Chronic cat kidney disease
The chronic renal disease of the cat in the older literature - (CNE) Chronic renal failure (CRF) or chronic renal failure called - is an incurable, progressive disease characterized by a gradual decrease of the nephrons and thus to a decreasing function ( failure ) of the kidney in is. It is one of the leading causes of death in older domestic cats . In the current literature, the term “kidney disease” is preferred to the term “renal insufficiency” because the disease initially proceeds without any measurable decline in kidney function. As a result of the different type of diet and the resulting metabolic peculiarities, the clinical picture and treatment differ significantly from chronic kidney failure in humans .
Chronic kidney disease occurs in cats as a result of inflammation of the kidney tubules and tissue between the kidneys for no apparent cause ( idiopathic tubulointerstitial nephritis ). The main symptoms are unwillingness to eat , increased drinking, increased urination, fatigue, vomiting and weight loss. Chronic kidney disease in cats is divided into four main stages based on the creatinine concentration in the blood plasma , which are further subdivided according to the protein-creatinine ratio in urine and blood pressure. The treatment is based primarily on reducing the protein and phosphate content of the food on the basis of the basic requirement ("kidney diet"). In addition, the numerous sequelae resulting from kidney dysfunction such as disturbances in the water, electrolyte and acid-base balance, rise in blood pressure, anemia and digestive disorders are treated with medication. Early detection and treatment can slow the progression of the disease, improve quality of life, and increase animal life expectancy.
Physiological basics
The kidney is a vital organ with a variety of tasks. It plays an important role in maintaining the water, electrolyte and acid-base balance , in the excretion of toxic metabolic breakdown products such as urea and in the recovery of valuable substances such as glucose, which are initially filtered out of the blood in the kidney corpuscles as part of ultrafiltration , Amino acids , peptides and minerals . In addition, the body's own and exogenous substances are converted and broken down in the kidney - the kidney is therefore a central metabolic organ alongside the liver . Finally, some hormone-active substances such as renin , erythropoietin and calcitriol (active form of vitamin D 3 ) are produced in the kidney . As a result, the organ is of essential importance for the regulation of blood pressure , new blood formation and calcium and phosphorus balance and thus bone metabolism.
As carnivores, cats are particularly dependent on the supply of animal proteins , because for them the formation of glucose from amino acids is the most important source of energy . The amino acid breakdown enzymes are adapted to the high protein intake and their activity is largely independent of the protein supply in the diet, so that cats break down the body's own proteins (especially from the muscles) when there is insufficient protein intake ( catabolic metabolism). Meat and offal also contain essential nutrients for the cat, such as vitamin A , taurine or arachidonic acid . Compared to normal human diet, cats consume around six times more dietary phosphate with commercially available cat food . This makes it difficult to achieve a phosphorus reduction in cat food similar to that which human medicine strives for in human kidney diets .
Pathophysiological basics
Symptoms of the disease only appear at an advanced stage, when more than two thirds of the original kidney function has already been lost. This is due to the body's own compensation mechanisms and the reserve capacity of the kidneys, which can compensate for the reduced kidney function for a long time and maintain the excretion of urinary substances. With the loss of functioning nephrons - the functional building block of the kidney - the filtering performance of the kidney corpuscles ( glomerular filtration rate ) decreases and with it the excretion capacity for urinary substances.
The increased urea levels in the blood ( uremia ) lead to nausea and vomiting for various reasons. On the one hand, they directly stimulate chemoreceptors in the chemoreceptor trigger zone in the brain. Second, they increase gastrin secretion and thus lead to an increase in gastric acid formation and thus to over-acidification of the stomach. Eventually, they cause inflammation of the blood vessels (uremic vasculitis ), which leads to further damage to the digestive tract.
As a result of the accumulation of phosphate in the blood ( hyperphosphataemia ) and the reduced formation of calcitriol in the remaining main pieces , there is a drop in the calcium blood level ( hypocalcemia ) and more parathyroid hormone is released from the parathyroid gland . Chronic kidney disease leads to an overactive parathyroid gland in 84% of cases (secondary renal hyperparathyroidism ). Among other things, the parathyroid hormone causes calcium and phosphate to be released from the bones, which ultimately leads to kidney-related bone disorders and calcification of the kidneys, skin, heart and blood vessels. In the kidneys, this calcification contributes to the further destruction of kidney tissue. The reduced responsiveness of the parathyroid cells to calcium disrupts the negative feedback of the parathyroid hormone secretion, so that despite the increase in the calcium level, parathyroid hormone is still released. Since less phosphate reaches the kidney tubules due to the reduced filtration rate, the inhibitory effect of the parathyroid hormone on the reuptake in the main part has only a minor effect on the blood phosphate level.
