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ECEIM consensus statements > Renal > Flashcards

Renal Flashcards

1
Q

What is azotemia?

A

Azotemia is the term for increased blood concentrations of urea, serum creatinine (sCr), and other nonprotein nitrogenous substances.

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2
Q

What causes prerenal azotemia?

A

Prerenal azotemia is caused by decreased renal blood flow (RBF), such as dehydration, hypovolemic shock, or cardiac failure.

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3
Q

What causes renal azotemia?

A

Renal azotemia is caused by decreased glomerular filtration rate (GFR) due to renal injury.

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4
Q

What causes postrenal azotemia?

A

Postrenal azotemia is caused by the failure of excretion due to urinary tract obstruction or rupture.

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5
Q

What are many cases of AKI linked with?

A

inflammatory changes, toxic insults

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6
Q

Describe the continuum between prerenal and renal azotemia.

A

There is a continuum between prerenal and renal azotemia, where poor perfusion eventually leads to intrinsic kidney damage.

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7
Q

How is serum creatinine (sCr) processed by the kidneys?

A

Serum creatinine (sCr) is freely filtered by the glomerulus and is neither reabsorbed nor secreted.

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8
Q

What is the relationship between serum creatinine (sCr) and glomerular filtration rate (GFR)?

A

Serum creatinine (sCr) is inversely proportional to GFR and acts as a functional marker for it.

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9
Q

How does serum creatinine (sCr) respond to a decrease in GFR in advanced kidney disease?

A

In advanced disease, a small decrease in GFR results in a large increase in serum creatinine (sCr).

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10
Q

How does serum creatinine (sCr) respond to a decrease in GFR in early kidney disease?

A

In early renal disease, a large decrease in GFR results in only a small increase in serum creatinine (sCr).

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11
Q

At what point does serum creatinine (sCr) increase above reference limits?

A

Serum creatinine (sCr) does not increase above reference limits until GFR is reduced by nearly 75%.

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12
Q

How do heavily muscled animals affect serum creatinine (sCr) values?

A

Heavily muscled animals can have serum creatinine (sCr) values above reference limits.

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13
Q

How is creatinine production affected in humans with sepsis?

A

In humans, the production of creatinine is reduced in sepsis.

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14
Q

Has reduced creatinine production in sepsis been demonstrated in horses?

A

No

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15
Q

Why is blood urea nitrogen (BUN) a less specific estimator of GFR?

A

Blood urea nitrogen (BUN) is influenced by many factors, including dietary protein and protein metabolism, making it a less specific estimator of GFR and not useful for diagnosing AKI.

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16
Q

What does Acute Kidney Injury (AKI) represent?

A

AKI represents a spectrum of kidney damage, ranging from inapparent nephron injury to acute renal failure (ARF), involving a sudden decline in kidney function and a failure to excrete waste products and maintain fluid and electrolyte balance.

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17
Q

What is the prevalence of AKI in hospitalized horses?

A

AKI affects approximately 3% to 23% of hospitalized horses.

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18
Q

What are the risk factors for decreased renal blood flow and hypoxia in AKI?

A

Hypotension: Low blood pressure reduces renal perfusion.

Dehydration: Decreases overall blood volume, reducing renal blood flow (RBF).
Hypovolemia: Significant loss of blood volume, leading to reduced kidney perfusion.
Anemia: Lower oxygen-carrying capacity of the blood, leading to renal hypoxia.

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19
Q

What is Systemic Inflammatory Response Syndrome (SIRS) and its effects on kidneys?

A

SIRS causes systemic inflammation, often due to sepsis or endotoxemia, leading to:

Hypotensive injury: Decreased blood pressure affecting kidney perfusion.
Renal microcirculatory dysfunction: Impaired blood flow within the kidneys.
Thrombotic injury and infarction: Blood clots causing localized tissue death.
Fibrin deposition: Accumulation of fibrin protein, leading to kidney damage.
Renal cortical necrosis: Death of kidney tissue due to prolonged hypoxia.

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20
Q

What are the nephrotoxic agents that can cause AKI?

A

Aminoglycosides: Accumulate in the proximal tubular cells, causing nephrotoxicity.

Oxytetracycline: Causes AKI in high doses.
Bisphosphonates: Cause proximal tubule degeneration and glomerulosclerosis.
NSAIDs: Inhibit cyclooxygenase (COX), causing medullary crest necrosis and interstitial nephritis.
Other medications like omeprazole and hydroxyethyl starches are nephrotoxic in humans, but evidence in horses is lacking.

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21
Q

What endogenous nephrotoxins can lead to pigment nephropathy?

A

Myoglobin and hemoglobin released during muscle injury or hemolysis.

