Identification of renal or urinary tract dysfunction

Question 1

What is often the first step of identification of renal or urinary tract dysfunction?

Answer 1

Azotaemia

Question 2

What is Azotaemia?

Answer 2

Azotaemia is defined as an increase in the nitrogenous compounds in the blood, generally identified by raised urea and creatinine compounds.

Question 3

Why are raised nitrogenous compounds an identifier of renal or urinary tract pathology?

Answer 3

The nitrogenous compounds are excreted by the kidneys therefore azotaemia is an indicator of renal or urinary pathology.

Question 4

How would one further classify the azotaemia?

Answer 4

It can be classified as pre-renal, renal (intrinsic) or post-renal azotaemia.

Question 5

At what % kidney function loss does azotaemia develop? And what conclusion can be drawn from this?

Answer 5

Azotaemia does not develop until there is at least 75% kidney loss. It is therefore now a very sensitive indication of intrinsic renal disease.

Question 6

What is a sightly more sensitive indicator of renal disease?

Answer 6

Isosthenuria is a slightly more sensitive indicator developing when there is 66% loss of renal function. (Isosthenuria is a condition in which urine has a consistent concentration, regardless of the body’s hydration status. In simpler terms, it means that no matter how much water you drink or how dehydrated you are, the concentration of substances in your urine remains the same. This condition usually indicates a problem with the kidneys’ ability to concentrate or dilute urine properly.)

Question 7

In pre-renal causes of azotaemia, how is the U.S.G. affected?

Answer 7

Hypersthenuric (increased concentration)(<1.040 in cats and 1.030 in dogs) unless there is a complicating disease, e.g. Addison’s, hypercalcaemia, E. Coli sepsis.

Question 8

In pre-renal causes of azotaemia, how are the dipstick affected?

Answer 8

(This box was blank but it did not say ‘generally unremarkable’ either)

Question 9

In pre-renal causes of azotaemia, what does the sedimentation exam show?

Answer 9

Generally unremarkable

Question 10

In pre-renal causes of azotaemia, how is the bladder size affected?

Answer 10

Generally small

Question 11

In pre-renal causes of azotaemia, what does diagnostic imaging show?

Answer 11

Kidneys and urinary tract generally unremarkable

Question 12

In pre-renal causes of azotaemia, what parameters should one look out for?

Answer 12

Hypersthenuria and small bladder

Question 13

In renal(intrinsic) causes of azotaemia, how is the USG. affected?

Answer 13

Variable depending on the stage of the disease but often isosthenuric (1.008-1.012) or poorly concentrated (<1.025). (This might not be right.)

Question 14

In renal(intrinsic) causes of azotaemia, what can be observed on the dipstick results?

Answer 14

Glucosuria and proteinuria are common.

Question 15

In renal(intrinsic) causes of azotaemia, what can be observed in the sedimentation exam?

Answer 15

Casts (tube-shaped particles made up of RBC/WBC/ kidney cells/protein/fat), erythrocytes, bacteria, leucocytes and/or neoplastic cells may be seen

Question 16

In renal(intrinsic) causes of azotaemia, how is the bladder size affected?

Answer 16

Variable depending on he stage of the disease.

Question 17

In renal(intrinsic) causes of azotaemia, what does diagnostic imaging show?

Answer 17

Renomegaly due to inflammation and edema, cellular infiltration and proliferation of inflammatory and regenerative kidney cells, bbstruction with cellular debris, casts, or inflammatory cells, vascular changes ( microangiopathies or vasculitis), fluid accumulation due to impaired fluid excretion OR small kidneys is the azotaemia is chronic.

Question 18

In renal(intrinsic) causes of azotaemia, what parameters should one look out for?

Answer 18

Isosthenuric/poorly concentrated urine, glucosuria, proteinuria, casts and other cells, renomegaly/small kidneys.

Question 19

In post causes of azotaemia, how is the USG affected?

Answer 19

Variable

Question 20

In post causes of azotaemia, what can be seen on the dipstick results?

Answer 20

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Question 21

In post causes of azotaemia, what can be seen in the sedimentation exam?

Answer 21

Erythrocytes are common.

Question 22

In post causes of azotaemia, how will the bladder appear?

Answer 22

Large and tense or absent

Question 23

In post causes of azotaemia, what could potentially be seen in diagnostic imaging?

Answer 23

1. Reno-, uretero-, cysto-, urethroliths
2. Ureteral dilation
3. Free abdominal fluid
4. Contrast studies may reveal urinary tract rupture or obstruction

Question 24

What are the four phases of AKI?

Answer 24

Induction, extension, maintenance, recovery.

Question 25

What is involved in the induction phase of AKI?