The loss of nephrons and the associated decrease in the number of sodium ion channels leads to a decrease in the concentration gradient in the kidney. However, this is the driving force for the water recovery in the middle section and - in the presence of ADH - also in the collecting pipes . The result is a loss of water through the urine and thus a dehydration of the body, which is intensified by the loss of fluid when vomiting.
One consequence of the kidneys' reduced ability to excrete hydrogen ions, phosphate and sulphate as well as the excessive loss of bicarbonate is metabolic acidification of the blood ( metabolic acidosis ). Metabolic acidosis occurs in 80% of cats with chronic kidney disease.
With increasing kidney damage, the autoregulation of kidney blood flow is also impaired, which normally ensures that the blood flow and thus the filter performance are independent of general blood pressure up to a threshold of 60 mm Hg . As a result, kidney performance is reduced when blood pressure is low, and high blood pressure, which is often associated with chronic kidney disease, causes further damage due to the pressure overload on the kidney corpuscles. The increase in blood pressure occurs as a result of the hardening of the blood vessels in the area of the kidney corpuscles, the reduced formation of vasodilating prostaglandins and the activation of the renin-angiotensin-aldosterone system .
Occurrence and causes
Chronic kidney disease is one of the leading causes of death in older domestic cats. In many animals, however, the disease initially remains undetected, since in the early stages of chronic kidney disease clinical symptoms are often absent due to the reserve capacity of the kidneys and sufficiently sensitive diagnostic tests are not available for routine use. The data on the frequency of the disease in cats are contradicting, they vary between 1.6 and 20%. Chronic kidney disease occurs more frequently in older cats: over 50% of the affected cats are seven years old or older and 30% of all cats over 9 years old have elevated blood levels of nitrogen compounds ( azotemia ). The disease can occur as early as 9 months. A breed predisposition has been demonstrated for Maine Coon , Abyssinian , Siamese , Russian Blue and Burmese .
Since the kidneys have a high reserve capacity and clinical symptoms do not appear until two thirds of the original kidney function has been lost, the triggering factors must damage both kidneys.
Chronic kidney disease in cats is idiopathic tubulointerstitial nephritis, i.e. inflammation of the kidney tubules and the tissue between the kidneys for no apparent cause. In addition to the damage that this primary disease directly affects the kidney tissue, the body's own repair mechanisms, such as the formation of connective tissue, are activated, leading to a further, partially self-sustaining, loss of functional kidney tissue. Causes the decreased ability of the kidney to excrete sodium and water retention of these substances and thus an increase in blood volume, which ultimately results in an increase in blood pressure result. It affects about two-thirds of all cats with CKD. High blood pressure, in turn, leads to increased connective tissue formation. A potassium deficiency or an excess of calcium that is secondary to other kidney damage causes further damage to the kidney tissue.
| root cause | Remarks |
|---|---|
| Damage to the kidney corpuscles | |
| chronic glomerulonephritis | Inflammation of the kidney corpuscles |
| Glomerulosclerosis | “Hardening” of the kidney corpuscles through the formation of connective tissue |
| Damage to the kidney tubules | |
| idiopathic tubulointerstitial nephritis (CKD) | Inflammation of the kidney tubules and the tissues between the kidneys |
| chronic pyelonephritis | Inflammation of the renal pelvis with involvement of the kidney tissue |
| Nephrocalcinosis | Kidney damage due to excess calcium in the blood |
| Hypokalemic nephropathy | Kidney damage due to lack of potassium in the blood |
| Granulomatous nephritis | nodular inflammation of the kidneys, in cats mainly due to feline infectious peritonitis (FIP) |
| Kidney tumors | Above all, malignant lymphomas , other tumors such as kidney cancer , transitional cell carcinoma , nephroblastoma and hemangiosarcoma do not usually occur on both sides |
| Kidney amyloidosis | pathological protein deposition, accumulated in Abyssinian and black-footed cats |
| Polycystic Kidney Disease | Hereditary cyst formation in Persian cats |
| Damage to the urinary tract | |
| Kidney stones | Deposits of concretions in the urinary tract |
| Hydronephrosis | "Water sac kidney" as a result of urinary retention |
| perirenal increases in size | only if bilateral: cysts, bruises , pseudocysts and other space-occupying processes in the area around the kidney |
| Kidney worm infestation | Infection with Dioctophyma renale , rare and only in southern Europe, Asia and North America |
| Damage due to vascular disease | |
| Arterial hypertension | general high blood pressure |
| Glomerular hypertension | High blood pressure in the kidney corpuscles |
| Disseminated intravascular coagulopathy | Blood clotting within the blood vessels |
Other diseases can also trigger kidney dysfunction, for example infections , autoimmune diseases , poisoning or tumors . Practically every infection or " lupus erythematosus " can lead to the deposition of antigen-antibody complexes in the basement membrane of the kidney corpuscles and thus to their damage. Many types of lily , ethylene glycol , melamine , cyanuric acid and some heavy metals ( cadmium , lead , mercury ) have a strong toxic effect on the kidneys (kidney toxicity ) in cats . But also many drugs such as amphotericin B , cholecalciferol , doxorubicin , polymyxins , aminoglycosides and numerous non-steroidal anti-inflammatory drugs (→ analgesic nephropathy ) can cause kidney damage.