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22
Q

How can the risk of nephrotoxicity be managed?

A

Hydration: Initiate IV fluid treatment (IVFT) before administering nephrotoxic drugs.

Clinical judgment: Weigh benefits of prompt drug administration against AKI risk.
Combination therapy: Avoid simultaneous use of multiple nephrotoxic drugs.

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23
Q

What are other causes (rather than nephrotoxic drugs, decreased RBF and SIRS) of AKI in horses?

A

Immune-mediated injury: Conditions like purpura hemorrhagica causing glomerular damage.

Idiosyncratic hypersensitivity reactions: Leading to acute interstitial nephritis.
Infections: Actinobacillus spp. (especially in foals) and leptospirosis.

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24
Q

What are the clinical signs of AKI?

A

Oliguria: Reduced urine output (<0.5 mL/kg/h).

Inappetence and lethargy: Persisting beyond the resolution of the primary disease.

Neurological signs: Uremic encephalopathy in severe azotemia, manifesting as altered mental status or seizures.

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25
Q

What is the Veterinary Acute Kidney Injury (VAKI) System?

A

Stage 0: <150% change from baseline sCr.
Stage 1: 150%-199% change or absolute increase >0.3 mg/dL (26.5 µmol/L).
Stage 2: 200%-299% change.
Stage 3: ≥300% change or absolute increase to >4.0 mg/dL (>354 µmol/L).

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26
Q

What are common laboratory findings in AKI?

A

Electrolyte abnormalities: Hyponatremia, hypochloremia, hyperkalemia.

Urine Specific Gravity (USG): >1.035 in hypovolemic states, <1.020 in ARF despite hypovolemia.

Urinalysis: Detects microscopic hematuria, casts, and glucosuria.

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27
Q

What imaging techniques are used for diagnosing AKI?

A

Renal ultrasonography: Often unremarkable but useful for ruling out obstructions and evaluating kidney size and structure.

Renal biopsy: Rarely alters management and is not recommended due to risk and limited diagnostic value.

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28
Q

What are the initial treatment steps for AKI?

A

Focus on treating the underlying cause.

IV Fluid Therapy (IVFT): Essential to restore intravascular volume, blood pressure, and renal perfusion.

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29
Q

What is the approach to fluid therapy in AKI?

A

Response monitoring: Assess sCr levels and urine output within 24-72 hours.

Persistent hypotension: Use inotropes (e.g., dobutamine) and vasopressors (e.g., norepinephrine) if fluid replacement is insufficient.

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30
Q

How should urine output be monitored during IVFT in AKI?

A

Detect oliguria or anuria.

Furosemide challenge test to induce diuresis in euvolemic AKI patients. Avoid further doses unless a positive response is seen. Mannitol is no longer recommended due to nephrotoxicity.

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31
Q

What are the prognostic indicators for AKI?

A

Azotemia is a poor prognostic indicator if secondary to many conditions.

Early detection and management improve outcomes significantly.
Response to IVFT is a favorable prognostic indicator. Horses producing adequate urine and showing a decrease in sCr within 72 hours have a better prognosis.

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32
Q

What are the prevention strategies for AKI?

A

Close monitoring: Regularly check sCr levels in at-risk patients.

Prompt treatment: Correct primary diseases, hypovolemia, and hypotension quickly.
Nephrotoxic drugs: Use cautiously and avoid simultaneous use of multiple nephrotoxic agents.
Supportive measures: Maintain hydration and monitor for early signs of AKI.
Intravenous sodium bicarbonate: Often suggested to protect against pigment nephrosis through urine alkalinization, although its superiority to IVFT without sodium bicarbonate is not demonstrated.

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33
Q

What is the dose and mechanism of action for furosemide in horses?

A

Bolus 0.5-2 mg/kg IV/IM q4h-q6h or CRI 0.25-2 mg/kg/h; it decreases sodium, chloride, and potassium tubular reabsorption.

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34
Q

What are the adverse effects of high doses of furosemide in horses?

A

High doses can be nephrotoxic, causing an increase in sCr due to tubuloglomerular feedback and electrolyte disturbances.

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35
Q

What is the consensus on using furosemide in foals and adult horses?

A

Single high-dose furosemide test is the first-line treatment for normotensive foals and adults with anuria/oliguria.

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36
Q

What is the dose and mechanism of action for mannitol in horses?

A

A: 0.25-1 g/kg IV q4h-q8h (20% solution); it increases osmotic pressure in renal tubules.

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37
Q

Why is mannitol not recommended for use in horses?

A

It is associated with increased risk of AKI and can cause osmotic renal tubular injury.

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38
Q

What is the dose and mechanism of action for dobutamine in horses?

