Title: Chronic kidney disease in cats

{{Short description|Incurable progressive feline disease}}
[[File:Katze CNI Infusion.JPG|thumb|A cat with chronic kidney disease and typical symptoms: fatigue, emaciation and dull, shaggy coat]]

The '''chronic kidney disease of the cat''' ('''CKD''' or '''CNE''')—also called ''chronic renal insufficiency'' (CRI or CNI) or ''chronic renal failure'' (CRF) in the older literature—is an incurable, progressive disease characterized by a gradual decrease in the [[nephron]]s and thus to a decreasing function (insufficiency) of the [[kidney]]s. It is one of the most common causes of death in older [[domestic cat]]s. In current literature, the term &quot;kidney disease&quot; is preferred to the term &quot;renal insufficiency&quot; because the disease initially progresses without any measurable decline in kidney function. Due to the different type of diet and the resulting metabolic peculiarities, the clinical picture and treatment sometimes differ significantly from [[chronic kidney failure|chronic renal failure in humans]].

Chronic kidney disease occurs in cats as a result of [[inflammation]] of the [[Tubule|renal tubules]] and the renal interstitial tissue without an identifiable cause (''[[Idiopathy|idiopathic]] tubulointerstitial nephritis''). The main [[symptom]]s are a reluctance to eat, increased drinking, increased urine output, 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 quotient in the urine and [[blood pressure]]. Treatment is mainly based on reducing the protein and phosphate content of the diet to the basic requirement (&quot;renal diet&quot;). In addition, the numerous secondary symptoms resulting from renal dysfunction, such as disorders of the water, [[electrolyte]] and [[acid-base balance]], increased blood pressure, [[anemia]] and digestive disorders are treated with medication. If detected and treated early, the progression of the disease can be slowed, the quality of life improved and the life expectancy of the animals increased.

== Physiological basics ==
[[File:Cat eating mouse.jpg|thumb|Cats are carnivores.]]

The [[kidney]] is a vital [[Organ (biology)|organ]] with a variety of tasks. It plays an important role in maintaining the [[Water-electrolyte balance|water, electrolyte]] and [[acid-base balance]], in the excretion of toxic metabolic degradation products such as [[urea]] and in the recovery of valuable substances such as [[glucose]], [[amino acids]], [[peptide]]s and [[minerals]] initially filtered out of the blood during [[ultrafiltration]] in the [[renal corpuscles]]. In addition, endogenous and exogenous substances are metabolized and broken down in the kidneys—the kidney is therefore a central metabolic organ alongside the [[liver]]. Finally, some [[Hormone|hormone-active substances]] such as [[renin]], [[erythropoietin]] and [[calcitriol]] (active form of [[Cholecalciferol|vitamin D&lt;sub&gt;3&lt;/sub&gt;]]). As a result, the organ plays an important role in the regulation of [[blood pressure]], [[Erythropoiesis|new blood formation]] and the [[Calcium homeostasis|calcium]] and [[phosphorus]] balance and thus the [[bone]]&lt;nowiki/&gt;metabolism.  As [[carnivores]], cats are particularly dependent on the intake of animal [[protein]]s because [[Gluconeogenesis|glucose formation]] from [[amino acids]] is their most important [[energy metabolism|energy source]]. The [[enzyme]]s of amino acid degradation 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 endogenous proteins (especially from the muscles) when there is a lack of protein intake ([[Catabolism|catabolic]] metabolic state).&lt;ref&gt;K. Sturgess: ''Nutritional management of Renal Disease''. In: Proceedings of the 33rd WSAVA/FECAVA Congress, Dublin 2008, p.&amp;nbsp;281–284.&lt;/ref&gt;&lt;ref name=&quot;Kirby&quot;&gt;R. Kirby: ''The cat is not a small dog'': In ICU: Parts I and II, Proceedings 29th World Congress oft the WSAVA, Rhodes 2004.&lt;/ref&gt; Meat and offal also contain vital nutrients for the cat, such as [[Retinol|Vitamin A]], [[Taurin]] or arachidonic acid.&lt;ref name=&quot;Kirby&quot; /&gt; Compared to a normal human diet, cats consume around six times as much [[phosphate]] in their diet with standard [[cat food]]. This makes it difficult to achieve a similar phosphorus reduction in cat food as is aimed at in human medicine for human kidney diets.&lt;ref name=&quot;chew&quot; /&gt;

== Pathophysiological basics ==
[[File:Nephron transports.svg|thumb|Basic transport processes in the nephron]]

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 compensatory mechanisms and the kidney's reserve capacity, which can compensate for the reduced kidney function for a long time and maintain the excretion of urine-requiring substances.&lt;ref name=&quot;chew&quot;&gt;D. J. Chew: ''The role of phosphorus in feline chronic renal disease''. In: ESFM Feline Congress 2008 Edinburgh, Scientific Proceedings, p. 59–65.&lt;/ref&gt;&lt;ref&gt;R. Heine: ''Labordiagnostik bei felinen Nierenerkrankungen''. In: Veterinary Focus 18 (2008), p. 16–22. {{ISSN|0965-4593}}&lt;/ref&gt; With the loss of functioning [[nephron]]s—the functional structural unit of the kidney—the filtering capacity of the renal corpuscles ([[glomerular filtration rate]]) decreases and with it the excretory capacity for urinary substances. Acute damage to the [[tubule]]s can regenerate again if the [[basement membrane]] is preserved. However, if a section of the nephron is irreversibly damaged, the entire nephron dies.&lt;ref name=&quot;Hey&quot;&gt;Karolin Hey: ''Chronische Nierenerkrankung der Katze – eine tägliche Herausforderung (Teil 1)''. In: ''Kleintierpraxis'' Band 69, No 3, 2024, p. 120–139. {{doi|10.2376/0032-681X-2252}}&lt;/ref&gt;

The increased [[urea]] levels in the blood ([[uremia]]) lead to nausea and vomiting for various reasons. Firstly, they directly irritate [[chemoreceptor]]s in the [[chemoreceptor trigger zone]] in the brain. Secondly, they increase [[gastrin]]&lt;nowiki&gt;secretion&lt;/nowiki&gt; and thus lead to an increase in gastric acid production and thus to hyperacidity of the stomach. Finally, they cause vascular inflammation (uraemic [[vasculitis]]), which leads to further damage to the digestive tract.&lt;ref name=&quot;Neiger406&quot;&gt;Reto Neiger: ''Chronische Niereninsuffizienz''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 4. Aufl. 2005, ISBN 3-8304-1049-2, p. 406.&lt;/ref&gt;&lt;ref name=&quot;Grauer&quot;&gt;Gregory F. Grauer: ''Chronic renal failure''. In: R. W. Nelson und C. G. Couto (Hrsg.): ''Small animal internal medicine''. Mosby, 3. Edition 2003, ISBN 0-323-01724-X, p. 617.&lt;/ref&gt;

