Kidney disease
There are many potential causes of chronic kidney disease (CKD), for example, infections, toxins, tumours or degenerative disease. Due to the massive functional reserve of the kidney, it is only possible to detect signs of kidney disease when less than about a third of renal function remains. By the time kidney failure occurs, the underlying cause can seldom be identified, but whatever the cause, the disease progression will be more or less the same.
Acute kidney injury (AKI) is less common than chronic kidney disease. AKI may occur as a primary disease, for example, due to a toxin. Some CKD patients may have an acute ‘crisis’ on top of their chronic disease (‘acute on chronic’) when the patient becomes dehydrated and needs intravenous fluids.
Effects of kidney disease
1. Reduced ability to concentrate urine
One of the first things to happen as the kidneys start to fail is that they can no longer produce concentrated urine. The ability of the body to retain or excrete electrolytes is also affected. This eventually leads to the clinical signs of polydipsia (excessive thirst) and polyuria (excessive urination). A loss of urinary concentrating ability is one of the first signs of CKD.
2. Protein loss in the urine
Due to the increase in glomerular filtration pressure (glomerular hypertension), the glomerular membrane becomes damaged. The damage allows leakage of larger molecules such as proteins into the plasma filtrate. This protein is detectable in urine (proteinuria) and this can be an important part in the diagnosis of CKD. The loss of protein from the body can cause weight loss and lethargy, and protein in the plasma filtrate also causes damage to the kidney tubules, leading to disease progression.
It has been recognised in recent years that the presence and severity of proteinuria is a useful prognostic indicator: studies have shown that the presence of even low levels of proteinuria are associated with significantly shorter survival1.
3. Azotaemia/uraemia
As the glomerular filtration rate (GFR) falls, the body can no longer remove all the waste products and these start to build up in the bloodstream. The major waste products are urea and creatinine and this build-up in the blood is referred to as azotaemia. If levels of waste products become high, clinical signs of uraemia occur (for example, anorexia, mouth ulcers, vomiting). Azotaemia is only detectable when about 25% of the renal function remains.
4. Systemic hypertension
The kidneys play an important role in regulating blood pressure, and in a significant proportion of patients with renal disease, an increase in systemic blood pressure (systemic hypertension) occurs. Approximately 30% of cats with CKD have systemic hypertension. This increased blood pressure may cause further damage to the kidneys and also to other organ systems. The eyes and central nervous system are particularly susceptible to hypertensive damage. Signs that may be seen include blindness due to detached retinas or bleeding into the eye, and behavioural changes or seizures.
Systemic hypertension leads to an increase in glomerular pressure although; conversely, a patient with glomerular hypertension may have normal systemic blood pressure.
5. Anaemia
As the kidneys deteriorate, they produce less erythropoietin, a hormone that stimulates red blood cell production. Anaemia may develop as the disease progresses, and is considered to indicate a poorer prognosis.
6. Elevated blood phosphate
As the kidneys fail, levels of parathyroid hormone increase, due to reduced excretion of phosphate and reduced production of calcitriol by the kidneys. As phosphate levels increase, calcium levels fall and calcium is released from the bones to compensate. This is called renal secondary hyperparathyroidism. The end result is bone weakness and calcification of organs, and this probably contributes to disease progression.
7. Reduced blood potassium
Excessive levels of potassium are lost through the kidneys so blood levels fall. If they become too low, muscle weakness develops.
Reference: 1. H. Syme et al. (2006) JVIM, 20, 528-553.