A

2-20 µg/kg/min; it is a beta-1 agonist with inotropic effects.

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39
Q

What are the consensus uses of dobutamine in foals and adult horses?

A

It is the first-line treatment for hypotension despite IVFT and for anesthesia-induced hypotension. Particularly foals.

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40
Q

What is the dose and mechanism of action for norepinephrine in horses?

A

0.2-0.3 µg/kg/min; it is an alpha-1 agonist causing peripheral vasoconstriction.

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41
Q

What are the consensus uses of norepinephrine in foals and adult horses?

A

Common treatment for hypotension despite IVFT and dobutamine, usually in conjunction with dobutamine, interchangeable with AVP.

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42
Q

What is the dose and mechanism of action for arginine vasopressin (AVP) in horses?

A

0.1-2.5 mU/kg/min; it increases water reabsorption in the distal tubule and collecting duct, vasoconstriction at high doses.

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43
Q

What are the consensus uses of arginine vasopressin (AVP) in foals and adult horses?

A

Treatment for hypotension despite IVFT and dobutamine, usually in conjunction with dobutamine, interchangeable with norepinephrine.

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44
Q

What is the dose and mechanism of action for fenoldopam mesylate in horses?

A

0.04 mg/kg/min; it is a selective dopamine (D1) agonist causing renal vasodilation.

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45
Q

What are the consensus uses of fenoldopam mesylate in foals and adult horses?

A

Potential treatment for normotensive foals and adults with anuria/oliguria.

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46
Q

What is the dose and mechanism of action for low-dose dopamine in horses?

A

1-5 µg/kg/min; it stimulates renal dopamine receptors causing vasodilation and natriuresis.

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47
Q

What are the consensus uses of low-dose dopamine in foals and adult horses?

A

Second-line treatment after unsuccessful furosemide challenge in normotensive foals and adults with anuria/oliguria.

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48
Q

What is the dose and mechanism of action for aminophylline in horses?

A

2-5 mg/kg slow IV q8h-q12h; it is an afferent arteriole vasoconstrictor with less potent and shorter action than theophylline. Adenosine antagonist.

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49
Q

What is the consensus use of aminophylline in foals and adult horses?

A

Potential treatment for normotensive foals and adults with ARF.

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50
Q

What is the dose and mechanism of action for theophylline in horses?

A

8 mg/kg IV q12h; it is an afferent arteriole vasoconstrictor.

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51
Q

What is the consensus use of theophylline in foals and adult horses?

A

Potential prophylactic treatment in foals with severe birth asphyxia; prophylactic treatment in adults is not established.

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52
Q

What is the mechanism of action for furosemide and its evidence of benefit in humans with AKI?

A

Furosemide decreases sodium, chloride, and potassium tubular reabsorption; it induces diuresis but without clinical benefit in AKI.

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53
Q

What adverse effects are associated with furosemide use in horses?

A

High doses can be nephrotoxic, causing increases in sCr through tubuloglomerular feedback and electrolyte disturbances.

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54
Q

What is the evidence of benefit for using dobutamine in humans with AKI?

A

Dobutamine has a beneficial effect on renal function for cardiorenal syndrome.

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55
Q

What adverse effects are associated with dobutamine use in horses?

A

: Increased blood pressure and arrhythmias.

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56
Q

What is the evidence of benefit for using norepinephrine in humans and its effects in horses?

A

Norepinephrine is recommended for treatment and prevention of AKI in humans with distributive shock; it increases blood pressure in anesthetized horses and critically ill foals.

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57
Q

What adverse effects are associated with norepinephrine use in horses?

A

Arrhythmias.

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58
Q

What is the mechanism of action for arginine vasopressin (AVP) and its adverse effects in horses?

A

AVP increases water reabsorption in the distal tubule and collecting duct, and causes vasoconstriction at high doses; adverse effects include arrhythmias and hyponatremia.

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59
Q

What is the mechanism of action and adverse effects of fenoldopam mesylate in horses?

A

Fenoldopam mesylate is a selective dopamine (D1) agonist causing renal vasodilation; it increases urine output in healthy foals but has no additional benefit to renal function when combined with norepinephrine.

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60
Q

What are the adverse effects of low-dose dopamine in horses?

A

Increased renal blood flow and urine production in healthy horses, and arrhythmias.

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61
Q

What is the evidence of benefit for using aminophylline in humans with AKI?

A

Aminophylline lowers sCr in pediatric patients with AKI but without improvement of urine production or outcome.

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62
Q

What adverse effects are associated with aminophylline use in horses?

A

Dose-related tachycardia, tachypnea, and nervous signs.

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63
Q

What is the mechanism of nephrotoxicity for aminoglycosides in horses?