As a result of the accumulation of phosphate in the blood ([[hyperphosphatemia]]) and the reduced formation of [[calcitriol]] in the remaining [[tubule|main parts]], there is a drop in the calcium blood level ([[hypocalcemia]]) and increased [[parathyroid hormone]] is released from the [[parathyroid gland]]. Chronic kidney disease leads to hyperparathyroidism in 84% of cases (secondary renal [[hyperparathyroidism]]).&lt;ref name=&quot;Francey-Müller&quot;&gt;Thierry Francey und Elisabeth Müller: ''Chronische Nierenerkrankung – Früherkennung und Bedeutung der Phosphate.'' In:veterinary mirror 3 (2010), p. 107–112.&lt;/ref&gt; Among other things, the parathyroid hormone causes calcium and phosphate to be released from the bones, which ultimately leads to [[renal osteodystrophy|renal bone disorders]] and calcification of the kidneys, skin, heart and blood vessels. In the kidneys, this calcification contributes to further destruction of the kidney tissue. The reduced responsiveness of the parathyroid cells to calcium disrupts the [[negative feedback]] of parathyroid hormone secretion, so that parathyroid hormone continues to be secreted despite the increase in calcium levels. As less phosphate reaches the renal tubules due to the reduced filtration rate, the inhibitory effect of parathyroid hormone on reabsorption in the main body has only a minor effect on the blood phosphate level.&lt;ref name=&quot;Francey-Müller&quot; /&gt;&lt;ref name=&quot;Neiger411&quot; /&gt;

The loss of nephrons and the associated decrease in the number of [[sodium channel|sodium ion channels]] leads to a decrease in the [[concentration gradient]] in the kidney. However, this is the driving force for water reabsorption in the [[Tubule|mid-piece]] and—in the presence of [[antidiuretic hormone|ADH]]—also in the [[collecting duct]]s. The result is a loss of water via the urine and thus drying out of the body, which is exacerbated by the loss of fluid during vomiting.&lt;ref name=&quot;Grauer&quot; /&gt;

One consequence of the kidneys' reduced ability to excrete [[hydrogen]] ions, phosphate and [[sulphate]] and the excessive loss of [[hydrogen carbonate|bicarbonate]] is the metabolic acidification of the blood ([[metabolic acidosis]]).&lt;ref name=&quot;Ettinger&quot; /&gt; Metabolic acidosis occurs in 80% of cats with chronic kidney disease.&lt;ref name=&quot;Neiger410&quot;&gt;Reto Neiger: ''Chronische Niereninsuffizienz''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 4. Edition 2005, p. 410&lt;/ref&gt;

With increasing kidney damage, the [[kidney#autoregulation of renal blood flow|autoregulation of renal blood flow]], which normally ensures that the blood flow and thus the filtering capacity up to a threshold of 60&amp;nbsp;[[Torr|mm Hg]] are independent of the general blood pressure, is also impaired. As a result, kidney performance is reduced at low blood pressure and, in the case of high blood pressure often associated with chronic kidney disease, further damage occurs due to pressure overload of the renal corpuscles.&lt;ref&gt;A. P. 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), p. 13–17. {{ISSN|1018-2357}}&lt;/ref&gt; The increase in blood pressure is due to [[arteriosclerosis|hardening of the blood vessels]] in the area of the renal corpuscles, the reduced formation of [[vasodilation|vasodilating]] [[prostaglandins]] and activation of the [[renin-angiotensin-aldosterone system]].&lt;ref name=&quot;Neiger409&quot; /&gt;

[[File:PKD cat.jpg|thumb|Cystic kidney in ultrasound image]]

== Occurrence and causes ==
Chronic kidney disease is one of the most common causes of death in older domestic cats.&lt;ref&gt;G. F. Grauer: ''Early detection of renal damage and disease in dogs and cats.'' In: Vet Clin Small Animal 35 (2005), p. 581–596.&lt;br /&gt;A. M. 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, p. 701–703.&lt;/ref&gt; In many animals, however, the disease initially remains unrecognized, as clinical symptoms are often absent in the early stages of chronic kidney disease due to the kidney's reserve capacity and sufficiently sensitive diagnostic tests are not available for routine use.&lt;ref&gt;A. Parotat, B. Kohn: ''Die chronische Niereninsuffizienz – Wie sieht ein effektives Management aus?'' In: ''kleintier konkret'' 12 (2009), p. 6–10.&lt;/ref&gt;&lt;ref name=&quot;Jepson&quot;&gt;R. E. Jepson et al.: ''Evaluation of predictors of the development of azotemia in cats.'' In: ''[[Journal of Veterinary Internal Medicine|J. Vet. Intern. Med.]]'' 23 (2009), p. 806–813. {{ISSN|0891-6640}}, PMID 19566846&lt;/ref&gt; The data on the [[prevalence|frequency]] of the disease in cats is contradictory, varying between 1.6 and 20%.&lt;ref name=&quot;Francey&quot;&gt;Thierry Francey, Ariane Schweighauser: ''Klinische Epidemiologie von Nierenerkrankungen bei der Katze.'' In: ''Vet. Focus'' 28 (2008), p. 2–7. {{ISSN|0965-4593}}&lt;/ref&gt; Chronic kidney disease occurs more frequently in older cats: Over 50% of affected cats are seven years old or older&lt;ref name=&quot;Francey&quot; /&gt; and 30% of all cats over 9 years of age show elevated blood levels of nitrogen compounds ([[azotemia]]).&lt;ref name=&quot;Jepson&quot; /&gt; However, the disease can occur as early as 9 months of age.&lt;ref name=&quot;Francey&quot; /&gt; Disposition predisposition has been proven for [[Maine Coon cat|Maine Coon]], [[Abyssinian cat|Abyssinian]], [[Siamese cat|Siamese]], [[Russian Blue]] and [[Burmese cat|Burmese]].&lt;ref name=&quot;Ettinger&quot;&gt;D. J. Polzin et al.: ''Chronic renal failure.'' In: S. J. Ettinger und E. C. Feldmann (Hrsg.): ''Textbook of Veterinary Internal Medicine.'' Saunders, 5. Edition, Philadelphia 2000, Band 2, p. 1634–1662. ISBN 0-7216-7256-6&lt;/ref&gt;

Since the kidneys have a high reserve capacity and clinical symptoms only appear when two thirds of the original kidney function has been lost, the triggering factors must damage both kidneys.&lt;ref&gt;Sarah Steinbach und Reto Neiger: ''Chronische Nierenerkrankung'': In: Hans Lutz et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 5. Ed. 2014, ISBN 978-3-8304-1243-4, p. 751.&lt;/ref&gt;

Chronic kidney disease in cats is an idiopathic tubulointerstitial nephritis, i.e. an inflammation of the renal tubules and the renal interstitial tissue without an identifiable cause.&lt;ref name=&quot;Francey&quot; /&gt;&lt;ref name=&quot;Jepson13&quot;&gt;Rosanne Jepson: ''Die Bedeutung von Nierenerkrankungen bei Katzen''. In: ''veterinärspiegel'' 2013, Heft 2, p. 59–64.&lt;/ref&gt; In addition to the damage that this primary disease causes directly to the kidney tissue, activated endogenous repair mechanisms such as connective tissue formation lead to further, partially self-sustaining destruction of functional kidney tissue. The reduced ability of the kidneys to excrete sodium and water causes retention (medicine) of these substances and thus an increase in blood volume, which ultimately leads to an increase in blood pressure. About two thirds of all cats with CNE are affected.&lt;ref name=&quot;Ettinger&quot; /&gt; High blood pressure in turn leads to increased connective tissue formation. A potassium deficiency or excess calcium secondary to other kidney damage also causes further damage to the kidney tissue.

