Kidneys play an important role in maintaining homeostasis (Lewis, 2012) being involved in the regulation of blood volume, pH, osmolarity, blood pressure and release of hormones (Breton, 2013). When kidneys start to fail this can lead to chronic kidney disease (CKD) where the kidneys irreversibly deteriorate (Somvanshi et al, 2012). CKD is a progressive loss of renal function due to nephron damage; these are the functional units of the kidneys where many homeostatic processes occur (Bartges, 2012). Signs of CKD include polyuria, polydipsia, vomiting and diarrhoea, anorexia and weight loss, dehydration, mucosal ulcers and uraemic breath.
Signs of chronic renal failure
One symptom of CKD is a rise in levels of blood urea nitrogen (BUN; normal reference range 17–29 mg/dl) (Brown, 2007) and creatinine (azotaemia being identified once the blood creatinine concentration >1.6 mg/dl) (Brown, 2007; Polzin, 2011). In healthy patients, urea is excreted in the urine but once kidneys begin to fail they are unable to remove the urea resulting in raised levels of BUN. Creatinine should be constantly filtered out through the kidneys but again when the kidneys begin to fail these levels also rise. These complications may show as typical gastrointestinal signs such as nausea, vomiting and diarrhoea (occasionally haemorrhagic) due to an increase in gastric acid where gastrin is not being metabolised within the kidneys as it once was. Mouth ulcers and a distinctive smell of ammonia on the breath occur due to nitrogenous waste such as ammonia and urea accumulating in the blood from the breakdown of proteins. Anorexia and subsequent weight loss and dehydration may then also be seen due to the build up of toxins in the blood combined with irritation and ulceration of the gastrointestinal tract making the patient feel unwell and painful (Acierno and Senior, 2011).
Glomerular sclerosis, proteinuria and hypertension
In healthy kidneys proteins and large molecules should not be leaving the blood as they are not usually able to pass through the glomerulus (Lewis, 2012). However, if this barrier becomes damaged proteins are able to pass from the blood, through the glomerular filtration barrier and into the renal tubules (Breton, 2013). The filtered protein is then normally reabsorbed in the proximal convoluted tubule where it is broken down by lysosomes before re-entering the blood as amino acids; increased filtration of proteins leads to proteinuria as protein filtration exceeds re-uptake (Mardell, 2009).
Break down of proteins releases oxygen free radicals which activates inflammatory mediators resulting in inflammation, further damaging tubular epithelial cells (Lewis, 2012). Inflammation activates renal fibroblasts causing collagen to be deposited in the glomeruli thus resulting in further sclerosis, damaging the glomeruli leading to a reduced glomerular filtration rate and decreased urine output (Acierno and Senior, 2011). As sclerosis develops there is a marked reduction in renal perfusion, this often presents as polyuria then secondary polydipsia and dehydration in the patient due to the inability to intake adequate volumes of fluid and to sufficiently concentrate urine (Caney, 2010). Once some damage has already occurred, blood may be shunted to healthier glomeruli by prostaglandins (Lewis, 2012); this causes increased blood flow and added pressure on the healthy glomeruli by increasing intraglomerular capillary pressure and hyperfiltration (Acierno and Senior, 2011).
The glomerulus can be further damaged by conditions such as hypertension and diabetes mellitus; these along with increased intraglomerular pressure and inflammation eventually cause sclerosis and occlusion of the glomerulus inhibiting correct filtration. This process is irreversible resulting in a decrease in glomerular filtration rates (Mardell, 2009). Hypertension can arise from sclerosis of the glomeruli, thus accelerating further sclerosis and causing a worsening hypertension, resulting in a vicious circle (Wong, 2012).
Kidneys play a vital role in blood pressure maintenance; loss of control of blood pressure may also be due to the over production of renin from the juxtaglomerular apparatus (hyperreninaemia), triggering excessive renin-angiotensinaldosterone activity (Lewis, 2012). Vasoconstriction then occurs with sodium and water being retained; signs in a patient may therefore be seen as reduced urinary concentrating ability, dehydration and hypertension. Hypertension promotes progression of CKD as well as proteinuria leading initially to ocular disease, retinal detachment and blindness then to left-sided heart failure, seizures and death (Forster-Van Hijfte, 2002).