A

Accumulation in proximal tubular cells caused by sustained drug exposure (frequent dosing), not individual high doses.

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64
Q

What are the risk factors for aminoglycoside nephrotoxicity in humans?

A

Risk factors include age, hypovolemia, preexisting renal dysfunction, and combination with furosemide. Gentamicin is more nephrotoxic than amikacin.

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65
Q

What is the evidence of nephrotoxicity for aminoglycosides in horses?

A

Reported nephrotoxicity; dosing schedules should be altered in neonates.

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66
Q

What is the panel recommendation for the use of aminoglycosides in at-risk patients?

A

Use aminoglycosides cautiously in at-risk patients.

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67
Q

What is the mechanism of nephrotoxicity for oxytetracycline in horses?

A

The mechanism of nephrotoxicity for oxytetracycline is unknown.

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68
Q

How common is nephrotoxicity from oxytetracycline in humans?

A

Nephrotoxicity from oxytetracycline is rare in humans.

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69
Q

What is the evidence of nephrotoxicity for oxytetracycline in horses?

A

AKI caused by high doses for flexural limb deformities in foals and normal antimicrobial doses in adults.

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70
Q

What is the panel recommendation for the use of oxytetracycline in at-risk patients?

A

Evaluate serum creatinine (sCr) before administration of high doses to foals.

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71
Q

What is the mechanism of nephrotoxicity for NSAIDs in horses?

A

Inhibition of COX blocks renal autoregulatory response to hypoperfusion, causing medullary crest necrosis and interstitial nephritis.

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72
Q

How common is nephrotoxicity from NSAIDs in humans?

A

Nephrotoxicity from NSAIDs is uncommon in humans.

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73
Q

What is the evidence of nephrotoxicity for NSAIDs in horses?

A

In healthy horses, phenylbutazone induced medullary crest necrosis with prolonged supraphysiological doses and AKI with normal doses. COX-2 selective drugs carry a similar but lower risk for nephrotoxicity.

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74
Q

What is the panel recommendation for the use of NSAIDs in at-risk horses?

A

NSAIDs, especially phenylbutazone, should be avoided in at-risk horses.

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75
Q

Which aminoglycoside is more nephrotoxic, gentamicin or amikacin?

A

Gentamicin is more nephrotoxic than amikacin.

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76
Q

What conditions in foals have been linked to AKI due to high doses of oxytetracycline?

A

Flexural limb deformities in foals have been linked to AKI due to high doses of oxytetracycline.

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77
Q

Which NSAID is specifically mentioned as inducing medullary crest necrosis in healthy horses?

A

Phenylbutazone is specifically mentioned as inducing medullary crest necrosis in healthy horses with prolonged supraphysiological doses.

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78
Q

What is Chronic Kidney Disease (CKD)?

A

An irreversible, progressive disease of the kidneys with a duration of more than 3 months, involving a gradual loss of kidney function over time.

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79
Q

What are the stages of CKD based on serum creatinine concentration?

A

Stage 1: <180 μmol/L (2.0 mg/dL), mild or absent clinical signs.

Stage 2: 180-250 μmol/L (2.0-3.0 mg/dL), mild clinical signs.

Stage 3: 251-450 μmol/L (3.1-5.0 mg/dL), moderate clinical signs.

Stage 4: >450 μmol/L (>6.0 mg/dL), severe clinical signs.

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80
Q

What are the congenital anomalies of development that can cause CKD?

A

Renal agenesis, hypoplasia, dysplasia, and polycystic kidney disease.

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81
Q

What is Chronic Interstitial Nephritis (CIN) and its causes?

A

A condition usually resulting from acute tubular necrosis due to ischemia or nephrotoxicity, adverse drug reactions, or progressing from AKI.

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82
Q

What is Pyelonephritis and how does it relate to CKD?

A

An ascending urinary tract infection causing inflammation of the kidney’s interstitial tissue, often a consequence of CKD.

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83
Q

What causes Nephrolithiasis and how is it related to CKD?

A

: Kidney stones, usually composed of calcium carbonate, found in the collecting ducts, often as a consequence rather than a cause of CKD.

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84
Q

What is Glomerulonephritis (GN) and what causes it?

A

A condition initiated by immune-mediated inflammation due to the deposition of immune complexes along the glomerular barrier, often associated with chronic infectious diseases.

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85
Q

What are the infiltrative causes of CKD?

A

Neoplasia (lymphoma, carcinoma, nephroblastoma), amyloidosis, and Halicephalobus gingivalis infection.

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86
Q

What is End-Stage Kidney Disease (ESKD)?

A

The final stage of CKD where kidneys are pale, shrunken, firm, with an irregular surface and adherent capsule, often with an indeterminate inciting cause.