{| class=&quot;wikitable&quot; align=&quot;center&quot; width=&quot;80%&quot;
|+ Possible causes of chronic kidney failure in cats
|- style=&quot;background:#DDFFDD;&quot;
! Cause
! Remarks
|- style=&quot;background:#FFCBCB;&quot;
| colspan=&quot;2&quot; align=&quot;center&quot;| '''Damage to the renal corpuscles'''
|-
| Chronic [[glomerulonephritis]]
| Inflammation of the renal corpuscles
|-
| [[Glomerulosclerosis]]
| &quot;Hardening&quot; of the renal corpuscles due to connective tissue formation
|- style=&quot;background:#FFCBCB;&quot;
| colspan=&quot;2&quot; align=&quot;center&quot;| '''Damage to the renal tubules'''
|-
| idiopathic [[tubulointerstitial nephritis]] (CNE)
| Inflammation of the renal tubules and the interstitial tissue of the kidney
|-
| Chronic [[pyelonephritis]]
| Renal pelvic inflammation with involvement of the kidney tissue
|-
| [[Nephrocalcinosis]]
| Kidney damage due to [[hypercalcemia|excess calcium]] in the blood
|-
| [[Hypokalemia|Hypokalemic]] Nephropathy
| Kidney damage due to a lack of potassium in the blood
|-
| [[granuloma]]atous nephritis
| Nodular inflammation of the kidneys, in cats mainly as a result of [[feline infectious peritonitis]] (FIP)
|-
| Kidney [[tumor]]s
| mainly malignant lymphoma, other tumors such as [[kidney cancer]], [[urothelial carcinoma|transitional cell carcinoma]], [[nephroblastoma]]s and [[hemangiosarcoma]]s do not usually occur on both sides
|-
| Nierenamyloidose
| Pathological protein deposition, more frequent in [[Abyssinian cat]] and [[black-footed cat]]s&lt;ref&gt;K. A. Terio et al.: ''Amyloidosis in black-footed cats (Felis nigripes).'' In: Vet. Pathol. 45 (2008), p. 393–400, PMID 18487501.&lt;/ref&gt;
|-
| Polycystic kidney disease
| Hereditary cysts&lt;nowiki&gt;formation&lt;/nowiki&gt; in [[Persian cat]]s
|- style=&quot;background:#FFCBCB;&quot;
| colspan=&quot;2&quot; align=&quot;center&quot;| '''Damage to the urinary tract'''
|-
| [[kidney stone]]s
| Deposits of [[concrement]]s in the urinary tract
|-
| Hydronephrose
| &quot;Water-sac kidney&quot; due to urinary retention
|-
| perirenal circumferential augmentation
| only if bilateral: cysts, [[hematoma|bruising]], pseudocysts and other space-occupying processes in the vicinity of the kidney
|-
| Kidney worm infestation
| Infection with ''[[Dioctophyma renale]]'', rare and only in southern Europe, Asia and North America
|- style=&quot;background:#FFCBCB;&quot;
| colspan=&quot;2&quot; align=&quot;center&quot;| '''Damage as a result of vascular diseases'''
|-
| [[Arterial hypertension]]
| General high blood pressure
|-
| Glomerular hypertension
| High blood pressure in the area of the renal corpuscles
|-
|[[Disseminated intravascular coagulopathy]]
| Blood clotting within the blood vessels
|}
[[File:Hemerocalis1.jpg|thumb|The yellow-red daylily—a popular ornamental plant with high kidney toxicity in cats]]
[[File:Katze CNI.JPG|thumb|Unresponsive cat with poor general condition—typical of chronic kidney disease]]

Other diseases can also be [[Etiology (medicine)|triggers]] of renal dysfunction, for example [[infection]]s, [[autoimmune disease]]s, [[poisoning]]s or [[tumor]]s. Virtually any infection or even [[lupus erythematosus]] can lead to the deposition of [[antigen-antibody reaction|antigen-antibody complexes]] in the [[basal lamina|basal membrane]] of the renal corpuscles and thus to their damage. Many [[lily]] species, [[ethylene glycol]], [[melamine]], [[cyanuric acid]] and some heavy metals ([[cadmium]], [[lead]], [[Mercury (element)|mercury]]) have a strong toxic effect on the kidneys (renal [[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.&lt;ref name=&quot;Fink&quot;&gt;Johanna Fink-Gremmels: ''Vergiftungen''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke-Verlag, 4. ed. 2005, p. 789–803. ISBN 3-8304-1049-2&lt;/ref&gt;

== Symptoms ==
The main [[symptom]]s of chronic kidney disease in cats are lack of appetite ([[Anorexia (symptom)|anorexia]]), increased drinking ([[polydipsia]]), increased urine output ([[polyuria]]), fatigue ([[apathy]]), [[vomiting]] and weight loss. In addition, diarrhea, inflammation of the oral mucosa ([[stomatitis]]) with the formation of ulcers ([[ulcus|ulcera]]), increased salivation ([[hypersalivation]]) and [[bad breath]] may occur as a result of uremia. Increased blood pressure ([[arterial hypertension]]) with damage to the eye ([[fundus hypertonicus]], hypertensive retinopathy), anemia ([[anemia]]), [[itching]], dehydration, [[Calcinosis|soft tissue calcifications]], [[bleeding]]s and accumulation of water in the tissues ([[oedema]]s) are also more frequent accompanying symptoms. In the case of severe uremia, [[Neurology|neurological neurology]] manifestations such as [[lethargy|apathy]], [[convulsion|seizures]], [[delirium]], [[coma]], abnormal movements and muscle disorders ([[myopathies]]).&lt;ref name=&quot;Ettinger&quot; /&gt; Typically, the symptoms—in contrast to [[Acute kidney failure|acute renal failure]]—occur gradually 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 (&quot;[[exacerbation]]&quot;) and thus becomes conspicuous to the cat owner. This can be the case, for example, if one kidney has already become a non-functioning shrunken kidney due to urinary retention and the second suddenly swells acutely due to urinary retention ([[hydronephrosis]]) and is damaged (&quot;large kidney-small kidney syndrome&quot;) or if [[feline hyperthyroidism|hyperthyroidism]] is treated and the glomerular filtration rate is suddenly reduced as a result.&lt;ref name=&quot;Francey&quot; /&gt;

[[File:Sono Nierenbeckenstauung Katze 0.jpg|thumb|Ultrasound image of [[hydronephrosis]] in a cat. The arrows point to the dilated ureter.]]

