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Kidney disease associated with lesions of the tubules and interstitium



Most forms of tubular damage also affect the interstitium. Ischemic or toxic damage to the tubules, leading to acute necrosis of the tubules and acute renal failure, as well as inflammatory changes in the tubules and interstitium (tubulointerstitial nephritis) are distinguished.

Acute tubular necrosis. This necrosis is characterized by the destruction of epithelial cells, which is the most common cause of acute renal failure, which is characterized by acute suppression of renal function and urination (less than 400 ml of urine are eliminated within 24 hours). Acute renal failure develops in the following diseases: vascular occlusion caused by diffuse involvement of the intrarenal vessels, for example, with nodular polyarteritis, malignant hypertension and hemolytic-uremic syndrome; severe glomerular diseases such as rapidly progressive glomerulonephritis; acute tubulo-interstitial nephritis, most often associated with drug hypersensitivity; massive infection (pyelonephritis), especially accompanied by papillary necrosis; disseminated intravascular coagulation; obstruction of urinary tract tumors, compression of the urethra hypertrophied prostate or blood clots; acute tubular necrosis.

Acute tubular necrosis is reversible damage to the kidneys and is associated with a period of inadequate blood flow in the peripheral organs, usually accompanied by severe hypotension and shock. A type of acute tubular necrosis that develops in shock is called ischemic acute tubular necrosis. Transfusion of incompatible blood and hemolytic crises of a different nature, causing hemoglobinuria, as well as severe damage to skeletal muscles, accompanied by myoglobulinuria, lead to the development of changes resembling ischemic acute necrosis of the tubules. This is the so-called acute necrosis of the tubules associated with pigments. The second type — nephrotoxic acute tubular necrosis — is associated with the use of numerous medications, such as gentamicin and other antibiotics, radiopaque substances, poisons, including heavy metals (for example, mercury) and organic solvents (for example, carbon tetrachloride) (see Chapter 9 ).

The critical phase in both ischemic and nephrotoxic acute necrosis of the tubules is their damage. The tubule epithelial cells are particularly sensitive to anoxia, they are also susceptible to toxins. Some factors predispose to toxic damage to the tubules: surface electrical charge required for tubular reabsorption, active transport systems for ions and organic acids, and the ability to be effective in concentration. Ischemia causes numerous structural and functional abnormalities in epithelial cells. A functionally important event is the loss of cell polarity. Since the medulla receives less blood flow, it is especially sensitive to ischemia. Thus, the cortical and medullary canaliculi are affected, including the functionally important thick section of the ascending part of the nephron loop. Once appeared, damage to the tubules leads to the development of acute renal failure. Damage to the tubules causes a spasm of preglomerular arterioles, leading to a decrease in the glomerular filtration rate through a glomerular-tubular feedback mechanism. Vasospasm activates the renin-angiotensin system. Renin, adenosine, thromboxanes and endothelium are involved in the development of vasospasm. In addition, the loss of activity of vasodilating factors (prostaglandin, nitric oxide) is important. Damage to the tubules can by itself lead to oliguria, since tubule residues can block the urine outflow pathways and cause an increase in intratubular pressure and at the same time a decrease in the glomerular filtration rate. Fluid from the destroyed tubules can penetrate into the interstices, leading to an increase in interstitial pressure and collapse of the tubules. There is evidence of the direct effect of toxins on the ultrafiltration coefficient of the wall of glomerular capillaries.

Which of these mechanisms is most important in the development of oliguria is not clear, but it is obvious that their development requires their combination. One of these mechanisms may be predominant depending on the damaging factor.