Symptoms
The main symptoms of chronic kidney disease in cats are unwillingness to eat ( anorexia ), increased drinking ( polydipsia ), increased urination ( polyuria ), fatigue ( apathy ), vomiting and weight loss. In addition, the oral mucosa (due to uremia diarrhea, inflammation stomatitis ) with formation of ulcers ( ulcers ), increased salivation ( drooling ) and bad breath occur. Increased blood pressure ( arterial hypertension ) with damage to the eye ( fundus hypertonicus , hypertensive retinopathy), anemia , itching , drying out ( dehydration ), soft tissue calcifications , bleeding and water retention in the tissues ( edema ) are also more common side effects. Severe uremia can also lead to neurological symptoms such as indifference , seizures , delirium , coma , abnormal movements and muscle disorders ( myopathies ).
Typically the symptoms - in contrast to acute kidney failure - creep in over weeks, months or even years, and the general condition is poor. In addition, acute kidney failure is initially characterized by reduced urine production. However, an existing mild or moderate chronic kidney disease is often suddenly worsened by an acute event (" exacerbation ") and thus conspicuous for the cat owner. This can be the case, for example, if one kidney has already passed into a non-functioning, shrunken kidney due to urinary accumulation and the second suddenly swells and is damaged ("large kidney-small kidney syndrome") due to urinary congestion ( hydronephrosis ) or if an overactive thyroid is being treated and the glomerular filtration rate is suddenly reduced.
A palpation examination can be used to check the kidneys for pain, firmness (consistency), enlargement or reduction, and changes in the surface structure. The healthy kidney is about 4 cm long, 3 cm wide and 2–3.5 cm thick. In the most common form - CKD due to tubulointerstitial nephritis - the kidneys are usually smaller and have an irregular surface; in tumors or pyelonephritis, they can be enlarged and sensitive to pain. Since the degree of protein loss via the urine is directly related to the increase in blood pressure, regular blood pressure measurement is useful.
With an X-ray examination , changes in size, density and position of the kidneys as well as some kidney stones ( struvite and calcium oxalate stones are "radiopaque") and soft tissue calcifications can be detected. In the case of severely emaciated cats or fluid accumulations in the retroperitoneal space, however, the kidney is only partially visible in the X-ray image due to the resulting decrease in contrast. Excretory urography , in which a radiopaque contrast agent (e.g. iopamidol , iohexol ) is injected into the bloodstream and its excretion via the kidneys is x- rayed, has a higher diagnostic value . This can be used to detect circulatory disorders, functional disorders of the kidney corpuscles and obstruction of the drainage channels.
The ultrasound examination allows to show morphological changes in the kidneys in more detail. In addition to changes in size and shape, kidney cysts, locally delimited (focal) organ damage, water sac kidneys and urinary congestion as well as tumors can also be shown. Hardly demarcated (diffuse) organ changes are associated with changes in echogenicity, but can only rarely be assigned to defined diseases. " Pulsed-Wave-Doppler " can also be used to detect circulatory disorders.
The kidney biopsy is not routinely used, but may be indicated in certain previous reports - for example, young Abyssinian cats with symptoms of kidney disease to detect amyloidosis. The computer and magnetic resonance imaging while having a very good detail recognition, but playing in veterinary medicine because of the high cost and limited availability of only a minor role.