By palpation, the kidneys can be checked for pain, firmness (consistency), enlargement or reduction in size and changes in surface structure. A healthy kidney is about 4&amp;nbsp;cm long, 3&amp;nbsp;cm wide and 2–3.5&amp;nbsp;cm thick. In the most common form—CNE due to tubulointerstitial nephritis—the kidneys are usually reduced in size and have an irregular surface; in the case of tumors or pyelonephritis, they may be enlarged and sensitive to pain.&lt;ref name=&quot;Jepson13&quot; /&gt; Since the degree of protein loss via the urine is directly related to the increase in blood pressure, regular [[blood pressure measurement]] is advisable.

[[File:Roentgen Katze CNI AP Kontrast.jpg|thumb|upright|Urography: Diffuse accumulation of contrast medium in the kidneys of a cat with high-grade CNE]]

An [[X-ray]] examination can be used to detect changes in the size, density and position of the kidneys as well as some urinary stones ([[struvite]] and [[calcium oxalate]] stones are &quot;radiopaque&quot;) and soft tissue calcifications. In severely emaciated cats or fluid accumulations in the [[retroperitoneal space]], however, the kidney can only be visualized to a limited extent on the X-ray image due to the resulting reduction in contrast. Excretory [[urography]], in which a radiopaque [[contrast medium]] (e.g. [[Iopamidol]], [[Iohexol]]) is injected into the bloodstream and its excretion via the kidneys is recorded radiographically. This makes it possible to detect circulatory disorders, dysfunctions of the renal corpuscles and obstructions of the outflow pathways.&lt;ref name=&quot;Seyrek&quot;&gt;Deniz Seyrek-Intas und Martin Kramer: ''Bild gebende Diagnostik der Niere bei Katzen.'' In: Vet. Focus 18 (2008), p. 23–30. {{ISSN|0965-4593}}&lt;/ref&gt;

[[File:RI Niere Katze CNI.jpg|thumb|left|PW-Doppler: Increased resistance index]]

The [[Sonography|ultrasound examination]] allows [[morphology (biology)|morphological]] changes in the kidneys in more detail. In addition to changes in size and shape, renal cysts, localized (focal) organ damage, water sac kidneys and urinary retention as well as tumors can also be visualized. Hardly defined (diffuse) organ changes are accompanied by changes in echogenicity, but can only rarely be assigned to defined diseases.&lt;ref name=&quot;Seyrek&quot; /&gt; Pulsed Wave Doppler&quot; can also be used to detect circulatory disorders.&lt;ref&gt;B.J. Rivers et al.: ''Duplex Doppler estimation of Pourcelot resistive index in arcuate arteries of sedated normal cats.'' In: J. Vet. Intern. Med. 10 (1996), p. 28–33. PMID 8965265&lt;br /&gt;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), p. 250–260. PMID 9298481&lt;/ref&gt; Calcification ([[nephrocalcinosis]]) is also common in chronic kidney disease and can also be detected sonographically.&lt;ref&gt;Pak-Kan Tang et al.: ''Risk factors and implications associated with ultrasound-diagnosed nephrocalcinosis in cats with chronic kidney disease''. In: ''J. Vet. Intern. Med.'' März 2024, [[doi:10.1111/jvim.17034]]&lt;/ref&gt;

Renal [[biopsy]] is not routinely used, but may be indicated in certain [[medical history|preliminary reports]]—for example, young Abyssinian cats with symptoms of kidney disease for the detection of amyloidosis.&lt;ref name=&quot;Francey&quot; /&gt; Although [[computed tomography]] and [[magnetic resonance imaging]] have very good detail recognition, they only play a subordinate role in veterinary medicine due to their high costs and limited availability.&lt;ref name=&quot;Seyrek&quot; /&gt;

== Laboratory diagnostic findings ==
[[File:Harnsediment Katze Pyelonephritis.jpg|thumb|Bacteria in urinary sediment in a cat with pyelonephritis]]

Urinalysis is essential in chronic kidney disease in cats. Damage to as little as two thirds of the [[nephron]]s results in a reduced ability to concentrate urine and the [[weight|specific weight]] falls below 1030&amp;nbsp;N-m&lt;sup&gt;−3&lt;/sup&gt;. Protein loss via the kidney is detected by an increase in the [[urinalysis#protein/creatinine quotient in spontaneous urine|protein/creatinine ratio]] in the urine (UPC), as [[urinalysis#24-h protein excretion|24-hour collection samples]] are impractical in cats. The UPC is a good marker for the early detection of CNE, as it reveals renal dysfunction even before the creatinine in the blood rises.&lt;ref name=&quot;Francey-Müller&quot; /&gt; The [[urine sediment]] can also show effusions from the renal tubules (cylinder), and in chronic bacterial renal pelvic inflammation [[bacteria]] or [[pus]] can also be detected. The detection of small amounts of albumin (&lt;&amp;nbsp;300&amp;nbsp;mg/l, &quot;[[microalbuminuria]]&quot;) is very [[sensitivity (test)|sensitive]], but not very [[Sensitivity and specificity|specific]] for chronic kidney disease.&lt;ref name=&quot;Heine&quot;&gt;{{cite magazine |first=Redun |last=Heine |title=Labordiagnostik bei felinen Nierenerkrankungen |magazine=Vet |issue=18 |date=2008 |pages=16–22 |issn=0965-4593 }}&lt;/ref&gt;

{| class=&quot;wikitable&quot; style=&quot;text-align:center; float:left; border:1px solid #999999; padding:4px; margin:1em 1em 1em 0em;&quot;
|+ Reference values of selected&lt;br /&gt;serum parameters in cats&lt;ref name=&quot;Schrey&quot;&gt;Christian F. Schrey: ''Leitsymptome und Leitbefunde bei Hund und Katze''. Schauttauer, 2. ed. 2005, ISBN 3-7945-2384-9&lt;/ref&gt;
|- style=&quot;background:#DDFFDD;&quot;
! Parameter
! Reference range
|-
| [[creatine]]
| &lt; 170 μmol/L (&lt; 2&amp;nbsp;mg/dL)
|-
|SDMA
|&lt; 14&amp;nbsp;μg/dL
|-
| [[Urea]]
| 5–11&amp;nbsp;mmol/L (30–65&amp;nbsp;mg/dL)
|-
| [[Phosphate|Phosphat]]
| 0,8–1,9&amp;nbsp;mmol/L
|-
| [[Calcium]]
| 2,3–3,0&amp;nbsp;mmol/L
|-
| [[Kalium]]
| 3,0–4,8&amp;nbsp;mmol/L
|-
| [[Natrium]]
| 145–158&amp;nbsp;mmol/L
|}

