Renal emergencies

Acute glomerulonephritis Acute glomerulonephritis (AGN) is a clinical syndrome caused by an immune-mediated injury to the glomerulus. Clinical features are reduction in glomerular filtration rate (GFR), oliguria or anuria, azotemia, proteinuria (possibly into the nephrotic range), gross hematuria with RBC casts, pyuria, and evidence of volume overload (hypertension, peripheral edema, vascular congestion). The degree of renal dysfunction and azotemia can range from very mild (subclinical) to severe. Most cases of AGN result from deposition of preformed immune complexes in glomerular structures (systemic lupus erythematosus) or in situ fixation of complement and specific antibody with antigen trapped within glomeruli (postinfectious glomerulonephritis). Other forms of AGN are caused by activation of the classic or alternative complement pathway (membranoproliferative glomerulonephritis), direct antibody-mediated injury (Goodpasture's syndrome), or damage from infiltrated inflammatory cells (Wegener's granulomatosis). Although hereditary nephritis (Alport syndrome) is considered a form of nephritis, it is caused by a genetic mutation resulting in a structural abnormality of the glomerular basement membrane with subsequent glomerular dysfunction. In IgA nephropathy (Berger's disease), deposition of IgA in the glomerular tuft leads to secondary inflammation. Systemic etiologies that can cause secondary renal injury, but are not a form of glomerulonephritis by definition, include Henoch-Schö nlein purpura (vasculitis), hemolytic uremic syndrome (thrombotic microangiopathy), subacute bacterial endocarditis, and shunt (ventriculoatrial) nephritis. Clinical presentation As the GFR falls, oliguria/anuria ensues, leading to the clinical symptoms that are the hallmark of AGN: edema (particularly periorbital), weight gain, hypertension (both systolic and diastolic), decreased urine output, and dark green to coca-cola colored urine due to gross hematuria (80% of patients).