Pathology of acute tubular inflammation

2021-01-26 12:00 AM

The main damage to this pathology is intercellular necrosis of the kidneys, which is a serious disease and the death rate is still very high if it is not managed in a timely and effective manner.


Acute tubular nephritis is a common condition that causes acute kidney failure, also known as acute tubular necrosis or acute tubular disease. The main damage to this pathology is intercellular necrosis of the kidneys, which is a serious disease and the death rate is still very high if it is not managed in a timely and effective manner.


There are many causes of acute tubular inflammation, but it can be divided into 3 large groups:

Tubular necrosis after anaemia

All of the causes that cause a prolonged decrease in renal perfusion can cause anaemia of the kidney and cause damage in the form of tubular necrosis.

Causes of decreased renal perfusion are divided into 2 groups:

Pre-kidney origins:

Shock reduction of blood volume: after surgery, after trauma, burns, abortion, dehydration, loss of salt.

Septic shock, poisoning.

Heart shock.

Origin in the kidneys:

The most common is due to adverse effects of certain drugs when used in specific locations: non-steroids anti-inflammatory drugs, antihypertensive drugs, ACE inhibitors when used in patients with dynamic stenosis. bilateral kidney vessels.

Acute tubular necrosis due to poisoning

It can be directed upon renal tubular cells or indirectly on the vascular mechanism and thereby causing renal anaemia.


Antibiotics, especially the Aminoxides group. In this group, the only one is Neomycin, the other less toxic ones are Streptomycin, Kanamycin, and Gentamycin. The most nephrotoxic cephalosporin is Cefaloridine.

Contrast iodine products.

Anti-U drugs: Ciplastine, Cyclosporine, Interferon.

Some other drugs such as aesthetic Phenylbutazone (methoxyflurane).

Some endogenous pigments such as haemoglobin (Hb), muscle pigment (myoglobin).

Commonly used chemicals such as Tetsra Chlorocarbon (CCl4), Methyl alcohol.

Toxins of the organism:

Molasses of carp, sesame, and carp.

Honey toad.


Also known as NIA immuo-allergique, drug-induced causes are common: Methicillin, Penicillin, non-Steroids anti-inflammatory, diuretics, Cimetidine.


Microscopic injury is in many different degrees and in particular it is not parallel with the severity of clinical manifestations. Injury included

In the interstitial organization

Swollen tissue, inflammatory cell infiltration.

In the kidney tubules

Tubular lesions are not the same for each segment of the renal tubule.

Mild with flattened or dilated tubular cytoplasm, especially in distal tubules.

On average with tubular intercellular necrosis, tubular cells lose the protoplasm and nucleus.

More severe than renal tubular necrosis and can rupture each section of the renal tubules.

In addition, the tubular lumen also contains tubules and corpses of renal tubular cells, chromaticity such as Hb, bile pigment.

In the glomeruli and blood vessels

In general, normal. In the early stage by immunofluorescent techniques, fibrin can be detected in the glomerular capillary lumen.

Mechanism of pathogenesis

Acute tubular inflammation-causing acute renal failure often has many mechanisms involved: decreased glomerular filtration, renal tubular obstruction, diffuse back of glomerular filtrate. Of these three mechanisms, the reduction of glomerular filtration is the most basic mechanism.

Decreased glomerular filtration

In general, decreased glomerular filtration is the result of three main mechanisms:

Decreased renal blood flow:

Or due to contraction of the incoming arterioles, which is due to increased Angiotensin II (Thurau's hypothesis).

Or due to the loss of self-regulation in the kidney due to the sensitivity of the capillary sphincter increased under the action of Catecholamine.

Reduced glomerular permeability:

Due to the reduction of the filtration area by contraction of the intervascular fibers.

Due to a decrease in membrane permeability coefficient (Kf) secondary to the action of Angiotension II or vasopressin.

