Glomerulonefritis agudas y rápidamente progresivas, glomerulonefritis proliferativa endocapilar y glomerulonefritis proliferativa extracapilar

Abstract

Acute (post-infectious) glomerulonephritis presents rapidly with hematuria (microscopic or causes), proteinuria, a decrease in glomerular filtration rate, and sodium and water retention that usually cause an increase in blood pressure and edema. In addition, various types of chronic glomerulonephritis may present as acute nephrotic syndrome and can be clinically indistinguishable from the onset of acute abnormalities. Rapidly progressive glomerulonephritis (RPGN) represents a clinical-pathological syndrome characterized by a rapid decline in renal function (weeks to months); proteinuria generally in a subnephrotic range; and the presence of fibrous, cellular crescents in the glomerular area. Its causes can be primary or secondary. Its classification depends on clinical, serological, and histological findings; they are divided into 3 types: 1, associated with anti-glomerular basement membrane antibodies; 2, associated with immune complexes; 3 pauci-immune (ANCA-associated), or 4, a combination of types 1 and 3. Diagnosis and treatment must be early. High-dose immunosuppressants and, sometimes, plasmapheresis can be used for the purpose of restoring renal function and avoiding rapid progression to advanced or end-stage chronic kidney disease. In cases with very high clinical suspicion, performing a renal biopsy must not delay starting immunosuppressive therapy.