Laboratory diagnostic findings
The urine test is essential for chronic kidney disease in cats. Damage to two thirds of the nephrons already results in a reduced ability to concentrate urine and the specific gravity drops below 1030 N · m −3 . The loss of protein via the kidneys is demonstrated by an increase in the protein-creatinine ratio in the urine (UPC), since 24-hour pool samples are not practical in cats. The UPC is a good marker for the early detection of CKD as it reveals kidney dysfunction even before the blood creatinine rises. In the urine sediment , effusions from the kidney tubules ( cylinders ) can also be detected, and in the case of chronic bacterial inflammation of the renal pelvis, bacteria or pus can be detected. Detection of small amounts of albumin (<300 mg / l, “ microalbuminuria ”) is very sensitive , but not very specific for chronic kidney disease.
| parameter | Reference range |
|---|---|
| Creatinine | <170 µmol / l (<2 mg / dl) |
| SDMA | <14 µg / dl |
| urea | 5–11 mmol / L (30–65 mg / dL) |
| phosphate | 0.8-1.9 mmol / l |
| Calcium | 2.3-3.0 mmol / l |
| potassium | 3.0-4.8 mmol / l |
| sodium | 145-158 mmol / L |
The content of nitrogenous substances such as urea and creatinine ( uraemia or azotemia ) and phosphate ( hyperphosphataemia ) is usually increased in the blood serum . The potassium content is usually reduced ( hypokalaemia ), but it can also be increased - with sodium it is the other way round. If the cause of the kidney disease lies in the kidney corpuscles, albumin deficiency ( hypoalbuminemia ) and excess cholesterol ( hypercholesterolemia ) also occur. The determination of cystatin C has not been evaluated for cats ; this protein can be increased in cats even with an overactive thyroid or glucocorticoid administration and can decrease sharply for several hours after eating. Recent research suggests that symmetric dimethylarginine (SDMA) is a suitable marker for kidney function in cats. The SDMA concentration shows close correlations with the glomerular filtration rate and the creatinine concentration. It can already detect a 40% loss of function in the kidney, i.e. before there is a rise in creatinine in the blood.
The most sensitive method of kidney function diagnostics is the direct determination of the glomerular filtration rate via the clearance , which is already reduced in chronic kidney disease before azotemia occurs. Various substances have been evaluated for cats, the most practical being creatinine and iohexol . Creatinine is eliminated more slowly than iohexol, but in many veterinary practices it can be determined immediately photometrically even without the involvement of a special laboratory.
In the blood image is shown in advanced kidney disease, a decrease in the number of red blood cells and thus the hematocrit without changing the blood pigment loading and the cell sizes of red blood cells and no signs of blood cell formation ( normochromic, normocytic, pure red cell aplasia anemia ).
Classification
Chronic kidney disease in cats is currently divided into four main stages by the International Renal Interest Society (IRIS) and, as adapted from it, the European Society for Veterinary Nephrology and Urology , with the creatinine concentration in the blood plasma being used as the main criterion. In addition, sub-stages are defined using the protein-creatinine ratio in the urine and blood pressure. The plasma creatinine concentration should be confirmed by at least two measurements at an interval of one to two weeks, the protein-creatinine quotient in the urine by two or three measurements over a period of two to four weeks.
| stage | Plasma creatinine concentration | Remarks |
|---|---|---|
| I. | <140 µmol / l (1.6 mg / dl) | no azotemia, but other abnormal kidney findings |
| II | 140–249 µmol / L (1.6–2.8 mg / dl) | low azotemia, clinical symptoms are weak or not at all pronounced in this area, residual kidney function about 33% |
| III | 249–442 µmol / L (2.9–5.0 mg / dL) | moderate azotemia, clinical symptoms are pronounced at this stage, residual kidney function about 25% |
| IV | > 442 µmol / l (5.0 mg / dl) | severe azotemia, usually accompanied by severe clinical symptoms, residual kidney function <10% |
| Lower stage | Protein-creatinine ratio in urine | Remarks |
|---|---|---|
| a | <0.2 | no protein loss through the urine |
| b | 0.2-0.4 | Protein loss via the urine is questionable, should be confirmed by repeated measurements |
| c | > 0.4 | Loss of protein in the urine ( proteinuria ) |
| Lower stage | Blood pressure in mmHg ( systolic : diastolic ) |
Remarks |
|---|---|---|
| 1 | <150: <95 | Blood pressure with no risk of organ damage occurring |
| 2 | 150-159: 95-99 | low risk of organ damage occurring |
| 3 | 160-179: 100-119 | moderate risk of organ damage occurring |
| 4th | > 180:> 120 | high risk of organ damage occurring |
Differential diagnoses
In the sum of all examination results, chronic kidney disease can hardly be confused with any other disease. There is only broad agreement with acute renal insufficiency. The clinical course (see symptoms) is particularly suitable as a delimitation criterion. In addition, in acute kidney failure, the blood pressure and the number of red blood cells are unchanged, and the kidneys are often enlarged and painful.