Renal blood flow redistribution:

From the shell to the medullary region due to the role of vasoconstrictive hormones, Catecholamine and Angiotensin II, perfusion is preferred for nephron with strong resorption.

Renal duct blockage

Due to the necrotic cells, the pigment blocks the renal tubules, causing symptoms of low urination, anuria.

Diffuse back to the dialysis solution

Tubular necrosis leads to increased local permeability and causes a quantity of glomerular filtrate to be diffused through the blood vessels around the renal tubule.

Clinical and subclinical


Clinical manifestation of acute tubular inflammation is a syndrome of acute renal failure sometimes accompanied by a history of acute hepatitis (seen in etiologic toxicity).

The situation to detect acute tubular inflammation varies widely: often found to be a symptom of minimal, anuria, sometimes detected by a serious complication such as extracellular fluid retention (hypertension, pulmonary oedema) or other electrolyte water disorders or a history of hyperuricemia syndrome.

Clinically goes through 5 stages:

Stage of kidney attack:

The duration of this stage depends on the cause: acute and sudden (shock, haemorrhage) or slow and prolonged (antibiotic toxicity to the kidney).

Minimize, primary anuria:

Show up 24 to 72 hours later. Clinical manifestations:

Extracellular fluid retention (weight gain, peripheral oedema, exertional dyspnoea)

Deposits of azotides: systemic signs, digestive disorders, sometimes spots of bleeding under the skin.

True stage of anuria:

Times vary from 7 to 21 days. The clinical course of this stage is the typical acute hyperuricemia syndrome (see the article Hyperuricaemia syndrome).

High stage of urination:

Usually appears around the third week of anuria, sometimes sooner, the amount of urine increases gradually. In this stage, sometimes it is still necessary to dialysis, but more importantly to replace the lost fluid, electrolytes.

Stage of renal function rehabilitation:

Blood urea and creatinine returned to normal or were similar to previous values ​​without acute renal failure.

In addition, in the clinical course of acute tubular inflammation, it is also important to note that the patients still have minimal urine output and anuria, the characteristics of this body are:

Diagnosis is usually slow.

Kidney damage is usually less severe, the prognosis is usually good.

This is a common form with early administration of Furosemide diuretic and or vasodilator.

Treatment for dialysis, nutrition is like anuria.


In addition to tests for the cause, there are also tests to determine acute kidney failure, including:

Increased urea, creatinine, acid unique in blood.

Electrolyte water disorders: hyperkalaemia, hyponatremia, hypocalcaemia, and hyperphosphatemia are common disorders in acute renal failure.

Acid alkaline disorder: acidosis.


Diagnosis based on

The onset of acute illness.

Clinical practice with oliguria, anuria at the onset, and a later stage of urinary retention.

Tests for urea, creatinine, and potassium increase gradually.

Differential diagnosis

It is important to distinguish acute renal failure due to acute tubular inflammation from entity acute renal failure from other etiologies (acute renal failure).

It is necessary to distinguish between the form of oliguria, oliguria, and conservative form.

Need to distinguish between acute tubular inflammation and other diseases such as glomerulonephritis, ureteral obstructive stones.


Includes symptomatic treatment, complications of acute tubular inflammation (depending on the stage of acute tubular inflammation for specific application), and treatment of the cause

In the early stage (the stage of a kidney attack)

Immediately manage the causes of acute tubular necrosis: Eliminate toxins in the cause of poisoning.

Immediately correct hypotension by infusion of colloidal solutions (albumin, plasma) or isotonic salts.

Drugs acting on blood vessels: dopamine dose 3 (g / kg/min to improve renal blood flow.

Little anuria stage

The basic goals in this stage are:

Keep homeostasis.

Limiting hyperkalaemia.

Limit blood urea increase.


In anuria, negative equilibrium means that the amount of water in is less than the amount of water out. Usually about 500ml of water, including eating and drinking. In cases of anuria due to loss of saltwater, the fluid must be compensated.