Acid–base balance
Kidneys are vital in the maintenance of acid–base balance in the blood (Chew et al, 2011); the renal tubules reabsorb and generate replacement bicarbonate, but as CKD progresses this function in the kidney begins to fail resulting in acidosis due to retention of normally excreted acids (hydrogen ions) (Acierno and Senior, 2011). Hypokalaemia is often seen with CKD due to reduced renal excretion and is a secondary effect of acidosis (Chew et al, 2011). Hypokalaemia also occurs due to hydrogen ions exchanging for potassium ions in the cells; potassium ions therefore enter the circulation and are excreted (Bartges, 2012). Hypokalaemia can present as muscle weakness, loss of muscle mass and anorexia due to malnutrition and excessive renal losses (Acierno and Senior, 2011).
Anaemia and resulting lethargy and weakness may be seen due to a failure to produce adequate erythropoietin by renal interstitial cells (Somvanshi et al, 2012). Erythropoietin increases the number of committed stem cells which will develop into erythrocytes; without erythropoietin, erythroid stem cells die (Breton, 2013).
Hyperphosphataemia, hypocalcaemia and secondary hyperparathyroidism result from vitamin D not being hydroxylated in the kidneys; phosphorus is retained and calcitriol metabolism is reduced (Polzin, 2011). Parathyroid hormone stimulates the release of the enzyme alpha-1 hydroxlase to convert calcidiol into calcitriol which is the active form of vitamin D3 (Al-Bard and Martin, 2008). Calcitriol stimulates absorption of calcium and phosphorus and inhibits parathyroid hormone which in turn not only stimulates renal absorption of calcium and excretion of phosphorus but also calcium and phosphorus release from bone and calcitriol production (Maltman, 2011). The resulting hyperphosphataemia leads to a risk of soft tissue mineralisation (Acierno and Senior, 2011). When CKD occurs there is decreased activation of calcitriol resulting in increased parathyroid hormone secretion (Wong, 2012).
Caring for the CKD cat
CKD is a leading cause of death in feline patients in veterinary practice. A detailed knowledge of chronic renal failure is therefore vital to correctly manage such a condition (Caney, 2010); by possessing a greater understanding of any disease, care can be tailored to ensure patients receive the best care possible that not only focuses on the disease, but looks at the patient in a holistic fashion with the aim of preventing potential complications. Before beginning treatment it is vital that a thorough assessment of the patient is conducted and a care plan then drawn up to ensure no areas of care are overlooked (Cherry, 2014).
Most felines admitted with CKD are dehydrated, the percentage dehydration should be calculated and intravenous fluid therapy (IVFT) started as appropriate to assist renal function. The IVFT line should be checked each time the patient is checked to ensure it remains patent and is delivering the correct amount of fluid. Due to the polydipsia and despite being on IVFT, the patient should be allowed constant access to water and encouraged to drink as much as possible; some may prefer water fountains and flavouring the water may also help. Whichever way, fluid intake should be recorded daily to ensure adequate amounts are being drunk (Caney, 2010). Feeding a wet diet or adding water to food will increase water intake however care should be taken to ensure a familiar food is used while hospitalised to avoid food aversion (Figure 1 and 2) and to also prevent potential diarrhoea from a sudden diet change. New food such as a renal diet should be introduced slowly once the patient has been discharged; a renal diet will eventually assist in managing hyperphosphataemia (Wakeling, 2009) and has been linked with increasing survival times in these patients (Plantinga et al, 2005). Those diets with low phosphorus and sodium and higher levels of potassium and arachidonic acid appear to promote the best results (Plantinga et al, 2005). Being specifically formulated to support cats with CKD, renal diets have been shown to not only slow the progression of CKD but also prolong survival times (Plantinga et al, 2005; Ross et al 2006; Korman and White, 2013).
Polyuria may already be present and with the increased water intake, litter trays should be constantly available being checked and cleaned regularly. It is useful to find out what the patient does at home and whether they are used to using a litter tray at all, if not the use of soil within a litter tray can be beneficial and more familiar to the patient. Any bedding or sheets contaminated with urine should be replaced immediately to prevent urine scalding and sores developing. Urine production (normal 1–2 ml/kg/day) and urine specific gravity (normal 1.013–1.034) (International Renal Interest Society, 2016) should be closely monitored by catheterisation or urine collection from an inert non-absorbent litter; this will allow monitoring of renal function by assessing whether water is being appropriately conserved or excreted (Wakeling, 2009). This also allows for the monitoring of losses of protein, bilirubin and glucose through the urine and assists in monitoring of patient hydration status (International Renal Interest Society, 2016).
