Renal diseases in dogs and cats
Renal disorders are some of the most common medical diseases we encounter in practice. This week we're chatting all about the kidney, its functions, and acute and chronic kidney disease.
The Kidney
The kidneys are the first organs in the urinary tract; they sit within the retroperitoneal space in the dorsocaudal abdomen at around the level of the 13th rib, and the left kidney is slightly more cranial than the right. Each kidney is formed of three main components:
The cortex is the outermost layer; here the blood filtration process begins and urine is formed;
The medulla is located beneath the cortex; here the urine is concentrated;
The pelvis is located centrally within the kidney; here urine collects prior to excretion.
The kidneys are made up of many nephrons. Each nephron consists of the glomerulus, Bowman’s capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule and collecting duct. The nephrons are responsible for filtering the blood, re-absorbing key solutes and electrolytes, and forming urine.
The glomerulus is a capillary bed which filters blood by forcing plasma through capillary membranes under pressure. Water and solutes are able to move through the membrane into the Bowman’s capsule, whereas larger molecules such as proteins remain in the circulation.
The ultrafiltrate then enters the proximal tubule. The renal tubules and loop of Henle are responsible for maintaining fluid, acid/base and electrolyte balance, as well as excreting waste products. Amino acids, glucose and electrolytes are re-absorbed into the bloodstream in the proximal tubule, and hydrogen moves from the bloodstream into the ultrafiltrate here too (maintaining a normal plasma pH level). The ultrafiltrate then enters the loop of Henle, where it is concentrated, as water moves out into the interstitial space via a concentration gradient. From here the ultrafiltrate enters the distal tubule, where sodium and water are re-absorbed into the bloodstream, due to the effects of antidiuretic hormone.
The ultrafiltrate has, at this point, become urine as all solutes required by the body have been absorbed back into the bloodstream. The urine then enters the collecting duct, where it flows to the renal pelvis for excretion. In addition to urine production and concentration, the kidneys have many other key roles within the body. These include:
red blood cell production, via the secretion of erythropoietin from specialised cells;
blood pressure regulation, through the production of renin;
maintenance of calcium and phosphorus balance, through the formation of calcitriol in the renal tubules.
Chronic Kidney Disease
CKD is the most commonly recognised renal disorder in dogs and cats. It is defined as renal damage or reduced renal function which has persisted for over 3 months. In response to short-term injury, the kidney can normally compensate through hypertrophy for short periods of time. In CKD, these compensatory mechanisms are exceeded and permanent damage occurs. This damage is progressive and irreversible, and renal function generally slowly declines over a period of months-to-years.
A number of causes of CKD have been identified, including:
congenital disorders such as renal dysplasia
pyelonephritis (infection of the kidney),
urolithiasis (e.g. following ureteral obstruction),
neoplasia (such as renal lymphoma)
glomerular diseases such as amyloidosis.
However, In many cases, the underlying cause is unknown.
Clinical signs of CKD vary and can include:
polyuria and polydipsia - as the kidneys lose their ability to concentrate urine, increased urine losses occur, leading to a compensatory polydipsia
lethargy
anorexia/hyporexia
weight loss
poor coat quality
signs of dehydration - sunken eyes, skin tenting and tacky mucous membranes
systemic hypertension is frequently seen secondary to CKD. Signs of target organ damage may be seen in a severely hypertensive patient; the most common organs affected are the eyes and central nervous system.
uraemia may be seen in severe, often end-stage CKD. This classically includes signs such as anorexia, lethargy, vomiting, severe weight loss, diarrhoea, halitosis and neurological signs.
secondary renal hyperparathyroidism may be seen where alterations to calcium/phosphate balance are present. Signs of this include depressed mentation, lethargy, weakness, anorexia, impaired muscle function and bone resorption in the skull/mandible, +/- mandibular fractures.
Acute Kidney Injury
AKI is a rapid and severe loss of renal function, which causes nitrogenous waste products (urea) to accumulate, and fluid/acid-base imbalance and electrolyte disturbances to occur. Unlike chronic disease, resolution of the acute injury, treatment of the underlying cause, and/or adaptation of the kidney can reverse the clinical signs. A number of factors can cause AKI, including toxin ingestion, infectious disease, urinary tract obstruction, and following the administration of certain medications.