The main characteristic that determines the staging - azotemia - can have a number of other causes, which can be located “in front of the kidney” (prerenal) or “behind the kidney” (postrenal). Prerenal causes in cats are primarily blood loss, dehydration, shock , congestive heart failure, hyperthyroidism , but also fever or intense physical exertion. Possible postrenal causes are, in addition to obstruction of the urinary tract by stones or tumors, tears of the urinary bladder , the ureter or the urethra .
treatment
The possibilities of renal replacement therapy are severely limited in cats, as kidney transplants or hemodialysis in veterinary medicine are only carried out in exceptional cases due to the high equipment, logistical and financial expenditure. The aim is therefore to detect chronic kidney disease as early as possible when the kidney still has sufficient reserve capacity. At the same time, attempts are being made to reduce the amount of urinary substances - especially nitrogen compounds and phosphate - in food through dietary measures. After all, metabolic imbalances and sequelae must be buffered. From a plasma creatinine level of 7 mg / dl (618.8 µmol / l), however, drug therapy is not very promising.
Dietary measures
One problem with diet therapy with low-phosphate and protein-reduced diets is their mostly poor palatability. In addition, cats with kidney disease have hardly any appetite and getting used to a new food is even more difficult due to the negative character - the cat associates its own physical discomfort with the new food. The loss of protein in the urine also creates a negative nitrogen balance , which also reduces appetite. Finally, affected animals often show gastrointestinal tract problems. In a clinical study by Elliott et al. 34% of the cats could not be switched to the kidney diet and Plantinga et al. it was even 54%. Attempts can be made to increase the acceptance of the feed by heating it or by adding tasty additives such as tuna juice or sardines. It is therefore recommended to start the feed change only after the uremia has been eliminated and to extend it over three weeks by gradually adding it in order to avoid feed aversion. With sorbents such as activated carbon or with probiotics the development of uremic substances in the gastrointestinal tract can be attempted to reduce. Cyproheptadine or mirtazapine may be used briefly to increase appetite ; if these measures do not work, force-feeding through an esophageal or gastric tube is necessary.
Phosphate reduction
A key goal in managing cat chronic kidney disease is to reduce dietary phosphate intake early in the course of the disease. As a rule of thumb, a reduction of the phosphate content to 170 mg / MJ UE (mega joule convertible energy, see also Physiological calorific value ), i.e. to two thirds of the maintenance requirement , can apply. Commercially available cat food usually contains twice the maintenance requirement, so it should not be mixed with the diet food. If the phosphate levels in the plasma are still increased, the absorption in the intestine can be reduced by using calcium salts and phosphate binders such as aluminum hydroxide , aluminum carbonate or lanthanum carbonate . Calcium carbonate can compensate for the calcium deficiency in the initial stages, but lead to hypercalcaemia in advanced stages . Several studies have found that a reduction in dietary phosphate is enough to slow the progression of the disease. If the phosphate reduction leads to a further deterioration in the general condition, a phosphate deficiency should also be considered. This manifests itself in a similar way to chronic kidney disease: shaggy hair, loss of appetite, weakness, exhaustion and anemia. Calcitriol can also be used to treat secondary hyperthyroidism , but only if the parathyroid hormone and calcium levels are controlled.
Protein reduction
To combat uremia, the protein content in feed and thus the amount of nitrogen supplied to the body can be reduced. This is only possible to a limited extent in cats because their energy balance is dependent on protein (see above). The protein content should be adjusted to the maintenance requirement of 15 g digestible crude protein per MJ AU and should never be reduced to below 11 g / MJ AU, whereby it should be noted that the protein amount declared on feed must be multiplied by a factor of 0.86 to determine the digestible Obtain crude protein. High-quality animal protein also reduces the amount of nitrogen compounds reaching the large intestine and thus the amount of ammonia produced by bacterial degradation processes in the intestinal flora .
Treatment of the side effects
Dehydration
Sufficient fresh drinking water should be provided to combat dehydration. Here, too, an attempt can be made to increase the cat's voluntary water intake by adding meat broth or tuna juice. If these measures are unsuccessful, sterile infusion solutions should be administered under the skin or through a feeding tube from stage III .