In those patients where the appetite is still poor, a feeding tube such as a naso-oesophageal or oesophagostomy, may be placed to ensure adequate nutrition is obtained. Once placed feeding tubes allow pain and stress free feeding until the patient feels able to eat for themselves; suitable liquid renal foods can be given via the tube in an attempt to start managing the condition early on (Webber, 2010). Food should always be offered to the patient first; warming and offering strong smelling foods may sometimes help. Nurses should take care however to monitor for signs of nausea and vomiting which may be causing anorexia. The attending veterinary surgeon (VS) should be alerted so that care may be tailored to perhaps include anti-emetics. Oral and gastric ulcers if present can be extremely painful therefore regular pain scoring alongside the use of analgesics may also be required to ensure the patient feels comfortable to eat (Cherry, 2014).
All observations and changes to care should be recorded on the hospitalisation sheet and care plan so that any improvement or deterioration can be noted and care altered accordingly. If vomiting and/or diarrhoea are present the use of incontinence sheets will absorb and save bedding; if soiled, any bedding should be changed quickly and the patient also cleaned using warm water as required. Cats are very clean, therefore being soiled may cause further depression especially if they are already not cleaning themselves adequately. Regular cleaning with warm water and brushing may improve a patient's demeanour, they will then also not always associate visits to the kennel with negative actions such as injections (Cherry, 2014).
Blood pressure monitoring
While hospitalised it is vital regular checks are made of not only the patient's demeanour but of vital signs and processes; regular blood pressure readings should be taken in the management of hypertension (normal systolic blood pressure of between 120–180 mmHg) (Figure 3). Regular pressure readings allow for monitoring of any medication to ensure the correct therapeutic dose is being given, if not complications such as blindness, seizures and cardiac changes can occur (Caney, 2010). Regular urine samples should also be taken over a patient's stay to monitor for changes in levels of protein and if any blood appears. Due to the possible combination of medications and increased water intake making the urine more dilute, there is an increased risk of the patient developing bacterial cystitis and infections (Barber, 2003; Mayer-Roenne et al, 2007).
Anaemia is commonly associated with lethargy, inappetance, weakness and weight loss, treatment may involve blood transfusions and iron supplementation. The nurse's role here is one of support for the patient ensuring they remain comfortable and as stress free as possible during any procedures. Those with CKD require intense levels of nursing care so it is vital that nurses are able to develop a bond quickly with patients to identify where changes in care need to be made. Taking a holistic view and implementing a care plan allows all members of staff to be involved in each individual's care encompassing the patient's mental wellbeing (Cherry, 2014).
Nursing care after discharge
The nurse's involvement with patients with CKD does not stop once the patient is discharged; check-ups and monitoring of the patient should initially be conducted monthly, this is where the nurse's role in supporting the owner is also very important so that any problems are treated quickly. Nurse clinics are useful for regular checks of blood pressure (ideally with an ultrasonic Doppler), appetite, fluid intake and taking routine blood samples, while also allowing owners time to discuss the care of their pet with a nurse and to learn how best to care for them at home (Figure 4). This could include how to give subcutaneous fluid therapy at home if indicated, preventing dehydration and the need for possible hospitalisation (Webber, 2010). Involving owners in this way shows empathy, consideration and trust of the veterinary team to the owner. The owner knows the practice is there to support them and appreciates the need for a ‘normal’ life at home where with correct management, care of cats with CKD need not be difficult, and that a good quality of life is possible (Caney, 2010).
Conclusion
On discharge of patients with CKD it is essential nurses develop a good relationship with the client and that the patient is seen regularly for checks within the clinic. It is a veterinary nurse's responsibility to ensure clients understand medication and care and are able to identify signs of distress in their animals; it is important the owner is made to feel involved to encourage compliance and ensure the patient has the best quality of life possible. Understanding disease physiology allows specific care to be given that not only addresses the disease in question but allows care to be tailored considering potential problems in different body systems that the disease may cause. By altering the provision of nursing care given, normal functions can aim to be restored and a positive outcome achieved for all involved.