focal Segmental Glomerulosclerosis (FSGS)

Volume status is deceptive - Total body water is high and the patient looks flooded, but hypoalbuminemia drops plasma colloid osmotic pressure and fluid sits in the interstitium, so the intravascular compartment can be depleted. Follow weight, pulse, and blood pressure rather than the look of the legs — diuretic-driven volume depletion is assessed that way. Expect an exaggerated pressure drop on induction.

Hypertension can be severe - Hypertension is a common feature and can be marked, with diastolic pressures over 120 mmHg, particularly in Black patients with renal impairment. ACE inhibitors and ARBs are first-line therapy to cut proteinuria, so most arrive on one. Expect a labile pressure in both directions.

Third spacing changes the chest - Pleural effusions and ascites are common in nephrotic-range disease; pericardial effusions are rare. That means reduced FRC, poorer tolerance of supine positioning and pneumoperitoneum, and less oxygen reserve at induction.

Edematous skin - Gross edema predisposes to infection and ulceration in dependent areas, especially the lower extremities. Pad generously, check heels and elbows, and be deliberate with tape and adhesives.

Thrombosis - Deep vein thrombosis or pulmonary embolism can be the first manifestation of nephrotic syndrome, and some of these patients are therefore on therapeutic anticoagulation. That decides the neuraxial question: identify the agent and the last dose, and check the interval against current ASRA guidance rather than working from memory.

Immunosuppressed by treatment - Corticosteroids, calcineurin inhibitors, rituximab, cyclophosphamide, mycophenolate, and plasma exchange all appear in FSGS regimens. Assume reduced host defense: strict asepsis for lines, neuraxial, and blocks. Abdominal pain in a nephrotic patient can mean peritonitis rather than a surgical abdomen.

Diuretics and albumin - Furosemide and spironolactone carry the edema management, but adequate diuresis is hard to achieve once serum albumin falls below 1.5 g/dL, and albumin is sometimes given to make it work. A patient diuresed hard on the ward arrives dry.

Advanced disease looks uremic - Severe renal failure brings nausea, vomiting, seizures, bleeding, and altered mental status. Uncommon in FSGS, but if any of those are present, get a current creatinine and electrolyte panel before induction rather than after.

Protect the function that's left - Avoid NSAIDs, be deliberate about IV contrast, and hold the perfusion pressure up — autoregulation is impaired in chronic renal disease, so intraoperative hypotension does more damage here. Hydroxyethyl starch is not recommended in patients at increased risk of AKI.

Focal segmental glomerulosclerosis (FSGS) is scarring of part of some — not all — glomeruli, driven by podocyte injury. Podocytes are terminally differentiated, so when they are damaged the survivors hypertrophy to cover the capillary surface, foot processes efface, protein leaks, and the involved segments sclerose. It accounts for roughly 40% of adult nephrotic syndrome and is the most common primary glomerular disease progressing to end-stage renal disease in the United States.

Primary disease is linked to circulating permeability factors. Genetic forms involve podocyte proteins such as nephrin, podocin, and alpha-actinin-4, with APOL1 variants raising risk markedly in patients of African descent. Secondary forms follow drugs, HIV and other viruses, obesity, reflux nephropathy, and reduced renal mass. Over 70% present with nephrotic syndrome, and 25% to 30% reach ESRD within five years.