Nephrotic syndrome

Nephrotic syndrome (NS) is not a single disease but a group of clinical syndromes in glomerular disease. Typical features are massive proteinuria (>3.5 g/1.73 m² body surface area per day), hypoalbuminemia (plasma albumin <30 g/L), edema with or without hyperlipidemia; the diagnostic criteria are massive proteinuria and hypoproteinemia. Massive proteinuria is characteristic of glomerular disease. Since hypoproteinemia, hyperlipidemia and edema all result from massive proteinuria, the diagnostic criterion should center on massive proteinuria.

Common Symptoms

Intraglomerular "three highs"; extrarenal obstruction; proteinuria; moth-eaten glomerular basement membrane; postrenal renal failure; half-moon nails; oily urine; hypoproteinemia

Causes

Any factor damaging the glomerular filtration barrier can cause nephrotic syndrome, classified as primary or secondary; primary is diagnosed by excluding secondary causes. Secondary causes: bacterial infection (post-streptococcal nephritis, endocarditis, shunt nephritis, leprosy, syphilis, TB, chronic pyelonephritis with reflux); viral infection (hepatitis B, CMV, EBV, HIV); parasites (malaria, toxoplasmosis, worms, schistosomiasis, filariasis). Toxins/allergy: organic or inorganic mercury, gold, penicillamine, heroin, probenecid, NSAIDs, trimethadione; bee sting, snake venom, pollen, vaccines. Tumors of lung, stomach, colon, breast, ovary, thyroid, leukemia, lymphoma, Wilms tumor. Systemic disease: SLE, mixed connective tissue disease, dermatomyositis, Sjögren syndrome, purpura, amyloidosis. Diabetes, thyroid disease. Hereditary: congenital nephrotic syndrome, Alport syndrome, Fabry disease, sickle cell anemia, nail-patella syndrome, familial nephrotic syndrome. Others: eclampsia, chronic transplant rejection, malignant nephrosclerosis, renal artery stenosis. In China, SLE, diabetic nephropathy and purpura are common secondary causes. Children mostly have minimal change; adults have focal segmental nephritis, membranous and minimal change. Etiology has shifted: in 1970-1980 membranous nephropathy was commonest; in 1976-1979 membranous 36%, minimal change 23%, FSGS 15%, while in 1995-1997 FSGS became the main cause at 35% (50% in blacks, 67% under 45). Pathologic types: minimal change (MCNS), mesangioproliferative GN (MsPGN), FSGS, membranoproliferative GN (MPGN), membranous nephropathy (MN) and IgA nephropathy (graded I-V by WHO). Immunologic and cellular mechanisms, complement activation, cytokines, growth factors, reactive oxygen species, prostaglandins and endothelin are all involved in glomerular injury.

Treatment

Medication, symptomatic treatment, rehabilitation therapy

Prevention

Prevention starts with personal health: reasonable diet, fitness, immunity, avoiding toxins and nephrotoxic drugs, and preventing infection; complications of nephrotic syndrome determine efficacy and long-term prognosis and must be actively prevented and treated.

Recommended Department

It is recommended to visit the nephrology department; before the visit you may first book an appointment and connect with experts through this platform.

Warm reminder: The above information is provided for health education reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek care at a regular hospital in time.