Glomerulonephritis

Excerpt

The structural and functional unit of the kidney, the 'nephron,' consists of a renal corpuscle (glomerulus surrounded by a Bowman capsule) and a renal tubule. Each kidney in an adult human contains around 1 million nephrons. A fenestrated endothelium forms the inner glomerular layer, followed by a layer composed of various extracellular proteins forming a meshwork called the glomerular basement membrane (GBM). The outer layer has visceral epithelial cells, podocytes, and mesangial cells. The intricate arrangement provides the basis for continuous plasma volume filtration at the glomerular level.

The term "glomerulonephritis" encompasses a subset of renal diseases characterized by immune-mediated damage to the basement membrane, the mesangium, or the capillary endothelium, resulting in hematuria, proteinuria, and azotemia.

Acute forms of glomerulonephritis (GN) can result from either a primary renal cause or a secondary illness that causes renal manifestations. For instance, acute post-streptococcal glomerulonephritis (PSGN) is a typical example of acute glomerulonephritis secondary to a streptococcal infection; similarly, Staphylococcus aureus infection can also lead to glomerulonephritis. In recent times, however, the incidence of glomerulonephritis associated with staphylococcal has increased as opposed to the reduction of PSGN in the United States and most developed countries.

Most forms of glomerulonephritis are considered progressive disorders. Without timely therapy, progress to chronic glomerulonephritis (characterized by progressive glomerular damage and tubulointerstitial fibrosis leading to a reduced glomerular filtration rate). This leads to the retention of uremic toxins with subsequent progression into chronic kidney disease (CKD) and end-stage renal disease (ESRD) along with their associated cardiovascular diseases.