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87
Q

What are the common clinical signs of CKD in horses?

A

Loss of body condition, polyuria/polydipsia (PU/PD), dental tartar accumulation, gingivitis/oral ulcers, decreased performance, hypertension, and ventral edema.

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88
Q

What laboratory findings are typically associated with CKD?

A

Moderate to severe azotemia, mild electrolyte imbalances, hypercalcemia (diet-dependent), hypophosphatemia, mild anemia, proteinuria, and isosthenuria.

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89
Q

What imaging techniques are useful in diagnosing CKD?

A

Rectal palpation and ultrasonography to evaluate kidney size, structure, presence of nephroliths, and cystic cavitation.

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90
Q

What are the main goals of dietary management in CKD?

A

Maintaining appetite and body condition, increasing carbohydrate and fat intake, monitoring BUN and serum protein levels, avoiding additional salt, and switching to low-calcium feeds for hypercalcemia.

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91
Q

What medications may benefit patients with CKD?

A

Corticosteroids for GN, ACE inhibitors (benazepril, ramipril) to control blood pressure and proteinuria, and nephrolith removal in specific cases.

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92
Q

What are the general management strategies for CKD?

A

IV fluid therapy (IVFT) as needed, free access to fresh water, appropriate dietary management, and careful use of medications.

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93
Q

How is CKD progression managed in horses?

A

Through long-term management including dietary adjustments, medication, regular monitoring, and individualized care to maintain quality of life until humane euthanasia becomes necessary.

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94
Q

What is pyelonephritis and how can it occur in horses?

A

Pyelonephritis is an uncommon condition characterized by bacterial infection of the renal pelvis and parenchyma, occurring via hematogenous spread or as an ascending infection from the lower urinary tract. Unilateral cases are more common than bilateral.

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95
Q

What mechanical obstructions or functional impairments can predispose horses to pyelonephritis?

A

Urolithiasis, recurrent cystitis, bladder paralysis, ectopic ureter, lower urinary tract neoplasia, urinary surgery, and foaling injury.

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96
Q

: What are the common bacterial isolates that cause pyelonephritis in horses?

A

Escherichia coli, Proteus spp., Klebsiella spp., Enterobacter spp., Streptococcus spp., Staphylococcus spp., Pseudomonas aeruginosa, Corynebacterium spp.

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97
Q

What are the general clinical symptoms of pyelonephritis in horses?

A

Fever, inappetence, lethargy, and weight loss.

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98
Q

What severe clinical signs can be observed in horses with pyelonephritis?

A

Renal hemorrhage, sepsis, renal failure, and death.

99
Q

Q: What inflammatory markers are commonly seen in horses with pyelonephritis?

A

A: Increased levels of inflammatory markers.

100
Q

How does serum creatinine (sCr) typically present in horses with unilateral pyelonephritis?

A

Serum creatinine (sCr) can be elevated or within normal range if the disease is unilateral.

101
Q

What might ultrasonography reveal in a horse with pyelonephritis?

A

A dilated renal pelvis, distortion of renal parenchyma, and presence of nephroliths.

102
Q

How is cystoscopy used in the diagnosis of pyelonephritis?

A

Cystoscopy assesses the appearance of urine from each ureter and allows collection of urine samples from each kidney.

103
Q

What does urinalysis typically include for diagnosing pyelonephritis?

A

Bacteriology and cytology to confirm infection and determine if the disease is unilateral or bilateral.

104
Q

What is the empirical antimicrobial therapy of choice for pyelonephritis in horses?

A

Trimethoprim-sulphonamides.

105
Q

How should ongoing treatment for pyelonephritis be guided?

A

Based on culture and susceptibility results, with long-term antimicrobial treatment until negative culture results and resolution of clinical signs and blood work abnormalities.

106
Q

What is the recommended follow-up after treating pyelonephritis?

A

Repeat urine culture 2 weeks after discontinuation of treatment to ensure infection clearance.

107
Q

When is surgical intervention indicated in pyelonephritis cases?

A

Nephrectomy is indicated if treatment of unilateral, non-azotemic pyelonephritis is unsuccessful

108
Q

What factors influence the prognosis of pyelonephritis in horses?

A

The underlying cause, concurrent nephrolithiasis, and the extent of renal damage

109
Q

What is renal haematuria?

A

Renal haematuria is the presence of blood in the urine originating from the kidneys, due to various underlying conditions affecting the upper urinary tract.

110
Q

What can cause lithiasis-related renal haematuria?

A

Mechanical irritation and damage to the renal tissues caused by kidney stones.

111
Q

How can NSAIDs lead to renal haematuria?

A

NSAIDs can cause renal papillary necrosis, leading to haematuria.

