Azoemia: Symptoms, Causes, Forms, Consequences

The azotemia is a condition characterized by the presence of nitrogen compounds in the blood. It is a term that results from the fusion of the Greek words “azote” (lifeless), used to designate nitrogen, and “haima”, which refers to blood.

It should be noted that the nitrogen referred to is not the one that can be present in the blood as dissolved gas or forming part of the molecular structure of plasma proteins or blood cells, but that of other small waste molecules.

Among the latter, urea and creatinine stand out. Urea is synthesized in the liver as the end product of protein catabolism, while creatinine is produced in muscle from phosphocreatine. Both substances are produced daily at a more or less constant rate.

Urea and creatinine are eliminated by the kidney at a daily rate that matches their production, thus keeping their blood concentrations within certain normal limits. The altered kidney function reduces the excretion of these substances and their blood values ​​increase.

Azotemia is thus a condition produced by alterations in renal function and characterized by the increase in blood concentrations of urea and creatinine, as a result of the kidneys’ inability to excrete the amounts produced daily by the body.

Causes

A part of the plasma that enters the kidney (renal plasma flow, RPF = 600-700 ml / min) is filtered at the level of the renal glomeruli and represents the glomerular filtration volume (GFR = 100-120 ml / min). What is contained in this filtrate and that is not reabsorbed, ends up being eliminated with the urine.

The kidney can reduce the filtered amount of a substance by returning it to the circulation by tubular reabsorption, or increase it by adding more from the circulation to the tube by secretion. The final excretion of the substance depends on the balance of these three processes.

Urea and creatinine begin their excretion by filtering at the level of the glomeruli. Urea undergoes tubular reabsorption, excreting 50% of the filtrate. Creatinine undergoes a small secretion process, which is why more is excreted than filtered.

The causes of azotemia are associated with those of renal failure, a syndrome characterized by a significant reduction in glomerular filtration volume (GFR) with retention of nitrogenous waste products (azotemia) and disturbance of the volume and composition of the extracellular fluid.

Forms of azotemia

According to its progression, kidney failure can be acute (ARF) when the kidneys stop working abruptly and its consequences manifest themselves within hours or days; or chronic (CRF), when over months or years there is a slow, progressive and irreversible loss of kidney function.

Although there is a form of azotemia associated with CRF and that would include the accompanying hyperazoemia of its final uremic stage, the forms of azotemia mentioned in the literature are rather associated with three types of ARF of various origins as described below.

Prerenal azotemia

It accompanies an ARF in which the kidney tissue is undamaged and alterations in previous structures reduce the blood supply to the kidney. Reduced renal blood flow reduces GFR and excretion of water (diuresis) and solutes that accumulate in body fluids.

Prerenal causal alterations could be the reduction of intravascular volume due to bleeding, diarrhea or vomiting, and burns; heart failure; peripheral vasodilation with arterial hypotension and renal hemodynamic abnormalities such as renal artery stenosis, embolism or thrombosis.

Intrarenal azotemia

It presents with direct alterations of the renal parenchyma that include lesions of small vessels and glomeruli (glomerulonephritis), damage to the tubular epithelium (acute, ischemic or toxic tubular necrosis) and lesions of the interstitium (pyelonephritis, allergic interstitial nephritis).

Postrenal azotemia

It results from the partial or total blockage or obstruction of the flow of urine somewhere in the urinary tract, with retrograde alteration of the glomerular filtration volume. These include: (1) bilateral ureter or renal pelvis obstruction, (2) bladder obstruction, and (3) urethral obstruction.

Symptoms

Although high levels of urea and creatinine are not toxic in themselves and do not imply specific symptoms, in moderate forms of azotemia nausea, vomiting, and a feeling of fatigue may occur. Other symptoms result from different accompanying alterations in kidney function.

With a very low glomerular filtration volume (<30%), little urine (oliguria and even anuria), fluid retention, and edema are produced. There are electrolyte disturbances such as acidosis, hyperkalemia, hyperphosphatemia, and hypocalcemia, and retention of phenols, sulfates, and guanidine bases. The production of kidney hormones also fails.

These alterations can lead to the condition known as uremia, in which edema, anorexia, nausea, vomiting, diarrhea, weight loss, itching, bone alterations, anemia, extreme oliguria, cardiac arrhythmias and neurological alterations, including coma and death.

Other symptoms in the various forms of azotemia can be very varied and complex, since it would include the manifestations not of renal failure itself, but of failures in other extrarenal systems.

Consequences

The kidney recovers its function after an acute injury, especially if the causes of the dysfunction are treated effectively. However, failure, especially chronic failure, can progress through about five stages in which the glomerular filtration volume is progressively reduced.

The last stage is the terminal stage or kidney failure. During it, the glomerular filtration volume can fall to values ​​below 15 ml / min and anuria with extreme azotemia and terminal uremia that is incompatible with life can be triggered, unless a replacement therapy is started.

Treatment

The objectives of the treatment of an azotemia are: on the one hand, to eliminate or reduce as much as possible the primary, renal or extrarenal causes of it, and on the other to reduce the impact of the specific physiological alterations of renal function in the organism.

In the first case, for example, whatever is causing the reduction in renal blood flow should be corrected, improving circulating volume (blood volume) or cardiovascular function to maintain blood pressure. Urinary tract obstruction and infections should be corrected.

The second objective is achieved by restricting the income of water, sodium, potassium and protein through the administration of appropriate solutions and a hypoprotein and hypercaloric diet. Anemia can be treated with recombinant human erythropoietin and iron and vitamin B12 supplements.

When the pre-terminal uremic state of renal failure is reached, the kidney can no longer fulfill its functions and to maintain the patient’s life, a replacement therapy must be resorted to, which may imply its intermittent connection to a dialysis machine or kidney transplantation. .

References

  1. Brady HR, Brenner BM: Acute renal failure, in Harrison’s Principles of Internal Medicine , 16 th ed, DL Kasper et al (eds). New York, McGraw-Hill Companies Inc., 2005.
  2. Skorecki K, Green J, Brenner BM: Chronic renal failure, in Harrison’s Principles of Internal Medicine , 16th ed, DL Kasper et al (eds). New York, McGraw-Hill Companies Inc., 2005.
  3. Huether SE: Alterations of renal and urinary tract function, in Pathophysiology, The Biologic Basis for Disease in Adults & Children , 4 th ed, KL McCance and SE Huether (eds). St. Louis, Mosby Inc., 2002.
  4. Guyton AC, Hall JE: Diuretic, Kidney diseases, in Textbook of Medical Physiology , 13 th ed, Guyton AC, Hall JE (eds). Philadelphia, Elsevier Inc., 2016.
  5. Stahl et RAK on: Niere und ableitende Harnwege, in Klinische Pathophysiologie , 8 th ed, W Siegenthaler (ed). Stuttgart, Georg Thieme Verlag, 2001.
  6. Silbernagl S: Die Funktion der nieren, in Physiologie , 6 th ed; R Klinke et al (eds). Stuttgart, Georg Thieme Verlag, 2010.

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