Ischemic acute tubular necrosis is characterized by focal necrosis of the tubules in many areas along the nephron and is often accompanied by ruptures of the basement membranes (tubulorexis) and occlusion of the tubular lumen with cylinders. Necrosis of the tubules is often barely noticeable, but sometimes it is very pronounced. The direct part of the proximal tubule and the ascending thick part of the nephron loop (loop of Henle) in the medulla of the kidneys are usually most vulnerable, but local necrotic changes are also found in the distal tubule, often near the cylinders.
Eosinophilic hyaline cylinders, as well as pigmented granular cylinders, are very common, especially in the distal tubule and collecting tubes. These cylinders consist mainly of the Tamm-Horsfall protein (E.Tamm, A.Horsfall), a specific urinary glycoprotein that is normally secreted by ascending cells of the nephron loop and distal tubules and is associated with hemoglobin, myoglobin and other plasma proteins. Other most common signs of ischemic acute necrosis of the tubules are interstitial edema and leukocyte accumulation in the dilated straight vessels that continue the outflow arterioles of the juxtaglomerular glomeruli (vasa recta). There are often signs of epithelial regeneration: flattened epithelial cells with hyperchromic nuclei and mitosis figures. Over time, the recovery processes can be so pronounced in the tubules that there is no trace of damage.

Toxic acute necrosis of the tubules begins with their damage, most noticeable in the proximal convoluted tubule. This necrosis can be non-specific, but is sometimes clearly associated with damaging agents. When poisoning with mercury chloride, some cells may contain large acidophilic inclusions. Later, these cells completely necrotic and exfoliated into the lumen of the tubules, and can also undergo calcification. When exposed to carbon tetrachloride, on the contrary, neutral lipids accumulate in damaged cells. Ethylene glycol causes marked swelling and hydropic or vacuolar dystrophy of the proximal convoluted tubules. Calcium oxalate crystals are often found in the lumen of the tubules when exposed to poisons.

The clinical course of acute necrosis of the tubules has three stages: the initial, the main and the stage of recovery. In the ischemic form of acute necrosis of the tubules, the initial stage is dominant, which lasts about 36 hours. A slight decrease in urination (oliguria) and an increase in blood urea nitrogen show evidence of kidney damage in this stage. Oliguria can be explained by a transitory decrease in blood flow in the kidneys. The main stage of acute necrosis of the tubules is characterized by stable oliguria, reaching 40–400 ml per day and occurring with salt and water retention, an increase in the level of urea nitrogen in the blood, hyperkalemia, metabolic acidosis and other manifestations of uremia that dominate this phase. With appropriate control over the balance of water and electrolytes, including dialysis, an oliguric crisis can be avoided. During the recovery stage, an increase in urine volume is observed, which can reach 3 liters per day. The canaliculi are still damaged, so the loss of water, sodium and potassium ions in the urine continues. The main clinical problem during this period is hypokalemia. In this stage, the susceptibility to infection is increased. At the same time, it is possible to restore the function of the renal tubules with an improvement in their concentrating ability. Blood urea nitrogen and creatinine levels can return to normal. Minor dysfunction of the tubules observed within months, but in the majority of patients who survived to the stage of recovery, the kidneys function are completely restored.

Tubulo-interstitial nephritis. It is characterized by histological and functional disorders affecting mainly the tubules and interstitium. Glomerular and vascular lesions also occur, although they are mild and develop only during the full clinical picture of the disease. Tubulo-interstitial nephritis has various causes and pathogenetic mechanisms. It is classified according to the cause or nature of the primary disease, for example, analgesic nephritis, radiation nephritis. In the latter case, the tubulo-interstitial nephritis acquires the status of a complication.

This disease can be acute or chronic. Acute nephritis has an acute onset clinically, and is histologically characterized by interstitial edema, often accompanied by leukocyte infiltration and focal necrosis of the tubules. In chronic nephritis, stromal infiltration with mononuclear cells, marked interstitial fibrosis, and widespread tubular atrophy are observed. Clinically, this disease in both forms differs from glomerular lesions in the absence at the early stages of such major signs of damage to the glomeruli of the kidneys as nephritic and nephrotic syndromes. Functional impairment may be minor. They include impaired ability to concentrate urine, clinically detectable due to polyuria; salt loss; reduced ability to secrete acids (metabolic acidosis); isolated defects of tubular reabsorption or secretion. Developed forms, however, are difficult to clinically distinguish from other diseases leading to renal failure.

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Kidney disease associated with lesions of the tubules and interstitium

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