112
Q

What characterizes Idiopathic Renal Haematuria (IRH)?

A

IRH is characterized by the sudden onset of gross haematuria with no identifiable cause, and a breed predisposition in Arabian and part-Arabian horses.

113
Q

How can intense physical activity lead to renal haematuria?

A

Intense physical activity can occasionally cause exercise-induced haematuria, although this is less common.

114
Q

What are the clinical presentations of gross haematuria?

A

The presence of visible blood in the urine.

115
Q

What systemic signs may be absent in idiopathic renal haematuria?

A

Signs of anaemia or hypovolemia may be absent in idiopathic renal haematuria cases.

116
Q

Why is a coagulation profile important in diagnosing renal haematuria?

A

To assess for coagulopathies that might contribute to bleeding.

117
Q

: How is cystoscopy used in the diagnosis of renal haematuria?

A

Cystoscopy involves visual examination of the bladder and ureters to determine the origin of the bleeding (unilateral or bilateral) and confirm that the source is from the upper urinary tract.

118
Q

What abnormalities can ultrasound detect in cases of renal haematuria?

A

Ultrasound can evaluate kidney size, structure, presence of stones, and other abnormalities.

119
Q

When might a biopsy be indicated in renal haematuria cases?

A

A biopsy may be indicated to rule out neoplasia or other specific conditions, though it is rarely performed.

120
Q

What laboratory tests are useful in diagnosing renal haematuria?

A

Urinalysis to assess the presence of red blood cells, protein, and other abnormalities; blood tests to check for signs of anaemia, renal function (creatinine, BUN), and electrolyte imbalances.

121
Q

What supportive care is essential for treating renal haematuria?

A

Fluid therapy to maintain hydration and renal perfusion, and blood transfusion in severe cases with marked anaemia.

122
Q

How is lithiasis managed to treat renal haematuria?

A

Through surgical or medical management of kidney stones.

123
Q

What is the treatment approach for pyelonephritis causing renal haematuria?

A

Long-term antimicrobial therapy guided by culture and sensitivity results.

124
Q

What specific treatments are available for Idiopathic Renal Haematuria (IRH)?

A

Acute management with supportive care for acute blood loss, and nephrectomy in severe cases with unilateral origin of bleeding.

125
Q

How is exercise-induced haematuria managed?

A

By restricting or modifying physical activity in affected horses.

126
Q

What factors influence the prognosis of renal haematuria?

A

The underlying cause and the severity of the condition.

127
Q

How does idiopathic renal haematuria typically resolve, and what is its prognosis?

A

IRH can resolve spontaneously but may recur, with episodes lasting months to years.

128
Q

What determines the prognosis of neoplastic causes of renal haematuria?

A

The type and stage of the tumor and the response to treatment.

129
Q

What is the prognosis for renal stones and infections causing haematuria?

A

Generally favourable if appropriately managed, but chronic cases can lead to long-term kidney damage.

130
Q

What is Renal Tubular Acidosis (RTA)?

A

A rare disorder characterized by the kidneys’ inability to properly acidify the urine, leading to metabolic acidosis despite normal glomerular filtration rate (GFR).

131
Q

What is the mechanism and result of Type I (Distal) RTA?

A

Impaired hydrogen ion (H⁺) secretion by the distal tubules, resulting in the inability to acidify the urine and causing systemic acidosis.

132
Q

What is the mechanism and result of Type II (Proximal) RTA?

A

: Impaired reabsorption of bicarbonate (HCO₃⁻) by the proximal tubules, resulting in loss of bicarbonate in the urine and causing systemic acidosis.

133
Q

What is the mechanism and result of Type IV (Hyperkalemic) RTA?

A

Impaired excretion of potassium (K⁺), often due to aldosterone deficiency or resistance, leading to a combination of type I and type II RTA features.

134
Q

What is Fanconi Syndrome and its mechanism?

A

: A subtype of proximal RTA with widespread proximal tubular dysfunction causing urinary loss of glucose, phosphate, uric acid, amino acids, and proteins.

135
Q

What are the primary disorders that can cause RTA?

A

: Idiopathic RTA, often congenital.

136
Q

What conditions can secondary RTA be associated with?

A

Chronic kidney disease (CKD), systemic diseases, and drug administration (e.g., certain antibiotics or chemotherapeutic agents).

137
Q

What general symptoms are associated with RTA?

A

Anorexia (reduced appetite), lethargy (generalized weakness and fatigue), and weight loss, particularly with chronic RTA.

138
Q

What are the acute symptoms of severe metabolic acidosis in RTA?

A

ow blood pH causing rapid breathing, confusion, and potential shock.

139
Q

What chronic symptoms might young animals with RTA exhibit?