In [[blood serum]], the content of nitrogenous substances such as [[urea]] and [[creatinine]] ([[uremia]] or [[azotemia]]) and phosphate ([[hyperphosphatemia]]). The increased phosphate concentration is the result of the reduced glomerular filtration rate. Among other things, [[fibroblast growth factor]] 23 (FGF-23) is involved here, which is more sensitive than the phosphate level in the event of an incipient disorder.&lt;ref&gt;{{cite journal |first1=R.F. |last1=Geddes |first2=N.C. |last2=Finch |first3=Jonathan |last3=Elliott |first4=Harriet M. |last4=Syme |title=Fibroblast Growth Factor 23 in Feline Chronic Kidney Disease |journal=Journal of Veterinary Internal Medicine |date=2013 |volume=27 |issue=2 |pages=234–241 |doi=10.1111/jvim.12044 }}&lt;/ref&gt; The [[potassium]] content is usually reduced ([[hypokalemia]]), but can also be increased—the reverse is true for the [[sodium]] content. If the cause of the kidney disease lies in the renal corpuscles, albumin deficiency (hypalbuminemia) and excess cholesterol ([[hypercholesterolemia]]) also occur.&lt;ref name=&quot;Neiger406&quot; /&gt; The determination of [[cystatin C]] is not [[Evaluation|evaluated]] for cats, this protein can also be elevated in cats with [[Feline hyperthyroidism|hyperthyroidism]] or with [[glucocorticoids]] and drop sharply for several hours after food intake.&lt;ref&gt;''Nierenerkrankungen – Diagnostik aus Blut und Urin.'' In: Laboklin aktuell 2/2009&lt;/ref&gt; Recent studies suggest that [[symmetric dimethylarginine]] (SDMA) is a suitable marker for renal function in cats. The SDMA concentration in serum shows close correlations with the glomerular filtration rate and the creatinine concentration.&lt;ref&gt;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.'' Band 28, Nummer 6, 2014 Nov-Dec, p.&amp;nbsp;1699–1701, [[doi:10.1111/jvim.12446]], PMID 25272985.&lt;/ref&gt; It can already detect a 40% loss of kidney function, i.e. before there is an increase in creatinine in the blood.&lt;ref&gt;{{cite web |url=https://www.idexx.com/small-animal-health/solutions/articles/sdma-diagnose-kidney-disease.html |title=SDMA: Diagnose kidney disease earlier |website=Idexx.com }}&lt;/ref&gt;

The most sensitive method of kidney function diagnostics is the direct determination of the [[glomerular filtration rate]] via the [[Renal clearance|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]]. Although creatinine is eliminated more slowly than iohexol, it can be determined immediately in many veterinary practices [[Photometer|photometric]] even without the involvement of a specialized laboratory.&lt;ref name=&quot;Heine&quot; /&gt;

In advanced kidney disease, the [[blood count]] shows a decrease in the number of [[erythrocyte|red blood cells]] and thus the [[hematocrit]] without a change in the blood pigment load and the cell sizes of the red blood cells and without signs of new blood cell formation ([[anemia#normochromic, normocytic anemia|normochromic, normocytic, aregenerative anemia]]).&lt;ref name=&quot;Neiger406&quot; /&gt;

== Classification ==
Chronic kidney disease in cats is currently divided into four main stages by the ''International Renal Interest Society'' (IRIS) and adapted by the ''European Society of Veterinary Nephrology and Urology'', with the [[creatinine]] concentration in [[blood plasma]] being used as the main criterion. In addition, sub-stages are defined on the basis of the protein-creatinine quotient in the urine and blood pressure.&lt;ref name=&quot;Heine&quot; /&gt;&lt;ref&gt;[http://www.iris-kidney.com/pdf/003-5559.001-iris-website-staging-of-ckd-pdf_220116-final.pdf#page=7 IRIS Guidelines für Katzen]&lt;/ref&gt; The plasma creatinine concentration should be ensured by at least two measurements at intervals 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.&lt;ref name=&quot;Arnell&quot;&gt;Katharine Arnell und Sheri Ross: ''Fortschritte in der Behandlung chronischer Nierenerkrankungen bei der Katze.'' In: Vet. Focus 19.3 (2009), p. 6–14.&lt;/ref&gt; As creatinine is also influenced by other factors, since 2019 the Symmetric dimethylarginine (SDMA) is also used for assessment.&lt;ref&gt;[http://www.iris-kidney.com/pdf/IRIS_Staging_of_CKD_modified_2019.pdf Aktualisierte Einteilung der IRIS]&lt;/ref&gt; In diabetic cats SDMA may be reduced.&lt;ref name=&quot;Hey&quot; /&gt;

&lt;div style=&quot;clear:left;display:inline-block;&quot;&gt;
{| class=&quot;wikitable&quot; align=&quot;center&quot; style=&quot;clear:both&quot;
|- style=&quot;background:#FFCBCB;&quot;
! Stage
! Plasma creatinine concentration
! SDMA
! Remarks
|-
| width=&quot;100&quot; |I
| width=&quot;200&quot; |&lt; 140 μmol/L (1,6&amp;nbsp;mg/dL)
| width=&quot;100&quot; |&lt;18&amp;nbsp;μg/dL
| width=&quot;600&quot; |No azotemia, but other pathological kidney findings
|-
| II
| 140–249 μmol/L (1,6–2,8&amp;nbsp;mg/dL)
| 18–25&amp;nbsp;μg/dL
| Low azotemia, clinical symptoms are weak or not pronounced at all in this area, residual kidney function approx. 33%
|-
| III
| 249–442 μmol/L (2,9–5,0&amp;nbsp;mg/dL)
| 26–38&amp;nbsp;μg/dL
| Moderate azotemia, clinical manifestations are pronounced at this stage, residual renal function about 25%
|-
| IV
| &gt; 442 μmol/L (5,0&amp;nbsp;mg/dL)
| &gt; 38&amp;nbsp;μg/dL
| Severe azotemia, usually accompanied by severe clinical symptoms, residual renal function &lt; 10%
|}

{| class=&quot;wikitable&quot; align=&quot;center&quot; style=&quot;clear:both&quot;
|- style=&quot;background:#FFCBCB;&quot;
! width=&quot;100&quot;|Sub-stage
! width=&quot;200&quot;|Protein-creatinine quotient in urine
! width=&quot;600&quot;|Remarks
|-
| a
| &lt; 0,2
| No protein loss via the urine
|-
| b
| 0,2–0,4
| Protein loss via urine questionable, should be confirmed by renewed measurements
|-
| c
| &gt; 0,4
| Loss of protein via the urine ([[proteinuria]])
|}

