Glomerulonephritis (GN)

Volume overload is an exam finding - Look for JVP distention, pitting edema, and crackles on auscultation, alongside elevated blood pressure and oliguria. That combination means reduced FRC, poor tolerance of supine and Trendelenburg positioning, and a low threshold for pulmonary edema with liberal fluids.

Hypertension is renin-driven - Salt and water retention through RAAS activation is the mechanism, so the pressure is volume-dependent and swings with induction and blood loss. Most patients are on an ACE inhibitor or ARB, prescribed to reduce proteinuria.

Anemia - Pallor and anemia are typical findings in active glomerulonephritis. Get a hemoglobin before any case with meaningful expected blood loss.

Potassium and the ECG - Reduced renal excretion is a core cause of hyperkalemia, and the first test in a suspected case is an ECG, because conduction abnormalities and dysrhythmias are the lethal complication. Rate of rise matters more than the absolute number, so a chronically elevated potassium may show a near-normal tracing. In renal disease also check serum calcium — hypocalcemia worsens the cardiac effects.

Immunosuppression on board - Corticosteroids, cyclophosphamide, mycophenolate, rituximab, calcineurin inhibitors, and plasma exchange are all used depending on subtype. Assume reduced host defense: strict asepsis for lines, neuraxial, and blocks.

Anti-GBM disease involves the lungs - Goodpasture syndrome is anti-glomerular basement membrane disease affecting both kidney and lung, often presenting as pulmonary hemorrhage with glomerulonephritis. In a patient carrying that diagnosis, hemoptysis, a falling hemoglobin, or new hypoxemia is alveolar hemorrhage until proven otherwise, and it changes airway and ventilation planning.

Find the infection driving it - Staphylococcus-associated GN typically hits a middle-aged or older man, often diabetic, concurrent with pneumonia, endocarditis, osteomyelitis, or an MRSA skin infection — a new murmur on exam in that setting points at endocarditis. Post-streptococcal GN in a child follows a throat or skin infection by weeks and is treated supportively plus antibiotics.

Rapidly progressive disease is a moving target - Crescentic (rapidly progressive) GN can lose renal function over weeks and may present as acute kidney injury. Draw a same-day creatinine and potassium rather than working from last week's labs — the number you have may already be stale.

Protect the function that's left - Avoid NSAIDs (interstitial nephritis) and be deliberate about IV contrast. Keep 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, and a large 0.9% saline load causes hyperchloremia and reduces renal blood flow.

Urine tells you where you are - Dark urine with a specific gravity above 1.020 and RBC casts is active nephritic disease. Intraoperatively, urine output under 0.5 mL/kg/hr for 6 hours meets the KDIGO threshold for acute kidney injury.

Uremia in advanced disease - Retained uremic toxins bring weakness, nausea, and vomiting, and encephalopathy in rapidly progressive disease. That means aspiration risk from active nausea and vomiting, plus a fluid and electrolyte picture worth correcting before induction rather than discovering after.

Glomerulonephritis (GN) is immune-mediated injury to the glomerular basement membrane, mesangium, or capillary endothelium, producing hematuria, proteinuria, and azotemia. Antigen-antibody deposition — or, in small-vessel vasculitis, T cell and macrophage infiltration — activates complement and the coagulation cascade, and the resulting cytokines drive glomerular cell proliferation and eventually glomerulosclerosis.

As GFR falls, salt and water are retained through renin-angiotensin-aldosterone activation, producing intravascular volume expansion, edema, and systemic hypertension: the nephritic picture of hematuria, hypertension, oliguria, and edema. IgA nephropathy is the most common form worldwide; post-streptococcal GN follows pharyngitis by 1 to 2 weeks or a skin infection by 2 to 4 weeks. Chronic GN is the third most common cause of end-stage renal disease in the United States, after diabetes and hypertension.