Metabolic acidosis and potassium
The bicarbonate content should ideally be between 17 and 22 mEq / l. For buffering purposes, sodium bicarbonate or potassium citrate are administered, with the latter at the same time compensating for any existing potassium deficiency. A diet rich in potassium and magnesium is recommended and is already implemented in most commercial kidney diets. Also potassium gluconate can a potassium deficiency are used to offset, potassium chloride on the other hand mostly bad accepted by cats and often causes disturbances in the gastrointestinal tract. It must be noted that through the renal excretion in stage IV, by ACE inhibitor or an aldosterone due renin lack a hyperkalemia may occur, which is why potassium levels should be monitored regularly and must be used a low-potassium diet may.
high blood pressure
Over 60% of cats with kidney disease develop high blood pressure. Amlodipine or atenolol are mainly used for treatment . If the blood pressure lowering effect of these active substances is insufficient , an ACE inhibitor such as benazepril , enalapril or ramipril can also be administered. The administration of an ACE inhibitor alone usually does not lead to a sufficient reduction in blood pressure, but can slow the progression of the disease up to stage III. In stage IV, ACE inhibitors are considered to be relatively contraindicated . Of these active ingredients, benazepril and ramipril are currently approved for cats in Germany; all others must be repurposed . The AT1 antagonist telmisartan has also been approved for the treatment of high blood pressure and proteinuria in cats since 2014 . Telmisartan can significantly reduce the level of proteinuria. In diet terms, the tendency to high blood pressure can be reduced by reducing the sodium content of the feed.
Anemia
To combat anemia , it is particularly useful to add iron to the feed in the form of organic iron compounds or iron sulfate . The iron content in the feed should be slightly above the maintenance requirement of 5 mg / MJ AU. If the hematocrit drops nevertheless, blood transfusions are indicated. Anabolic steroids to increase the formation of new blood only work slowly in cats, their benefit is questionable. Recombinant human erythropoietin can be indicated from a hematocrit <20%. The treatment is expensive, however, and about a third of all cats form antibodies against this active ingredient, which results in anemia that is no longer treatable. With darbepoetin , the risk of antibody formation is apparently significantly lower, it also has a longer plasma half-life and is more potent.
Gastrointestinal tract
Secondary consequences of uremia on the gastrointestinal tract in cats are primarily fibrosis and mineralization of the gastric mucosa , but not gastric ulcers , so that gastric acid blockers such as omeprazole, which have long been recommended for therapy , must be critically reviewed. Mirtazapine has proven itself to stimulate the appetite and reduce uraemic nausea .
Kidney transplant
A kidney transplant is only possible in a few specialized facilities and is costly. The basic requirements are decompensated renal insufficiency in the early stages, which no longer responds to conventional treatment, a previous weight loss of a maximum of 20%, the absence of serious comorbidities and negative tests for chronic viral infections such as feline leukemia or the immunodeficiency syndrome in cats . Also, urinary tract infections should not have occurred in the recent past.
Interactions with other treatments
Since the kidney is an important excretory organ for numerous drugs, chronic kidney disease must be taken into account in the drug therapy of other diseases. The plasma half-life can be significantly extended (for example with numerous antibiotics) and the dose must be reduced accordingly. Active ingredients that can only be administered with caution in cats with kidney disease include atenolol , carbimazole , chlorothiazide , digoxin, and thiamazole .
Treatment prospect
It is not possible to restore lost nephrons, so that all therapeutic measures only increase the quality of life and the lifespan. The prospect of treatment depends heavily on the degree of azotemia, the loss of protein via the urine, hyperphosphataemia and uremia, and the hematocrit. In stage 2, a low hematocrit and a high urine-protein-creatinine ratio, and in stage 3, hyperphosphataemia are prognostic for progression of the CKD. In a recent study, the mean survival time in stage IIb cats was 1151, stage III 778 and stage IV only 103 days. The consistent use of phosphate-reduced kidney diets shows quite good results up to stage III. If the measures taken do not respond, the only thing left to do with advanced kidney disease is euthanasia .
literature
- Sarah Steinbach and Reto Neiger: Chronic kidney disease : In: Hans Lutz et al. (Ed.): Diseases of the cat . Enke, 5th edition 2014, ISBN 978-3-8304-1243-4 , pp. 751-755.
- Gregory F. Grauer: Chronic renal failure . In: RW Nelson and CG Couto (eds.): Small animal internal medicine . Mosby, 3rd Edition 2003, ISBN 0-323-01724-X , pp. 615-623.