Answer 25

This begins with the ischaemic or nephrotoxic insult, and continues until there is a change in renal function such as decreased urine output or an increased urea or creatinine level. The length of time necessary t see the changes is variable and depends on the nature and severity of the insult. During this early stage, early intervention may prevent progression; clinical signs are often not apparent, which makes intervention difficult, but anticipation of the risk of AKI.

Question 26

What is involved in the extension phase of AKI?

Answer 26

The kidney is further injured by alterations in renal perfusion, continued hypoxia, secondary inflammation and ongoing epithelial and endothelial injury.

Question 27

What is involved in the maintenance phase of AKI?

Answer 27

This occurs after a critical amount of damage is established. The resulting decreased GFR results in azotaemia and clinical signs of uraemia, especially if combined with ongoing renal hypoperfusion. Elimination of inciting factors at this phase will not decrease existing damage or expedite the rate of recovery.

Question 28

What is involved in the recovery phase of AKI?

Answer 28

This is the phase where renal tissue undergoes regeneration and repair with varying restoration of renal function.

Question 29

IRIS AKI Grade 1 includes serum creatinine values that fall within the reference range for most veterinary, chemistry analysers, thus highlighting the need for monitoring trends in laboratory parameters. What value of increase in serum creatinine over 24hours would represent AKI?

Answer 29

Greater than or equal to micromoles/litre.

Question 30

Other than azotaemia, give another indicator of renal dysfunction.

Answer 30

Proteinuria

Question 31

How can proteinuria causses be classified?

Answer 31

Pre, intrinsic and post.

Question 32

What are pre-renal causes of proteinuria? (3)

Answer 32

1. Bence-Jones (fragments of immunoglobulins, which are antibodies produced by the immune system to help fight infections and lead to renal damage)
2. Haemolysis (haemoglobin is a protein and when RBC are broken down the haemoglobin is released)
3. Rhabdomyolysis (rapid breakdown of skeletal muscle tissue> release of myoglobin> kidney damage)

Question 33

What are post-renal causes of proteinuria? (4)

Answer 33

1. Cystitis
2. Prostatitis
3. Vaginitis
4. Neoplasia

Question 34

What are renal causes of proteinuria? (2)

Answer 34

1. Glomerular (resulting from abnormal permselectivity of the glomerular filtration barrier)
2. Tubular (caused by failure of tubular protein reabsorption or damage to the tubular epithelium)

Question 35

After excluding pre and post renal causes of proteinuria, what should be evaluated next?

Answer 35

The magnitude of the proteniuria should be evaluated next to evaluate the magnitude of the proteinuria by measuring the urine protein:creatinine ration (UPC).

Question 36

What can the UPC not be used to differentiate?

Answer 36

Tubular and Glomerular origins of the proteinuria nor can it be used to suggest the type of (glomerulo)pathy present. e.g. amyloidosis, immune complex glomerulonephritis, non-immune complex glomerulonephritis).

Question 38

What type of damage can proteinuria cause to the epithelium of the tubules?

Answer 38

Oxidative damage leading to AKI.

Question 39

What clinical states define nephrotic syndrome? (4)

Answer 39

1. Proteinuria
2. Hypalbuminaemia
3. Ascites/Oedema
4. Hypercholesterolaemia

Question 40

In addition to albumin that may be lost in the case of nephrotic syndrome, what glycoprotein can also be lost? And as a result, what can it lead to?

Answer 40

Anti-thrombin may be lost leading to a hypercoagulable state.

Question 41

Can serum albumin concentration be used to to predict antithrombin deficiency?

Answer 41

No

Question 42

What are the complications that can arise from proteinuria? (3)

Answer 42

1. Thromboembolism
2. Systemic Hypertension
3. Reduced tolerance towards crystalloid therapy

Question 43

Why can proteinuria lead to thromboembolism?

Answer 43

Proteinuria can induce hypercoagulability through a combination of endothelial dysfunction, inflammation and immune activation, alterations in blood rheology, direct activation of coagulation factors, and renal dysfunction

Question 44

Why can proteinuria lead hypertension?

Answer 44

Proteinuria can lead to hypertension through a combination of RAAS activation, endothelial dysfunction, inflammation and oxidative stress, and alterations in fluid and sodium balance.

Question 45

Why can proteinuria lead to reduced tolerance towards crystalloid therapy?

Answer 45

Hypoalbuminemia: Proteinuria often results in the loss of albumin, the most abundant protein in the blood. Albumin helps maintain oncotic pressure, which is necessary to keep fluids within the blood vessels and prevent them from leaking into the tissues.
Also..edema formation, renal dysfunction, risk of volume overload, electrolyte imbalances.