A

: Growth retardation and bone pain due to demineralization.

140
Q

What serum chemistry findings are indicative of RTA?

A

Metabolic acidosis with hyperchloremia and a normal anion gap,

low blood pH and bicarbonate levels, low potassium levels, possible azotemia, and increased serum PTH and 1-25 OHD3 concentrations in some cases.

141
Q

What does urinalysis typically reveal in cases of RTA?

A

Alkalotic urine (high urine pH of 7.5-9) despite systemic acidosis, glycosuria, aminoaciduria, and phosphaturia indicative of Fanconi syndrome.

142
Q

What blood tests might be elevated in RTA cases?

A

Elevated serum parathyroid hormone and 25-hydroxyvitamin D levels in some cases.

143
Q

Are bicarbonate or ammonium chloride challenge tests commonly used in horses with RTA?

A

: No, they are rarely used as treatment is the same regardless of type

144
Q

How is metabolic acidosis corrected in RTA?

A

: With intravenous sodium bicarbonate to quickly correct severe acidosis, and oral sodium bicarbonate for long-term management, with dose adjustments based on severity and response.

145
Q

How is hypokalemia corrected in R

A

With potassium chloride supplementation (IV or oral depending on severity) and regular monitoring of potassium levels, especially during sodium bicarbonate therapy

146
Q

What supportive care measures are important for RTA?

A

Ensuring adequate fluid intake to prevent dehydration, dietary management with high-quality diet to support overall health and kidney function.

147
Q

What does long-term management of RTA involve?

A

Treatment duration can be unpredictable, with some horses requiring lifelong management, and monitoring for recurrence, particularly if there is ongoing renal disease.

148
Q

What is the prognosis for horses with a favorable clinical response to RTA treatment?

A

A: Most horses show improvement within 24 to 72 hours of starting treatment.

149
Q

What is the prognosis for chronic RTA cases?

A

They may require ongoing treatment for months or longer, with possible recurrence, especially with underlying renal disease.

150
Q

What is the long-term outlook for horses with RTA?

A

With proper management, many horses can maintain good health and quality of life; regular monitoring and adjustments in treatment are essential to manage the condition effectively.

151
Q

What is Polyuria (PU) and Polydipsia (PD)?

A

Polyuria (PU) is characterized by excessive production of urine, and Polydipsia (PD) is characterized by excessive intake of water (>100 ml/kg/day).

152
Q

What is the difference between physiological and pathological PU/PD?

A

Physiological PU/PD is temporary and influenced by external factors like hot weather and exercise, while pathological PU/PD is persistent and indicates underlying health conditions requiring investigation.

153
Q

How can alpha2-agonists cause PU/PD?

A

Drugs like xylazine and detomidine can induce transient diuresis by affecting the kidneys and systemic circulation.

154
Q

How do corticosteroids cause PU/PD?

A

: Corticosteroids can cause PU/PD by affecting the kidney’s ability to concentrate urine and altering electrolyte balance.

155
Q

How does glucose administration lead to PU/PD?

A

: High levels of glucose (e.g., from IV dextrose solutions) can cause osmotic diuresis, where excess glucose in the urine draws water along with it, increasing urine output.

156
Q

What role do diuretics play in causing PU/PD?

A

Diuretics are medications designed to increase urine output to manage conditions like edema or hypertension

157
Q

How can excessive intravenous fluid therapy (IVFT) cause PU/PD?

A

Excessive administration of IV fluids can lead to increased urine output as the body works to excrete the excess fluid.

158
Q

Q: What is psychogenic polydipsia and how is it diagnosed?

A

A: Psychogenic polydipsia is a behavioral condition where horses drink excessive amounts of water due to boredom, anxiety, or stress. It is diagnosed primarily by excluding other causes and monitoring water intake.

159
Q

What are the symptoms and diagnostic methods for PU/PD caused by chronic kidney disease (CKD)?

A

Symptoms include weight loss, decreased appetite, lethargy, polyuria, and polydipsia. Diagnosis is based on clinical signs, blood tests (elevated serum creatinine, BUN), and imaging (ultrasound).

160
Q

: What is the difference between neurogenic and nephrogenic diabetes insipidus (DI)?

A

: Neurogenic DI is caused by a deficiency in vasopressin (ADH) production or release, while nephrogenic DI is caused by the kidneys’ insensitivity to vasopressin.

161
Q

: What are the symptoms and diagnostic methods for diabetes insipidus (DI)?

A

Symptoms include marked polyuria and polydipsia, with dilute urine despite dehydration. Diagnosis involves a water deprivation test and response to desmopressin administration.

162
Q

How does diabetes mellitus (DM) cause PU/PD and what are the diagnostic methods?

