Acute renal failure - Causes and pathogenesis

The causes of acute renal failure are not completely clear, but four main mechanisms of its development are noted:

• tubular obstruction;
• interstitial edema and passive reverse flow of glomerular filtrate at the level of the tubules;
• renal hemodynamic disorder;
• disseminated intravascular coagulation.

Based on a large amount of statistical material, it has now been proven that the morphological basis of acute renal failure is damage to the predominantly tubular apparatus in the form of nephrothelial necrosis with or without damage to the basement membrane; with poorly defined damage to the glomeruli. Some foreign authors use the Russian term "acute tubular necrosis" as a synonym for the term "acute renal failure". Morphological changes are usually reversible, therefore, the clinical and biochemical symptom complex is also reversible. However, in a few cases, with severe endotoxic (less often exotoxic) effects, the development of bilateral total or subtotal cortical necrosis is possible, characterized by morphological and functional irreversibility.

There are several stages of development of acute renal failure:

• initial stage (of exposure to a damaging factor);
• stage of oliguria or anuria (increase in clinical signs of the disease). The period of kidney dysfunction is characterized by instability of diuresis, the condition periodically shifts from anuria to oliguria and vice versa, therefore this period is called oligoanuric;
• diuretic stage (beginning of disease resolution);
• stage of recovery.

The action of damaging factors causes damage to the tubular apparatus and, above all, the tubular epithelium in the form of necrobiotic and dystrophic processes, which leads to the development of the oligoanuric stage. From the moment of damage to the tubular apparatus, anuria becomes persistent. Moreover, another factor is characteristic of advanced acute renal failure - tubular obstruction, which occurs as a result of the destruction of the nephrothelium, its loading with pigment slags. If the basal membrane is preserved and functions as a framework, then the regeneration process develops in parallel with nephrothelium necrosis. Regeneration of the tubule is possible only if the integrity of the nephron is preserved. It has been established that the newly formed epithelium is functionally inferior at first, and only by the 10th day from the onset of the disease do signs of restoration of its enzymatic activity appear, which clinically corresponds to the early diuretic stage.

In surgical patients undergoing inpatient treatment, the causes of acute renal failure can be divided into two groups:

• progression of the underlying disease or development of complications;
• complications of drug, infusion therapy or blood transfusion complications.

In patients who have undergone surgery, in the postoperative period, determining the etiologic factors of acute renal failure presents a significant diagnostic difficulty. These are factors directly related to the trauma of the operation and complications of the postoperative period, among which the most likely are peritonitis, destructive pancreatitis, intestinal obstruction, etc. In this case, it is necessary to take into account significant changes in some reactions of the body characterizing the purulent-inflammatory process. Fever in the purulent-septic process often softens, chills are not always accompanied by a corresponding increase in body temperature, especially in patients with hyperhydration. The development of acute renal failure in surgical patients who have undergone surgery complicates the diagnosis of purulent complications in the abdominal organs. A significant improvement in the patient's condition after hemodialysis indicates the absence of complications.

Anesthesia may cause toxic and toxic-allergic effects on the kidneys. For example, there is information about the nephrotoxicity of halothane. In these cases, anuria is often preceded by arterial hypertension during surgery or in the first day of the postoperative period; prolonged recovery from narcotic sleep; prolongation of artificial ventilation.

Postrenal acute renal failure is most often caused by acute urinary tract obstruction.

• Ureteral obstruction:
  • stone;
  • blood clots;
  • necrotic papillitis.
• Compression of the ureters:
  • tumor;
  • retroperitoneal fibrosis.
• Bladder damage:
  • stones;
  • tumor;
  • schistosomiasis
  • inflammatory obstruction of the bladder neck;
  • prostate adenoma;
  • disorders of the innervation of the bladder (spinal cord damage, diabetic neuropathy).
• Stricture of the urethra.

In acutely developed anuria accompanied by pain, urolithiasis should be excluded. Even with unilateral obstruction of the ureter with severe pain (renal colic), cessation of urine flow by the healthy kidney is possible (reflex anuria).

In necrotic papillitis (necrosis of the renal papillae), both postrenal and renal acute renal failure develop. Postrenal acute renal failure is more common due to obstruction of the ureters by necrotic papillae and blood clots in diabetes mellitus, analgesic or alcoholic nephropathy. The course of postrenal acute renal failure in necrotic papillitis is reversible. At the same time, renal acute renal failure caused by acute total necrotic papillitis complicating purulent pyelonephritis often develops into irreversible renal failure.

Acute renal failure may also develop with TUR syndrome, which complicates TUR of the prostate for adenoma (occurs in approximately 1% of cases). TUR syndrome occurs 30-40 minutes after the start of prostate resection and is characterized by increased blood pressure, bradycardia, increased bleeding from the wound; many patients experience agitation and convulsions, and coma may develop. In the early postoperative period, arterial hypertension is replaced by hypotension, which is difficult to correct; oliguria and anuria develop. Jaundice appears by the end of the day. During the operation, it is necessary to constantly or fractionally wash the surgical wound and bladder with distilled water under a pressure of 50-60 cm H2O. Since the pressure in the venous vessels of the surgical area does not exceed 40 cm H2O, the irrigation fluid enters the venous vessels. The possibility of fluid absorption through the paravesical space when the gland capsule is opened has been proven. The rate of absorption of irrigation fluid from the surgical site is 20-61 ml/min. From 300 to 8000 ml of fluid can be absorbed within an hour. When using distilled water, hypoosmolarity of blood plasma develops with subsequent intravascular hemolysis of erythrocytes, which was considered the main cause of TUR syndrome. However, subsequently, using non-hemolyzing solutions, it was not possible to completely avoid TUR syndrome and acute renal failure, despite the absence of hemolysis. At the same time, all researchers note hyponatremia, hypocalcemia and general hyperhydration. According to literary data, the following causes of acute renal failure are likely:

• mechanical blockage of the renal tubules by deposition of blood pigment;
• the appearance of nephrotoxin when electric current acts on tissue;
• circulatory problems in the kidneys.

In TUR syndrome, acute renal failure occurs in 10% of patients and leads to death in 20% of cases.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ], [ 10 ]