Renal failure

Question 1

What are the two responses of the remaining parenchyma in the event of kidney damage?

Answer 1

1. Remaining functional glomeruli will increase their filtration rate in compensation
2. Tubular epithelial cells can undergo hyperplasia to replace lost cells

Question 2

What are three factors that might contribute to the dehydration of an animal in renal failure?

Answer 2

Loss of ability to concentrate urine (especially medullary/juxtamedullary nephron lesions)

Inadequate fluid intake to compensate for the polyuria

Vomiting or diarrhoea

Question 3

What are three mechanisms that can contribute to the oedema or anasarca seen in renal failure patients?

Answer 3

1. Loss of protein via the glomerulus reducing the oncotic pressure of the blood
2. Uremic toxin damage to vascular endothelial cells causing increased permeability
3. Activation of RAAS causing fluid conservation at the kidney, leading to dilution of remaining albumin and increased plasma hydrostatic pressure, promoting leak into tissues

Question 4

What is one potential consequence of hyperphosphataemia in renal failure?

Answer 4

Tissue mineralisation

Question 5

What is one potential consequence of hyperkalaemia in renal failure?

Answer 5

Interference with cardiac electrical activity (especially anuric/oliguric renal disease)

Question 6

What is one potential consequence of hypokalaemia in renal failure?

Answer 6

Muscle weakness - especially polyuric renal failure, especially if patient has poor appetite

Question 7

What is one potential consequence of hypocalcemia in renal failure?

Answer 7

Can lead to secondary renal hyperparathyroidism

Question 8

What is one potential consequence of hypercalcemia in renal failure?

Answer 8

Can lead to soft tissue mineralisation

Question 9

What are four mechanisms for acidosis in renal failure patients?

Answer 9

1. Decreased ability of the DCT to generate NH4+ ions
2. Increased retention of H+ ions
3. Failure of the kidneys to excrete anions such as sulphates, phosphates causes them to be titrated in the blood by remaining HCO3-, consuming it
4. impaired reabsorption of HCO3- ions by the tubules

Question 10

What are two benefits of acidosis for the patient?

Answer 10

1. If the patient becomes hypocalcemic, the acidic blood encourages Ca2+ ions out of cells into circulation
2. Acidosis shifts the O2 saturation curve to the right, promoting O2 supply to the tissues

Question 11

Name two conditions that could result from secondary renal hyperparathyroidism

Answer 11

1. Osteoporosis

2. Osteodystrophia fibrosa (rubber jaw)

Question 12

What are five factors that might contribute to anemia in a chronic renal failure patient?

Answer 12

1. Decreased RBC production due to reduced EPO synthesis by damaged kidney
2. Negative effects of circulating uremic toxins on bone marrow haematopoiesis e.g PTH
3. Increased RBC fragility due to circulating uremic toxins
4. Platelet dysfunction
5. Blood loss through uraemic ulceration of GIT

Question 13

Is it possible to see abnormal glucose metabolism in chronic renal failure? Why?

Answer 13

Yes - due to increased retention of insulin, which is normally excreted via the kidneys

Question 14

Why are renal failure animals immunosuppressed?

Answer 14

Due to retention of proteins that inhibit leukocyte chemotaxis and degranulation. May be predisposed to secondary bacterial infection, also due to urea in secretions being metabolisable by urease + bacteria

Question 15

All animals in chronic renal failure should have their BP monitored. What are three potential consequences of systemic hypertension?

Answer 15

1. Hypertrophy and fibrinoid change of arterioles due to persistent vasoconstriction +/- dystrophic mineralisation can lead to narrowing of the lumen, perpetuating hypertension
2. May get thrombosis and infarction due to the above changes
3. May get sudden onset blindness due to acute retinal haemorrhage or detachment as a result of systemic hypertension

Question 16

In which species does uremic gastritis occur? What clinical signs might be seen? What factors might compound the damage to the gastric mucosa? What is one microscopic change that might be seen?

Answer 16

Dogs
See vomiting, haematoemesis, melena
Secondary bacterial infection of the mucosa, gastric hyperacidity due to increased renal gastrin retention , platelet dysfunction.
Microscopically may see dystrophic mineralisation of middle-deep mucosal layers +/- tunica muscularis

Question 17

Other than left ventricular hypertrophy, name two cardiac lesions associated with uraemia and briefly describe their pathogenesis.

Answer 17

1. Hydropericardium - distension of the pericardial sac with non-inflammatory fluid due to hypoalbuminaemia +/- endothelial injury via uremic toxins
2. Ulcerative uremic mural endocarditis of left atrium (more common in acute) - subendothelial oedema and glycoasminoglycan deposition as a result of circulating uremic toxins that may progress to necrosis and ulceration. Can get thrombosis OR scarring and dystrophic mineralisation OR rupture of the left atrial wall and fatal haemopericardium

Question 18

Most animals with terminal uremia develop pulmonary oedema. What is “uremic pneumopathy”, and which species does it occur in?

Answer 18

Uremic pneumopathy is severe pulmonary mineralisation and oedema with fibrin exudation into the alveolar lumina. Occurs in dogs.

Question 19

Which three major factors contribute to renal secondary hyperparathyroidism?

Answer 19

1. Hyperphosphataemia decreases concentration of ionised Ca2+ in blood, triggering PT gland response
2. Damaged kidney synthesises less vitamin D
3. Reduced GFR causes retention of circulating PTH, prolonging its effect

Question 20

Describe the lesions of uremic encephalopathy. Is it more common in acute or chronic renal failure?

Answer 20

Acute. Similar / identical to hepatic encephalopathy:

• vaculoation of white matter due to intra-myelinic oedema
• reactive swelling of astrocytes