Glomerulonephritis glomerular filtration rate

A prerenal mechanism secondary to the vascular leak syndrome is commonly involved in the pathophysiology of acute renal insufficiency. In addition it has been suggested that a direct intrinsic intrarenal effect of aldesleukin with a higher than expected reduction in glomerular filtration rate or tubular dysfunction (85,89) is involved. Several isolated cases of acute interstitial or tubulointerstitial nephritis with predominant T lymphocjde infiltration of the kidneys (90-92) and the exacerbation of a subchnical IgA glomerulonephritis (93) suggested altered cell-mediated immunity. 

Nephrotic syndrome characteristic of excretion of protein in urine in excess of 2.5 g per day is not present in most patients with glomerulonephritis. These patients may present with a reduced glomerular filtration rate and varying degrees of proteinuria with or without hematuria, a condition referred to as the nephritic syndrome. Patients with nephritic syndrome may recover or worsen with chronic renal failure. 

The marked inflammatory changes in the glomerular capillaries that accompany poststreptococcal glomerulonephritis significantly reduce the flow of blood to the filtering surfaces of these vessels. As a result, creatinine, urea, and other circulating metabolites that are filtered into the urine at a normal rate (the glomerular filtration rate or GFR) in the absence of kidney disease now fail to reach the filters, and, therefore, they accumulate in the plasma. 

---