Azotemia or creatinine and urea increase, can occur in cats due to various situations. Azotemia, depending on its origin, can be divided into prerenal azotemia (when renal perfusion decreases), renal azotemia (due to kidney damage) or post-renal azotemia (alteration in the elimination of urine from the body). The causes can be very diverse, from dehydration or alteration of the circulatory flow, intoxication, an electrolyte alteration, a nephrotoxic drug or a kidney pathology, to an obstruction of the urinary tract or a uroabdomen.
What is azotemia in cats?
Azotemia is defined as the increase in non-protein nitrogenous waste products in the blood, with urea and creatinine being the most commonly measured. So to say that a cat has azotemia is to say that the cat has increased urea and creatinine or only one of the two.
What is urea?
Urea is a small molecule and the end product of protein metabolism formed in the liver in the urea cycle. This substance is filtered by the glomerulus of the kidney and reabsorbed into the renal tubule and collecting ducts of the kidney.
What is creatinine?
Creatinine is a compound that is formed through the breakdown of creatine, an importantnutrient for muscles. Creatinine is the waste product created in normal muscle metabolism and is produced at a constant rate, depending on the feline's muscle mass. Finally it is also filtered in the glomerulus of the kidney but it is not reabsorbed afterwards, being secreted in the urine.
Types of azotemia in cats
There are three types of azotemia in cats. However, in all three there is a decrease in renal glomerular filtration with the consequent increase in creatinine and urea.
Feline prerenal azotemia
Prerenal azotemia develops as a consequence of reduced kidney perfusion due to a alteration in blood flow, such as hypovolemia, inadequate cardiac output, marked vasodilation, or dehydration. In these cases, by decreasing renal perfusion, the glomerular filtration rate decreases, which causes a slower elimination of urea and creatinine, appearing in higher concentrations in blood. Urea is reabsorbed much more, appearing faster in the analysis due to the slower transit in the tubules and ducts. Creatinine is the one that will increase the slowest, since it is not reabsorbed.
In these cases, the cats must continue to concentrate the urine, its density being equal to or greater than 1.035. As the nephrons remain intact, without damage or alteration in their functionality, when perfusion is restored, renal function returns to normal.
Feline renal azotemia
In renal azotemia, as its name indicates, there has been damage to the kidney A reduction in renal function between 66-75% results in increased blood urea, after creatinine, with insufficient urine gravity (1.008-1.012).
However, a density between 1.013 and 1.034 indicates that part of the concentration capacity of the urine is intact, but it is insufficient to compensate for the losses. In addition, cats with chronic kidney disease retain the ability to concentrate urine for longer than dogs, and a density greater than 1 can be expected.020, but will remain inadequate to prevent azotemia.
Postrenal azotemia
In post-renal azotemia, renal function and glomerular filtration rate are completely normal and efficient, however the excretion products do not leave the body through the urine for a blocking the flow of urine downstream to the kidneys.
What causes azotemia in cats?
The increase in creatinine and urea can occur in various situations, so it will also depend on the type of azotemia in question.
Causes of feline prerenal azotemia
Prerenal azotemia occurs when there is no kidney damage or renal outflow obstruction and develops as a consequence of reduced perfusion of the kidney due to an alteration in the blood flow, such as:
- Hypovolemia.
- Inadequate cardiac output.
- Important vasodilation.
- Dehydration.
Causes of renal azotemia in cats
Renal azotemia occurs when there is damage to the kidneys themselves. Therefore, azotemia in these cases is produced by:
- Acute kidney disease: Sudden and intense onset with reduced glomerular filtration rate. Sometimes it can be reversible. The most common causes in cats are nephrotoxins (drugs, ethylene glycol, heavy metals, lilies, and iodinated contrast agents), hypercalcemia, hypophosphatemia, disorders that cause poor renal perfusion (hypovolemia, thrombosis, infarction, polycythemia, or hyperviscosity), or renal parenchymal disease. (pyelonephritis, glomerulonephritis, urinary tract obstruction).
- Chronic kidney disease: Progressive reduction in glomerular filtration rate and kidney function, which gives time to activate compensatory mechanisms. It is common not to find an original cause in cats, and it can derive from some cause of acute kidney disease such as urinary tract infections, non-steroidal anti-inflammatory drugs or hypovolemia. It can also be caused by high blood pressure.
Causes of postrenal azotemia in cats
Postrenal azotemia occurs when the flow of urine is blocked by extrarenal causes. In this way, the causes can be:
- Obstruction of the urethra.
- Obstruction, rupture or ligation in the ureters.
- Bladder leak or bladder rupture.
Other causes of azotemia in cats
On the other hand, high urea in cats without increased creatinine can occur after eating a protein-rich food when there is a intestinal bleeding. Elevated urea and normal creatinine may also occur in cats when protein catabolism is increased secondary to pyrexia or corticosteroid use.
However, the high creatinine in cats may simply be due to the cat having a lot of muscle mass, since the more mass muscle has, the higher the normal creatinine concentration.