{| class=&quot;wikitable&quot; align=&quot;center&quot; style=&quot;clear:both&quot;
|- style=&quot;background:#FFCBCB;&quot;
! Sub-stage
! Blood pressure in mmHg&lt;br /&gt;([[Systole|systolic]]: [[Diastole|diastolic]])
! Remarks
|-
| width=&quot;100&quot; |1
| width=&quot;200&quot; |&lt; 150: &lt; 95
| width=&quot;600&quot; |Blood pressure without risk of organ damage
|-
| 2
| 150–159: 95–99
| Low risk of organ damage
|-
| 3
| 160–179: 100–119
| Medium risk for the occurrence of organ damage
|-
| 4
| &gt; 180: &gt; 120
| High risk of organ damage
|}
&lt;/div&gt;

In stage 1, creatinine and SDMA values are still within the normal range. However, there are other disorders of kidney function, such as an inadequate ability to concentrate, protein loss via the urine, morphological kidney changes or an increase in the values on repeated measurements. Creatinine and SDMA values often indicate a different stage. This may be due to the biological fluctuation range, concomitant diseases, influencing factors outside the kidney and pre-analytical causes. In this case, staging should be based on the higher value and the determination should be repeated after two to four weeks.&lt;ref name=&quot;Hey&quot; /&gt;

== Differential diagnosis==
In the sum of all examination findings, chronic kidney disease can hardly be confused with any other disease. There is only extensive agreement with acute renal insufficiency. Here, the clinical course (see symptoms) is particularly suitable as a differentiation criterion. In addition, in acute renal failure the blood pressure and red blood cell count are unchanged and the kidneys are often enlarged and painful.&lt;ref name=&quot;Schrey&quot; /&gt;

The main feature that determines the staging—azotemia—can have a number of other causes that can be localized &quot;before the kidney&quot; (prerenal) or &quot;after the kidney&quot; (postrenal). Prerenal causes in cats are mainly blood loss, dehydration, [[Shock (circulatory)|shock]], [[congestive heart failure]], [[Feline hyperthyroidism|hyperthyroidism]], but also [[fever]] or severe physical exertion. Possible postrenal causes include obstruction of the urinary tract due to [[Feline lower urinary tract disease|bladder stones]] or tumors, tears of the [[urinary bladder]], [[ureter]], or [[urethra]].&lt;ref name=&quot;Schrey&quot; /&gt;

== Treatment==
The options for [[Chronic kidney failure#Renal replacement therapy|kidney replacement therapy]] are severely limited in cats, as [[kidney transplant]]s&lt;ref&gt;L. Bernsteen et al.: ''Renal transplantation in cats.'' In: Clin. Tech. Small Anim. Pract. 15 (2000), p. 40–45, PMID 10911684.&lt;/ref&gt; and [[hemodialysis]]&lt;ref&gt;J.R. Fischer et al.: ''Veterinary hemodialysis: advances in management and technology.'' In: ''Vet. Clin. North Am. Small Anim. Pract.'' 34 (2004), S. 935–967, PMID 15223210.&lt;/ref&gt; in veterinary medicine are only carried out in exceptional cases due to the high equipment, logistical and financial costs involved. The aim is therefore to detect chronic kidney disease at the earliest possible stage, when the kidneys still have sufficient reserve capacity. At the same time, attempts are made to reduce the amount of urinary substances—especially nitrogen compounds and phosphate—in the diet by means of [[dietary]] measures. Finally, metabolic imbalances and sequelae must be buffered. From a plasma creatinine level of 7&amp;nbsp;mg/dL (618.8&amp;nbsp;μmol/L), however, drug therapy is not very promising.&lt;ref name=&quot;Arnell&quot; /&gt;

=== Dietary measures===
One problem with dietary therapy with phosphate—and protein-reduced diets is that they are usually not very palatable. In addition, cats with kidney disease have little appetite and getting used to a new food is made even more difficult due to the negative imprinting (behavior)—the cat associates its own physical discomfort with the new food.&lt;ref name=&quot;Neiger406&quot; /&gt; The loss of protein via the urine also results in a negative [[nitrogen balance]], which also reduces appetite. Finally, affected animals often show gastrointestinal tract problems. In a clinical study by Elliott et al.&lt;ref name=&quot;Elliott&quot; /&gt; 34% of cats could not be switched to the renal diet and in Plantinga et al.&lt;ref name=&quot;Plantinga&quot; /&gt; the figure was as high as 54%. An attempt can be made to increase the acceptability of the feed by warming it or by adding tasty additives such as tuna juice or sardines. It is therefore recommended to start the feed change only after the uraemia has been eliminated and to extend it over three weeks by gradually mixing it in to avoid feed aversion. Adsorbents such as [[activated charcoal]] or [[probiotics]] can be used in an attempt to reduce the formation of uraemic substances in the gastrointestinal tract. Cyproheptadine or [[mirtazapine]] may be used for a short time to increase appetite; if these measures do not work, force-feeding via an esophageal or gastric tube is necessary.&lt;ref name=&quot;Arnell&quot; /&gt; The administration of feed supplements based on [[Rheum palmatum|Chinese rhubarb]] or with [[Prebiotic (nutrition)|prebiotics]] and [[probiotics]] had no discernible effect in clinical studies; there is only one small manufacturer's study on the activated charcoal-based absorber for [[indole]] in the large intestine (trade name ''Porus one''), but this did not include any cats with kidney disease.&lt;ref name=&quot;Hey2&quot; /&gt;

==== Phosphate reduction ====
A key goal in the management of chronic kidney disease in cats is to reduce dietary phosphate intake early in the course of the disease.&lt;ref name=&quot;chew&quot; /&gt;&lt;ref name=&quot;Elliott2&quot;&gt;J. Elliott: ''The role of phosphate in chronic kidney disease (CKD) progression''. In: ''Small Animal Medicine UK Vet.'' 13 (2008), p. 23–28 and p. 37–46.&lt;/ref&gt; As a rule of thumb, the phosphate content can be reduced to 170&amp;nbsp;mg/MJ UE (Mega[[joule]] metabolizable energy, see also Physiological calorific value), i.e. to two thirds of the maintenance requirement. Commercially available cat food usually contains twice the maintenance requirement and should therefore not be mixed with the diet food. If the phosphate levels in the plasma remain elevated despite the renal diet, 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 calcium deficiency in the early stages, but can lead to [[hypercalcemia]] in advanced stages.&lt;ref name=&quot;Francey-Müller&quot; /&gt; The use of phosphate binders should be monitored by blood tests and their dose adjusted on the basis of phosphate levels.&lt;ref name=&quot;Hey2&quot; /&gt;