Electrolytes and acidosis:

Treatment of hyperkalaemia.

Limit the introduction of potassium from the outside: potassium-rich vegetables, fluids with potassium.

Eliminate necrotic foci, fight infection.

Diuretic: to eliminate electrolyte water, especially potassium, is indicated when there is no evidence of post-renal blockage, the dose can be detected with Lasix 20mg x 4 intravenous syringes, high doses are possible. 200mg - 500mg / 24 hrs. Very high dose can be ordered as Furosemide 1000mg / 24 hrs by slow infusion via electric syringe. In addition to furosemide can use bumetanide or etacrynic acide.

Natribicarbonate infusion: Natribicarbonate can be infused 1.4% or 4.2% when the patient has a certain amount of urine (For example 300 - 500ml). Sodium bicarbonate can be injected provincially 8.4% if you want to limit water intake, Sodium bicarbonate helps to improve acidosis, thereby limiting the transfer of potassium from intracellular to extracellular.

Hypertonic glucose infusion with fast-acting insulin aims to push potassium into the intracellular region.

Give calcium by slow intravenous injection in cases of severe hyperkalaemia, emergencies (especially with cardiovascular manifestations).

You can use ion exchangers such as resonium, Kayexalate (30 grams / 24 hours) to excrete potassium through the stool.

If blood potassium ≥ 6.5 mmol / l, then need to indicate dialysis outside the kidney.

Treatment of other electrolyte disorders:

Sodium and chlorine: Low blood sodium is usually caused by water retention. It is best to limit water. When blood sodium is much lower, it is necessary to compensate for sodium.

Calcium: In acute tubular inflammation in the presence of hypocalcaemia. If Tétani occurs due to hypocalcaemia, calcium chloride or calcium gluconate can be given.

Treatment of hyperuricemia:

Diet reduced protein, enough calories at least 35 kcal/kg / 24 hours, enough vitamins.

The drugs that increase protein anabolism such as Durabolin 25 mg/day, Testosterone 25 mg/day.

Additional ketosteroid tablets: 1 600mg tablet for 5 kg of body weight / day.

Eliminate foci of infection.

Dialysis indication: should prescribe early dialysis by artificial kidney or peritoneal dialysis. Dialysis is indicated when:

Blood potassium ≥ 6.5 mmol /.

Blood urea> 35mmol / l.

Creatinine blood> 600mmol / l.

There are manifestations of acidosis.

During the period of multiple urination

At this stage, although the urination is much, kidney function has not recovered. In the early days of the urinary period, the concentration of urea, blood creatinine increases, so the treatment of hyperuricemia is sometimes the same as when urinating less and anuria. . Treatment aims to:

Continue to restrict food protein, increase protein only when blood urea has decreased to a safe level (10 mmol / l). Give a diet containing potassium (fruit) when blood potassium is normal.

Infusion or drink to prevent dehydration, loss of electrolytes. In the case of urine volume> 3 liters / 24 hours, it is necessary to compensate by intravenous infusion. The amount of rehydration fluid depends on the amount of urine. After 5-7 days of excessive urination can gradually limit the amount of infusion and follow up because the kidneys have begun to function to concentrate.

In the recovery stage

On average, after 4 weeks of treatment, kidney function began to recover well and patients were discharged from the hospital

Monthly monitoring is required until complete renal function is restored.

When blood urea returns to normal, gradually increase protein ratio, ensure enough calories, vitamins to ensure good health recovery.

Treat the cause.

Depending on the cause of the acute tubular inflammation.

Antibiotic treatment in infectious etiology.

Eliminate toxins in poisoning causes.

Stop anti-inflammatory drugs other than steroids, ACE inhibitors.

Antibiotics, Contrast iodine products, Anti-U drugs: Ciplastine, Cyclosporine, Interferon, Phenylbutazone ... if the cause is drug.

Treatment of malaria in haemolytic malaria.