Symptoms of azotemia in cats
Depending on the type of azotemia in cats, the symptoms may be:
Feline prerenal azotemia symptoms
The symptoms in this case are those related to low perfusion due to alteration of normal blood flow. In these cases, the feline may manifest:
- Anemia.
- Pale mucous membranes.
- Weak pulse.
- Skinfold increase.
- Dry mucous membranes.
- Low hematocrit.
- Decreased blood pressure.
- Alterations in heart rate and breathing.
Symptoms of renal azotemia in cats
Renal azotemia due to acute kidney disease can cause symptoms such as:
- Oliguria (reduced urine volume).
- Anuria (not urinating).
- Arched back due to kidney pain.
- Tachypnea.
- Arrhythmias.
- Temperature increase.
- Depression.
- Vomiting and/or diarrhea.
- Normal or enlarged kidneys.
Renal azotemia due to chronic kidney disease can produce symptoms such as:
- Oral ulcers.
- Halitosis.
- Dehydration.
- Anemia of chronic disease.
- Gastrointestinal signs.
- Polyuria-polydipsia.
- Kidneys reduced in size.
- Lack of appetite with weight loss.
- Vomiting.
- Acute blindness.
Symptoms of post-renal azotemia
Blockage of the flow of urine due to obstruction of the urethra by stones or mucous plugs in FLUTD (feline lower urinary tract disease), damage to the ureters or bladder rupture can produce symptoms such as:
- Dysuria (painful urination).
- Strangury (painful urination, drip).
- Frequency (urinating small amounts many times a day).
- Hematuria (urinating blood).
- Urogenital area lick.
- Urinating outside the litter box.
- Hyperkalemia (increased potassium).
Diagnosis of azotemia in cats
To detect azotemia, it is necessary to take blood to determine the concentration of urea in serum or plasma. Later it will be necessary to see if this azotemia is pre-renal, renal or post-renal.
Diagnosis of prerenal azotemia
Dehydration in cats can be determined by performing the following tests:
- Skin fold.
- Check for dryness of the mucous membranes.
- Check for sunken eyeball.
- Blood work to check for an increase in hematocrit and total protein.
A thorough physical examinationshould be performed to detect hypovolemia.
Diagnosis of renal azotemia
Glomerular filtration rate is reduced in kidney disease and the creatinine concentration has been considered as an indirect indicator of the rate of glomerular filtration. However, SDMA more accurately reflects this rate and diagnoses kidney disease earlier than creatinine, as SDMA increases when at least 25% kidney function has occurred and creatinine does not increase until this loss. is at least 75%. In addition, it must be considered that creatinine depends on the muscle mass of a cat, and may give false results in a very muscular or very thin cat such as hyperthyroids, which does not occur with this parameter.
To diagnose the stage of kidney disease, a series of measurements and parameters must be made, such as SDMA, creatinine, UPC (protein/creatinine ratio in urine) and systolic blood pressure.
A good history should be taken to find out if he has been in contact with a nephrotoxic drug or substance, if there is a urinary tract infection, hypertension or low renal perfusion and determine the concentrations of phosphorus and calcium to find the cause of kidney disease.
You should also perform a ultrasound of the kidney to assess its size and shape and to see the rest of the structures of the urinary system.
Diagnosis of post-renal azotemia
To diagnose urethral or ureteral obstruction or bladder rupture, the following tests should be performed:
- Blood biochemistry to detect azotemia, hyperkalemia, hyperphosphatemia and metabolic acidosis.
- Imaging techniques to detect fluid in the abdomen (uroabdomen) and sometimes even an obstruction may be seen. Analysis of the liquid after its extraction to know if it is urine.
- Urinalysis for crystals, mucous plugs, or blood.
Treatment of azotemia in cats
In the face of prerenal azotemia, what must be done immediately is replace the fluids and perfusion to the feline, through fluid therapy and sometimes blood transfusion.
In cases of renal azotemia, it is necessary to treat the cause of the acute kidney disease, as well as correct dehydration and electrolyte disturbances. It is important to treat concomitant diseases if they exist (diabetes, hyperthyroidism, heart disease, tumor). Specific treatment for kidney disease consists of:
- Treat dehydration with fluid therapy.
- Treat hypertension with amlodipine.
- Treat proteinuria with ACE inhibitors, such as benazepril.
- If there is hyperphosphatemia, start with a kidney feed and after a month, if the phosphate is still high, give a phosphate binder.
- Appetite stimulants such as mirtazapine.
- Antiemetics such as maropitant or metoclopramide.
- If there is gastric ulcer, omeprazole or ranitidine.
- If food is not tolerated, feed tube.
- Dietary treatment: reduction of protein, phosphorus, sodium and increase of potassium, fat and B vitamins.
- If there is anemia with hematocrit less than 20%, erythropoietin.
- Antibiotics, if there is a urinary tract infection.
In post-renal azotemia, the feline must be unblocked, damage repaired, urinary stones eliminated with diet (struvite) or surgery (calcium oxalate), and in cases of bladder rupture, surgery to restore the damage.