Several studies have shown that a reduction of phosphate in the diet is sufficient to slow down the progression of the disease.&lt;ref name=&quot;Elliott&quot;&gt;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), p. 235–242. {{ISSN|0022-4510}}&lt;/ref&gt;&lt;ref name=&quot;Plantinga&quot;&gt;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), p. 185–187, PMID 16100367.&lt;/ref&gt;&lt;ref name=&quot;Barber&quot;&gt;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), p. 62–70, PMID 10088085.&lt;/ref&gt; If the general condition continues to deteriorate during phosphate reduction, a phosphate deficiency should also be considered. This manifests itself in a similar way to chronic kidney disease: shaggy coat, loss of appetite, weakness, exhaustion and anaemia.&lt;ref name=&quot;Neiger411&quot;&gt;Reto Neiger: ''Chronische Niereninsuffizienz''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 4. Aufl. 2005, p. 411.&lt;/ref&gt; Calcitriol can also be used to treat secondary hyperparathyroidism, but only if parathyroid hormone and calcium levels are monitored.&lt;ref name=&quot;Arnell&quot; /&gt; For cats in the early stages with normal blood phosphate levels, a less phosphate-reduced diet (&quot;Senior&quot;, &quot;Early-Renal&quot; or a mixture of kidney and normal food) is usually sufficient.&lt;ref name=&quot;Hey2&quot; /&gt;

==== Protein reduction ====
In order to combat uraemia, the amount of protein in the diet and thus the amount of nitrogen supplied to the body can be reduced. However, this is only possible to a limited extent in cats, as 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 UE and should never be reduced below 11 g/MJ UE, whereby the amount of protein declared on feed must be multiplied by a factor of 0.86 to obtain the digestible crude protein. High-quality animal protein also reduces the amount of nitrogen compounds entering the large intestine and thus the amount of [[ammonia]] produced by bacterial degradation processes through the [[intestinal flora]].&lt;ref&gt;Reto Neiger: ''Chronische Niereninsuffizienz''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 4. Aufl. 2005, p. 405–407.&lt;/ref&gt; If there are severe acceptance problems or there is a loss of body mass and muscle, complicating factors (metabolic acidosis, intestinal bleeding) must be clarified. The necessary nutritional requirements must be guaranteed in any case, in problematic cases even without a kidney diet.&lt;ref name=&quot;Hey2&quot; /&gt;

=== Treatment of the accompanying symptoms ===
[[File:Infusion-cat.jpg|thumb|Subcutaneous fluid administration in a cat]]

==== Dehydration ====
To combat dehydration, sufficient fresh drinking water should be provided. Here, too, you can try to increase the cat's voluntary water intake by adding meat broth or tuna juice.&lt;ref name=&quot;Arnell&quot; /&gt; Switching to wet food also often leads to increased fluid intake. Dehydrated cats or animals with [[hypovolemia|volume deficiency]] require fluid administration with correction of electrolytes. Renal azotemia cannot be influenced in this way. The administration of sterile [[infusion]] solutions under the skin by the owner must be viewed critically. These also ultimately enter the vascular system and conventional infusion solutions inevitably lead to a permanent excess of sodium. This form of treatment should therefore only be carried out if the condition and hydration status improve and there are no disturbances in blood pressure or potassium levels. Infusion solutions for cats in stage IV should contain a maximum of 40&amp;nbsp;mmol/L sodium and about 13&amp;nbsp;mmol/L (max. 30&amp;nbsp;mmol/L) potassium (half-electrolyte solution with potassium substitution).&lt;ref name=&quot;Hey2&quot;&gt;Karolin Hey: ''Chronische Nierenerkrankung der Katze – eine tägliche Herausforderung (Teil 2)''. In: ''Kleintierpraxis'' Band 69, No 4, 2024, p. 192–210. {{doi|10.2377/0023-2076-69-192}}&lt;/ref&gt;

==== Metabolic acidosis and potassium ====
The [[Sodium hydrogen carbonate|bicarbonate content]] should ideally be between 17 and 22 mEq/L. Sodium bicarbonate or [[potassium citrate]] is administered for buffering, whereby the latter also compensates for any existing potassium deficiency. A diet rich in potassium and magnesium is recommended &lt;ref name=&quot;Neiger410&quot; /&gt; and is already used in most commercial kidney diets. Potassium gluconate can also be used to compensate for a potassium deficiency, but [[potassium chloride]] is usually poorly accepted by cats and often causes gastrointestinal disorders.&lt;ref name=&quot;Arnell&quot; /&gt; The restriction of renal excretion in stage IV, [[ACE inhibitors]] or [[aldosterone]] deficiency due to [[renin]] deficiency can also lead to [[hyperkalemia]], which is why potassium levels must be checked regularly and a low-potassium diet may also need to be used.&lt;ref name=&quot;Arnell&quot; /&gt;

[[File:Blood pressure cat oscillometric.JPG|thumb|Blood pressure measurement in a cat]]

==== High blood pressure ====
Over 60% of cats with kidney disease develop high blood pressure. Amlodipine is the main drug used for treatment.&lt;ref name=&quot;Neiger409&quot;&gt;Reto Neiger: ''Chronische Niereninsuffizienz''. In: Marian C. Horzinek et al. (Hrsg.): ''Krankheiten der Katze''. Enke, 4. Ed. 2005, p. 409.&lt;/ref&gt; If the antihypertensive effect is not sufficient, the AT1 antagonist, which has been approved for cats since 2014 [[telmisartan]] can also be used to treat high blood pressure and proteinuria. Telmisartan can significantly reduce the extent of proteinuria.&lt;ref&gt;Ulrike Sent et al.: ''Gegenüberstellung der Wirksamkeit einer oralen Langzeitbehandlung mit Telmisartan und Benazepril bei Katzen mit chronischer Nierenerkrankung.'' In: ''Kleintierpraxis'' 61 (2016), p. 245–257.&lt;/ref&gt; However, the active ingredient can only be used as the sole antihypertensive agent if the blood pressure is below 200&amp;nbsp;mg Hg. It is important to monitor the effect of telmisartan at the beginning and after one week if the dose is changed by determining creatitinine, blood pressure and potassium levels; after four weeks, the urine protein-creatinine quotient should be checked. The reduction in [[systole|systolic]] blood pressure must not be lowered below 120&amp;nbsp;mm Hg; it should be around 140&amp;nbsp;mm Hg. Telmisartan should also be discontinued in phases of volume or fluid deficiency, during acute episodes of illness or before anesthesia.&lt;ref name=&quot;Hey2&quot; /&gt;