Azotaemia (increased serum urea and creatinine levels) is described as pre-renal, renal or post-renal, depending on the underlying cause, and different causes result in injury to different areas of the urinary tract:
pre-renal azotaemia occurs when there is reduced blood flow to the kidney. This can be caused by severe hypotension, shock, and general anaesthesia (any cause of significant, sustained hypotension).
renal azotaemia results from injury to any part of the kidney itself. Causes of renal azotaemia include toxins, medications and/or infection.
post-renal azotaemia occurs due to urinary tract obstruction. In these cases the obstruction puts pressure on the kidneys, reducing glomerular filtration and causing azotaemia. Obstructions can be present in the lower urinary tract (urethra) or upper tract (ureters), or both, and can be caused by stones, crystalline sludge, or due to neoplasia.
Clinical signs of acute kidney injury are varied, and include:
polyuria and polydipsia
lethargy or depressed mentation
hyporexia or anorexia
vomiting
halitosis and/or oral ulceration
anuria or oliguria (in cases of urinary tract obstruction or severe loss of renal function)
stranguria (in cases of urinary tract obstruction)
bradycardia or bradyarrhythmias (in cases of hyperkalaemia)
neurological signs (in cases of toxin ingestion)
AKI patients typically present as an emergency and have extensive triage and stabilisation requirements. On presentation to the clinic, the veterinary nurse should undertake an immediate major body systems assessment, in order to identify and correct any life-threatening changes to the cardiovascular, respiratory and central nervous systems. Following initial stabilisation, a more detailed 'secondary survey' assessment should be performed.
Priorities after triage include securing intravenous access, attaching monitoring equipment such as an ECG where bradycardia is present, to check for cardiac arrhythmias, providing appropriate warming to a collapsed, hypothermic patient (whilst ensuring that warming does not worsen any hypotension/shock by dilating peripheral circulation). Following this, fluid resuscitation and treatment of any hyperkalaemia present should be performed as a priority.
Diagnostics in the Renal Patient
A variety of diagnostics are performed in patients with renal diseases. These include:
non-invasive blood pressure, ideally using the Doppler method if available. This should be performed before other diagnostic methods and in a way that minimises stress, in order to prevent 'white coat hypertension'.
biochemistry testing is the main diagnostic used in our renal patients. Urea and creatinine are the parameters typically used to monitor renal function. In CKD patients azotaemia is present when >75% of kidney function is lost. Other changes include hyperphosphataemia, hypercalcaemia, hypokalaemia (in the CKD patient), hyperkalaemia (in the AKI patient) and hypoalbuminaemia (due to increased protein loss through the kidneys - seen in patients with glomerular diseases). SDMA is a relatively new biochemical test which acts as an early indicator of renal insufficiency (before elevations in creatinine/urea are seen).
haematology may reveal anaemia (due to reduced erythropoietin levels) or signs of inflammation/infection where pyelonephritis is present.
blood gas analysis may reveal metabolic acidosis
urine analysis should be performed in all renal patients. This should include specific gravity (to determine the urine concentrating ability), dipstick analysis, sediment examination, and submission for a urine protein:creatinine ratio and bacterial culture.
abdominal ultrasound may be used to visualise the kidneys, and assess their size, presence of structural abnormalities, masses, stones or other abnormalities. Guided FNA sampling (where required) of the kidneys can also be performed via ultrasonography, as can cystocentesis sample collection.
Treatment and Nursing Care
Fluid Therapy
A mainstay of both CKD and AKI treatment is fluid therapy. An appropriate isotonic crystalloid solution should be used; typically this is Lactated Ringer’s Solution, as it is suitable for correcting metabolic acidosis, whilst not containing sufficient potassium to contribute to any hyperkalaemia that may be present. The administration of intravenous fluids restores hydration and perfusion status in dehydrated and hypovolaemic patients, corrects acid/base disturbances and can correct electrolyte imbalances as well as initiating diuresis. Fluid requirements should be calculated based on assessment of dehydration or hypovolaemia, and administered accordingly. Fluid balance should be regularly re-assessed to detect any over or under-hydration, and rates adjusted as appropriate.