Individual evidence
- ↑ K. Sturgess: Nutritional Management of Renal Disease . In: Proceedings of the 33rd WSAVA / FECAVA Congress, Dublin 2008, pp. 281-284.
- ^ A b R. Kirby: The cat is not a small dog : In ICU: Parts I and II, Proceedings 29th World Congress of the WSAVA, Rhodes 2004.
- ↑ a b c D. J. Chew: The role of phosphorus in feline chronic renal disease . In: ESFM Feline Congress 2008 Edinburgh, Scientific Proceedings, pp. 59-65.
- ↑ R. Heine: Laboratory diagnostics in feline kidney diseases . In: Veterinary Focus 18 (2008), pp. 16-22. ISSN 0965-4593
- ↑ a b c d Reto Neiger: Chronic renal insufficiency . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke, 4th edition 2005, ISBN 3-8304-1049-2 , p. 406.
- ^ A b Gregory F. Grauer: Chronic renal failure . In: RW Nelson and CG Couto (eds.): Small animal internal medicine . Mosby, 3rd edition 2003, ISBN 0-323-01724-X , p. 617.
- ↑ a b c d Thierry Francey and Elisabeth Müller: Chronic kidney disease - early detection and importance of phosphates. In: veterinärspiegel 3 (2010), pp. 107-112.
- ↑ a b Reto Neiger: Chronic renal insufficiency . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke, 4th ed. 2005, p. 411.
- ↑ a b c d e D. J. Polzin et al .: Chronic renal failure. In: SJ Ettinger and EC Feldmann (Eds.): Textbook of Veterinary Internal Medicine. Saunders, 5th Edition, Philadelphia 2000, Volume 2, pp. 1634-1662. ISBN 0-7216-7256-6
- ↑ a b Reto Neiger: Chronic renal insufficiency . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke, 4th ed. 2005, p. 410
- ^ AP Carr, B. Egner: Blood pressure in small animals - Part 2: Hypertension - Target organ damage, heart and kidney . In: Eur. J. Comp. Anim. Pract. 19 (2009), pp. 13-17. ISSN 1018-2357
- ↑ a b c Reto Neiger: Chronic renal insufficiency . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke, 4th ed. 2005, p. 409.
-
^ GF Grauer: Early detection of renal damage and disease in dogs and cats. In: Vet Clin Small Animal 35 (2005), pp. 581-596.
AM Wolf: Chronic Progressive Renal Disease in the Cat: Recognition and Management In: North American Veterinary Conference Orlando, NAVC Proceedings, Vol. 20, Small Animal Edition, 2006, pp. 701-703. - ↑ A. Parotat, B. Kohn: Chronic Renal Insufficiency - What does an effective management look like? In: kleintier specifically 12 (2009), pp. 6–10.
- ↑ a b R. E. Jepson et al .: Evaluation of predictors of the development of azotemia in cats. In: J. Vet. Intern. Med. 23 (2009), pp. 806-813. ISSN 0891-6640 , PMID 19566846
- ↑ a b c d e f g Thierry Francey, Ariane Schweighauser: Clinical epidemiology of kidney diseases in cats. In: Vet. Focus 28 (2008), pp. 2-7. ISSN 0965-4593
- ↑ Sarah Steinbach and Reto Neiger: Chronic kidney disease : In: Hans Lutz et al. (Ed.): Diseases of the cat . Enke, 5th edition 2014, ISBN 978-3-8304-1243-4 , p. 751.
- ↑ a b Rosanne Jepson: The Importance of Kidney Disease in Cats . In: veterinärspiegel 2013, issue 2, pp. 59–64.
- ↑ KA Terio et al .: Amyloidosis in black-footed cats (Felis nigripes). In: Vet. Pathol. 45 (2008), pp. 393-400, PMID 18487501 .
- ↑ a b Johanna Fink-Gremmels: Poisonings . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke-Verlag, 4th edition 2005, pp. 789–803. ISBN 3-8304-1049-2
- ↑ a b c Deniz Seyrek-Intas and Martin Kramer: Image-giving diagnostics of the kidney in cats. In: Vet. Focus 18 (2008), pp. 23-30. ISSN 0965-4593
-
^ BJ Rivers et al .: Duplex Doppler estimation of Pourcelot resistive index in arcuate arteries of sedated normal cats. In: J. Vet. Intern. Med. 10 (1996), pp. 28-33. PMID 8965265
B.J. Rivers et al .: Duplex doppler estimation of intrarenal pourcelot resistive index in dogs and cats with renal disease. In: J. Vet. Intern. Med. 11 (1997), pp. 250-260. PMID 9298481 - ↑ a b c d Redun Heine: Laboratory diagnostics in feline kidney diseases. In: Vet. Focus 18 (2008), pp. 16-22. ISSN 0965-4593
- ^ A b c Christian F. Schrey: Key symptoms and key findings in dogs and cats . Schauttauer, 2nd edition 2005, ISBN 3-7945-2384-9
- ↑ Kidney diseases - diagnostics from blood and urine. In: Laboklin aktuell 2/2009
- ↑ J. Braff, E. Obare, M. Yerramilli, J. Elliott, M. Yerramilli: Relationship between serum symmetric dimethylarginine concentration and glomerular filtration rate in cats. In: Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Volume 28, number 6, 2014 Nov-Dec, pp. 1699-1701, doi: 10.1111 / jvim.12446 , PMID 25272985 .