ACE inhibitors such as [[benazepril]], [[enalapril]] or [[ramipril]] alone do not usually lead to a sufficient reduction in blood pressure, but they can slow down the progression of the disease up to stage III.&lt;ref&gt;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), p. 1074–1079, PMID 17063698&lt;/ref&gt; In stage IV, ACE inhibitors are considered relatively [[contraindication|contraindicated]].&lt;ref name=&quot;Francey&quot; /&gt; Of these active substances, benazepril and ramipril are currently approved for cats in Germany, all others must be reclassified. Dietetically, the tendency to high blood pressure can be reduced by reducing the sodium content of the feed.&lt;ref name=&quot;Ettinger&quot; /&gt;

==== Anemia ====
To combat anaemia, an [[iron]] &lt;nowiki&gt;addition&lt;/nowiki&gt; to the feed in the form of organic iron compounds or [[iron(II) sulphate|iron sulphate]] is particularly useful. The iron content in the feed should be slightly above the maintenance requirement of 5&amp;nbsp;mg/MJ UE. However, the [[parenteral]] administration of iron is more potent.&lt;ref name=&quot;Hey2&quot; /&gt; If the [[hematocrit]] (Hct) nevertheless falls, [[blood transfusion]]s are indicated. Anabolic steroids [[Steroids]] to increase [[erythropoiesis|new blood formation]] are slow-acting in cats and their benefit is questionable. [[Recombinant protein|recombinant]] human [[erythropoietin]] may be indicated from a hematocrit &lt; 20%. However, the treatment is expensive and around a third of all cats form [[antibodies]] against this substance, which results in anemia that can no longer be treated.&lt;ref name=&quot;Neiger409&quot; /&gt; With [[darbepoetin]], the risk of antibody formation is apparently significantly lower, it also has a longer [[plasma half-life]] and is more potent.&lt;ref name=&quot;Arnell&quot; /&gt; Darbepoetin is used when the hematocrit is permanently below 20, the target range is a Hct of 25–35. This is usually achieved after two to three weeks, then the dose can be gradually reduced.&lt;ref name=&quot;Hey2&quot; /&gt;

==== Gastrointestinal tract ====
Secondary consequences of uremia on the gastrointestinal tract in cats are mainly [[fibrosis]] and [[Mineralized tissues#Diseased mineralized tissues|mineralization]] of the [[gastric mucosa]], but no [[gastric ulcer]]s, so that the gastric acid blockers such as [[omeprazole]], which have long been recommended for therapy, are no longer indicated.&lt;ref name=&quot;Hey2&quot; /&gt;&lt;ref&gt;S. M. McLeland, K. F. Lunn, C. G. Duncan, K. R. Refsal, J. M. 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.'' Band 28, Nummer 3, 2014 May-Jun, p.&amp;nbsp;827–837, [[doi:10.1111/jvim.12342]]. PMID 24628683.&lt;/ref&gt; Mirtazapine has been shown to stimulate the appetite and reduce uraemic nausea.&lt;ref&gt;J. M. Quimby, K. F. 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).'' Band 197, No 3, September 2013, p.&amp;nbsp;651–655, [[doi:10.1016/j.tvjl.2013.05.048]]. PMID 23838205.&lt;/ref&gt;

=== Kidney transplantation ===
Kidney transplantation is only possible in a few specialized facilities and is cost-intensive. The basic requirements are decompensated renal insufficiency at an early stage that no longer responds to conventional treatment, a previous weight loss of no more than 20%, the absence of serious concomitant diseases and negative tests for chronic viral infections such as [[feline leukemia]] or feline immunodeficiency syndrome. Urinary tract infections should also not have occurred in the recent past.&lt;ref name=&quot;Arnell&quot; /&gt;

== Interactions with other treatments ==
Since the kidney is also an important excretory organ for numerous drugs, chronic kidney disease must be taken into account in the drug therapy of other diseases. For example, the [[plasma half-life]] may be significantly prolonged (e.g. with numerous antibiotics) and the dose must be reduced accordingly. Drugs that can only be administered with caution in cats with kidney disease include [[atenolol]], [[carbimazole]], [[chlorothiazide]], [[digoxin]] and [[thiamazole]].&lt;ref name=&quot;Fink&quot; /&gt;

== Treatment prospects==
It is not possible to restore lost nephrons, so that all therapeutic measures only result in an increase in quality of life and lifespan. The [[prognosis|treatment prospects]] is strongly dependent on the degree of azotemia, protein loss via the urine, hyperphosphatemia and uremia as well as the hematocrit.&lt;ref name=&quot;Heine&quot; /&gt;&lt;ref&gt;J.N. King et al.: ''Prognostic factors in cats with chronic kidney disease.'' In: J. Vet. Intern. Med. 21 (2007), p. 906–916, PMID 17939542&lt;/ref&gt; In stage 2, a low hematocrit and a high urine protein-creatinine ratio, and in stage 3 hyperphosphatemia are prognostic for progression of CNE.&lt;ref&gt;S. Chakrabarti, H. M. 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.'' Band 26, No 2, 2012 Mar-Apr, p.&amp;nbsp;275–281, [[doi:10.1111/j.1939-1676.2011.00874.x]], PMID 22269057.&lt;/ref&gt; A new prognostic parameter is [[fibroblast growth factor]] 23, as it indicates an early derailment of mineral metabolism.&lt;ref name=&quot;Hey2&quot; /&gt; The [[median|average]] survival time in a recent study was 1151 days in stage IIb cats, 778 days in stage III and only 103 days in stage IV.&lt;ref&gt;L. M. Boyd et al.: ''Survival in cats with naturally occurring chronic kidney disease (2000–2002).'' In: J. Vet. Intern. Med. 22 (2008), p. 1111–1117, PMID 18691369&lt;/ref&gt; The consistent use of phosphate-reduced kidney diets shows quite good results up to stage III.&lt;ref name=&quot;Elliott&quot; /&gt;&lt;ref name=&quot;Plantinga&quot; /&gt;&lt;ref name=&quot;Barber&quot; /&gt; If the measures taken do not work, the only option for advanced kidney disease is often [[euthanasia]].

== Further reading==
* Sarah Steinbach and Reto Neiger: ''Chronische Nierenerkrankung'': In: Hans Lutz et al. (Ed.): ''Krankheiten der Katze''. Enke, 5. Aufl. 2014, ISBN 978-3-8304-1243-4, S. 751–755.
* Gregory F. Grauer: ''Chronic renal failure''. In: R. W. Nelson und C. G. Couto (Hrsg.): ''Small animal internal medicine''. Mosby, 3. 2003, ISBN 0-323-01724-X, p.&amp;nbsp;615–623.

==See also==
{{Commons category|Feline chronic kidney disease|Chronische Nierenerkrankung der Katze}}
*[[List of feline diseases]]

== References ==
&lt;references responsive /&gt;

== External links ==
* [https://www.iris-kidney.com/ International Renal Interest Society]

{{Domestic cat}}
{{Authority control}}

[[Category:Cat diseases]]
[[Category:Kidney]]