Etiology and mechanism of chronic renal failure

  I. Etiology
  Chronic renal failure has a wide range of causes, and almost all kidney diseases can lead to chronic renal failure if they develop and deteriorate. Acute renal failure without cure and without death within a short period of time can also directly transition to chronic renal failure. The common causes are described as follows.
  1, chronic glomerulonephritis The most common cause of chronic renal failure is the development and deterioration of the disease to an advanced stage.
  2, Interstitial Nephritis (Interstitial Nephritis) is a group of diseases that mainly involve the renal interstitium and renal tubules, so also known as tubular interstitial nephropathy (Tubulo-Interstitia Nephropa-thy). Its etiology is complex, and it is a common clinical disease, accounting for 25%-33% of urological diseases and ranking second in chronic renal failure.
  (1) Infection: Bacteria, viruses, mycobacteria, Plasmodium, etc. invade the renal interstitium and tubules, and its representative diseases such as chronic pyelonephritis. Malignant hernia disease, etc.
  (2) Immune damage: common drug allergies such as penicillin, sulfonamide, autoimmune disorders such as systemic lupus erythematosus, scleroderma, dermatomyositis involving the kidney.
  (3) Toxic substance damage: such as aminoglycoside antibiotics, contrast agents damage the kidneys, heavy metal salts such as mercury, lead, arsenic, gold, etc. damage the kidneys.
  (4) Renal blood supply disorders: such as renal arteriosclerosis, renal artery stenosis, etc.
  (5) Metabolic abnormalities: such as hyperuricemia, hypercalcemia, long-term hypokalemia, etc.
  (6) Physical factors: long-term exposure to X-rays, X-ray radiotherapy for malignant tumors, etc.
  (7) Urinary tract obstruction: obstruction causes urinary reflux from bladder and ureter, which increases the pressure of renal pelvis and ureter and damages the renal interstitium, and if combined with infection, it will aggravate the disease.
  (8) Tumor directly infiltrates the renal interstitium: such as leukemia, lymphoma, metastasis of cancer cells cause renal interstitial damage.
  (9) Hereditary diseases: such as polycystic kidney, renal cysts.
  (10) Balkan nephritis: belongs to the interstitial renal disease of unknown cause, mainly occurs in southern Europe.
  3, hypertensive arteriosclerosis At this time, the tubules are damaged first and then the glomeruli, which is different from glomerulonephritis that damages the glomeruli first and then the tubules.
  4, secondary to metabolic diseases such as diabetes mellitus, gout kidney, amyloidosis, etc.
  Mechanism
  1, glomerular hyperfiltration theory When glomerular destruction more and more residual kidney units due to compensatory hyperfiltration, eventually leading to successive glomerular sclerosis and loss of function, such as 85% of nephrectomized animals, 3 months can be seen in the residual glomerular hypertrophy, epithelial cell vacuole formation, pedicle fusion, 6 months can be seen in the thylakoid area enlargement; glomerular basement membrane endothelium, epithelial cell shedding, and finally lead to focal, segmental glomerular sclerosis, further reduction of renal filtration rate, and further deterioration of renal function.
  2.The theory of corrective imbalance In chronic renal failure, the toxic substances in the body increase, and the body compensates for the removal of certain toxic substances, resulting in a new imbalance, such as decreased glomerular filtration rate, reduced urinary phosphorus excretion, high blood phosphorus, low blood calcium, stimulating increased secretion of parathyroid glands, acting on the renal tubules, increasing urinary phosphorus excretion, so that blood phosphorus is reduced and blood calcium is increased and restored to normal levels. Elevated blood calcium is deposited in all systems including the kidney itself, causing a further decrease in glomerular filtration rate and further deterioration of renal function.
  In chronic renal failure, the glomerular filtration rate is low and sodium excretion is reduced, at which time natriuretic hormone secretion increases and sodium reabsorption by the proximal tubules is reduced, but natriuretic hormone has an inhibitory effect on Na+-K+-ATPase, thus making many tissues impaired for steel transport and causing a new imbalance.
  3, toxin theory In uremia there are more than 200 kinds of substances increased in the body, including more than 20 kinds of toxic substances, divided into small molecules (molecular weight <500 people medium molecules (molecular weight 500 ~ 5000) and large molecules substances (molecular weight > 5000) three categories. Small molecule substances are the main cause of clinical symptoms such as urea, guanidine, amines. Medium molecular substances such as peptides, cellular and bacterial lysis products.
  Medium molecular substances can cause peripheral neuropathy, uremic encephalopathy, erythropoietin suppression, insulin activity suppression, lipoprotein lipase activity suppression, platelet function impairment, cellular immune hypofunction, sexual dysfunction and exocrine gland atrophy. In chronic renal failure, high blood phosphorus and low blood calcium stimulate increased parathyroid secretion, causing tissue calcium deposition, slowed nerve conduction and increased calcium content in brain cells, while parathyroid glands are an important cause of renal anemia, in addition to affecting cardiac function and cardiomyocyte metabolism.