Glomerular nephritis results from inflammation of the filtration membrane within the renal corpuscle. It is characterized by an increased permeability of the filtration membrane and the accumulation of numerous white blood cells in the area of the filtration membrane. As a consequence, a high concentration of plasma proteins enters the filtrate along with numerous white blood cells. Plasma proteins in the filtrate increase the osmolality of the filtrate, causing a greater-than-normal urine volume.
Acute glomerular nephritis often occurs 1 to 3 weeks after a severe bacterial infection such as streptococcal sore throat or scarlet fever. Antigen-antibody complexes associated with the disease become deposited in the filtration membrane and cause its inflammation. This acute inflammation normally subsides after several days.
Chronic glomerular nephritis is long-term and usually progressive. The filtration membrane thickens and eventually is replaced by connective tissue. Although in the early stages chronic glomerular nephritis resembles the acute form, in the advanced stages many of the renal corpuscles are replaced by fibrous connective tissue, and the kidney eventually becomes nonfunctional.
Pyelonephritis is inflammation of the renal pelvis, medulla, and cortex. It often begins as a bacterial infection of the renal pelvis and then extends into the kidney itself. It can result from several types of bacteria, including Escherichia coli. Pyelonephritis can destroy nephrons and renal corpuscles, but because the infection starts in the pelvis of the kidney, it affects the medulla more than the cortex. As a consequence, the ability of the kidney to concentrate urine is dramatically affected.
Renal failure can result from any condition that interferes with kidney function. Acute renal failure occurs when kidney damage is extensive and leads to the accumulation of urea in the blood and to acidosis. In complete renal failure death can occur in 1 to 2 weeks. Acute renal failure can result from acute glomerular nephritis, or it can be caused by damage to or blockage of the renal tubules. Some poisons such as mercuric ions or carbon tetrachloride that are common to certain industrial processes cause necrosis of the nephron epithelium. If the damage does not interrupt the basement membranes surrounding the nephrons, extensive regeneration can occur with 2 to 3 weeks. Severe ischemia associated with circulatory shock resulting from sympathetic vasoconstriction of the renal blood vessels can cause necrosis of the epithelial cells of the nephron.
Chronic renal failure results when so many nephrons are permanently damaged that those nephrons remaining functional cannot adequately compensate. Chronic renal failure can result from chronic glomerular nephritis, trauma to the kidneys, absence of kidney tissue caused by congenital abnormalities, or tumors. Urinary tract obstruction by kidney stones, damage resulting from pyelonephritis, and severe arteriosclerosis of the renal arteries also cause degeneration of the kidney.
In chronic renal failure the GFR is dramatically reduced, and the kidney is unable to excrete excess excretory products, including electrolytes and metabolic waste products. The accumulation of solutes in the body fluids causes water retention and edema. Potassium levels in the extracellular fluid are elevated, and acidosis occurs because the distal convoluted tubules cannot excrete sufficient quantities of potassium and hydrogen ions. Acidosis, elevated potassium levels in the body fluids, and the toxic effects of metabolic waste products cause mental confusion, coma, and finally death when chronic renal failure is severe.