Potassium Management
CKD patients typically require potassium supplementation in additional to IVFT. An appropriate level of supplementation should be provided based on the patient's serum potassium level, and this re-checked regularly.
Patients with AKI are frequently hyperkalaemic and require correction of this to prevent life-threatening consequences. Potassium levels may be managed or reduced by administering
Calcium gluconate, which protects the heart from the effects of the hyperkalaemia (but does not actually lower the potassium level);
Glucose, which reduces serum potassium by stimulating the body to release insulin, to drive potassium from the bloodstream into cells;
Neutral insulin, which reduces serum potassium levels by driving it into cells. As hypoglycaemia can result, glucose is typically given at the same time.
Phosphate Management
Hyperphosphataemia is common in CKD patients, and adjustment of dietary phosphate intake is indicated. This is achieved through feeding a restricted-phosphate diet (e.g. a renal diet), or through adding a phosphate binder to the patient's normal food.
Hypertension Management
Where systemic hypertension is present, calcium channel blockers or angiotensin-converting enzyme (ACE) inhibitors may be administered. Patients receiving antihypertensive medications should be monitored regularly, especially in the early stages of treatment. Regular blood pressure assessment during hospitalisation is recommended.
Supportive Care
Supportive treatments include appetite stimulants, analgesics, anti-emetics and gastroprotectant medications. Patients with gastrointestinal upset due to renal disease may require H2-blockers, mucosal protecting agents, or anti-emetics to minimise GI-side effects of the renal disease, prevent nausea and pain, and encourage voluntary appetite. Appetite stimulants may be used in anorexic patients where any other causes of anorexia have been addressed.
Nutritional Support
Renal patients are frequently anorexic or hyporexic, and nutritional support forms a large part of nursing care. These patients should be weighed regularly and their resting energy requirement calculated each day (based on their current or admitted weight). Percentage of RER consumed each day should be recorded, and enteral feeding support given where less than 80% of RER is consumed for 3+ days. Naso-oesophageal tubes can be beneficial in these patients and are quick and simple to place, can be placed conscious, and can be placed by nurses.
Following correction of anorexia, patients with chronic disease should be transitioned onto a renal diet, since these are designed to maintain renal health and slow progression of disease. This should be performed at home once the patient is over their initial period of illness, since introduction of a new diet in the hospital can cause food aversion, which can persist long-term.
General Nursing Care
General nursing care of the renal patient is varied and includes:
Clinical examination and recording vital signs at appropriate intervals, based on patient stability
Monitoring urine output - ideally through a urinary catheter in AKI patients, or through weighing bedding/litter trays and collecting urine when walking dogs outside
Urinary catheter care as appropriate
Considering venous access - in the long-term patient, or those where multiple blood samples are required, a central venous catheter or sampling line may be a more appropriate IV choice. These allow repeated blood sampling without repeated venipuncture. Any IV catheter should be checked and re-dressed at regular intervals (every 12 hours or more often as appropriate)
Monitoring for signs of pain, nausea, bradycardia, cardiac arrhythmias or other complications of disease
Provision of an appropriate kennel environment, including wicking, padded bedding, frequent opportunities for urination in the polyuric patient
Grooming and maintenance of skin integrity, especially around the perineal area in polyuric or catheterised patients
Let me know below... what are your experiences with renal patients, and your nursing top tips?
References
1. Ettinger, S., Feldman, C., and Cole E. Textbook of Veterinary Internal Medicine. 8th ed. Missouri: Elsevier, 2016.
2. Merrill L. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell, 2012.
3. Nelson, R W. and Couto, C G. Small Animal Internal Medicine. 5th ed. Missouri: Elsevier Mosby, 2014.
4. Taylor S, Sparkes A, Briscoe K, et al. ISFM Consensus Guidelines on the Diagnosis and Management of Hypertension in Cats. J Feline Med Surg 2017; 19: 288-303.