- ↑ SDMA: Diagnosis kidney disease earlier
- ↑ IRIS guidelines for cats
- ↑ a b c d e f g h i Katharine Arnell and Sheri Ross: Advances in the treatment of chronic kidney disease in cats. In: Vet. Focus 19.3 (2009), pp. 6-14.
- ↑ L. Bernsteen et al .: Renal transplantation in cats. In: Clin. Tech. Small Anim. Pract. 15 (2000), pp. 40-45, PMID 10911684 .
- ↑ JR Fischer et al .: Veterinary hemodialysis: advances in management and technology. In: Vet. Clin. North Am. Small Anim. Pract. 34 (2004), pp. 935-967, PMID 15223210 .
- ↑ a b c J. Elliott et al .: Survival of cats with naturally occurring renal failure: Effect of conventional dietary management . In: Journal of Small Animal Practice 41 (2000), pp. 235-242. ISSN 0022-4510
- ↑ a b c E. A. Plantinga et al .: Retrospective study of the survival of cats with acquired chronic renal insufficiency offered different commercial diets . In: Veterinary Record 13 (2005), pp. 185-187, PMID 16100367 .
- ^ J. Elliott: The role of phosphate in chronic kidney disease (CKD) progression . In: Small Animal Medicine UK Vet. 13 (2008), pp. 23-28 and pp. 37-46.
- ↑ a b P. J. Barber et al .: Effect of dietary phosphate restriction on secondary renal hyperparathyreoidism in the cat. In: Journal of Small Animal Practice, 40 (1999), pp. 62-70, PMID 10088085 .
- ↑ Reto Neiger: Chronic renal failure . In: Marian C. Horzinek et al. (Ed.): Diseases of the cat . Enke, 4th ed. 2005, pp. 405-407.
- ↑ H. Mizutani et al .: Evaluation of the clinical efficacy of benazepril in the treatment of chronic renal insufficiency in cats. In: J. Vet. Intern. Med. 20 (2006), pp. 1074-1079, PMID 17063698
- ↑ Ulrike Sent et al .: Comparison of the effectiveness of long-term oral treatment with telmisartan and benazepril in cats with chronic kidney disease. In: Kleintierpraxis 61 (2016), pp. 245–257.
- ↑ SM McLeland, KF Lunn, CG Duncan, KR Refsal, JM Quimby: Relationship among serum creatinine, serum gastrin, calcium-phosphorus product, and uremic gastropathy in cats with chronic kidney disease. In: Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Volume 28, Number 3, 2014 May-Jun, pp. 827-837, doi: 10.1111 / jvim.12342 . PMID 24628683 .
- ↑ JM Quimby, KF Lunn: Mirtazapine as an appetite stimulant and anti-emetic in cats with chronic kidney disease: a masked placebo-controlled crossover clinical trial. In: Veterinary journal (London, England: 1997). Volume 197, number 3, September 2013, pp. 651-655, doi: 10.1016 / j.tvjl.2013.05.048 . PMID 23838205 .
- ↑ JN King et al .: Prognostic factors in cats with chronic kidney disease. In: J. Vet. Intern. Med. 21 (2007), pp. 906-916, PMID 17939542
- ↑ S. Chakrabarti, HM Syme, J. Elliott: Clinicopathological variables predicting progression of azotemia in cats with chronic kidney disease. In: Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Volume 26, number 2, 2012 Mar-Apr, pp. 275-281, doi: 10.1111 / j.1939-1676.2011.00874.x , PMID 22269057 .
- ↑ LM Boyd et al .: Survival in cats with naturally occurring chronic kidney disease (2000-2002). In: J. Vet. Intern. Med. 22 (2008), pp. 1111-1117, PMID 18691369