A

Chronic hyperglycemia leads to glucosuria, causing osmotic diuresis and subsequent PU/PD. Diagnosis involves elevated blood glucose levels and the presence of glucose in the urine.

163
Q

What are the clinical signs and diagnostic methods for PU/PD caused by Pituitary Pars Intermedia Dysfunction (PPID)?

A

Clinical signs include long, curly coat, muscle wasting, laminitis, polyuria, and polydipsia. Diagnosis is based on clinical signs and endocrine testing (ACTH levels, dexamethasone suppression test).

164
Q

How do sepsis and endotoxemia cause PU/PD and what are the diagnostic methods?

A

Severe infections cause systemic inflammation, impairing kidney function and water balance, leading to PU/PD. Diagnosis involves blood cultures, inflammatory markers, and clinical presentation.

165
Q

: How does hepatic insufficiency contribute to PU/PD?

A

Liver disease can disrupt fluid and electrolyte balance, contributing to PU/PD. Diagnosis involves liver function tests, imaging, and liver biopsy.

166
Q

: What is medullary washout and what causes it?

A

Medullary washout is a condition resulting from prolonged polyuria, leading to an inability of the kidneys to concentrate urine effectively. It can occur secondary to psychogenic PU.

167
Q

What should be included in the initial assessment of a horse with PU/PD?

A

History and physical examination, medication use, recent changes in environment or behaviors, physical examination for signs of systemic disease, and blood tests to measure serum electrolytes, creatinine, BUN, glucose, and liver enzymes.

168
Q

What urine analysis tests are useful in diagnosing PU/PD?

A

: Urine specific gravity (USG) to assess the kidneys’ concentrating ability and urinalysis to evaluate for the presence of glucose, protein, ketones, and signs of infection.

169
Q

What is the purpose and procedure of the water deprivation test in diagnosing PU/PD?

A

To differentiate between causes of PU/PD, particularly psychogenic polydipsia and diabetes insipidus. The procedure involves gradual water restriction under controlled conditions, monitoring weight, hydration status, and urine output.

170
Q

How is psychogenic polydipsia managed?

A

By gradually limiting water intake to prevent rapid dehydration, providing environmental enrichment to reduce boredom, and addressing underlying anxiety or stress.

171
Q

What supportive care is important in managing chronic kidney disease causing PU/PD?

A

Dietary adjustments, ensuring adequate hydration, and providing appropriate medications as needed (e.g., phosphorus binders, antihypertensive drugs).

172
Q

How is neurogenic diabetes insipidus (DI) treated?

A

With hormone replacement therapy using desmopressin acetate.

173
Q

How is diabetes mellitus (DM) managed in horses with PU/PD?

A

By controlling blood glucose levels through diet, exercise, and potentially insulin therapy, with regular monitoring of blood glucose and urine ketones.

174
Q

What medications are used to treat Pituitary Pars Intermedia Dysfunction (PPID)?

A

Medications such as pergolide to manage hormone levels, along with supportive care including dietary management and regular monitoring of ACTH levels.

175
Q

How are sepsis and endotoxemia causing PU/PD treated?

A

Through aggressive management of the underlying infection with antibiotics, supportive care to maintain hydration and electrolyte balance, and anti-inflammatory medications to control systemic inflammation.

176
Q

What is the prognosis for psychogenic polydipsia?

A

Generally good with appropriate behavioral management and environmental enrichment.

177
Q

What is the prognosis for chronic kidney disease and PPID causing PU/PD?

A

These are managed but progressive conditions requiring ongoing care and monitoring.

178
Q

What is the prognosis for diabetes insipidus and mellitus causing PU/PD?

A

They require lifelong management, with the prognosis depending on response to treatment and management of complications.

179
Q

How does renal blood flow (RBF) in neonatal foals compare to adult horses?

A

Neonatal kidneys receive less RBF than adult kidneys but constitute a larger percentage of body mass.

180
Q

What is the glomerular filtration rate (GFR) like in neonatal foals?

A

Similar to adult horses.

181
Q

How do blood urea nitrogen (BUN) and serum creatinine (sCr) levels change in neonatal foals after birth?

A

These levels are often above adult reference ranges at birth but normalize within 24 to 72 hours.

182
Q

Why do neonatal foals have low BUN and sCr values?

A

Due to high fluid intake from milk.

183
Q

When is urination expected in neonatal foals?

A

Within 12 hours of birth.

184
Q

How does urine specific gravity (USG) change in neonatal foals?

A

It is initially variable but rapidly becomes hyposthenuric (<1.008).

185
Q

What is the typical urine pH in neonatal foals?

A

Typically neutral.

186
Q

Why can proteinuria occur in neonatal foals?

A

: Due to the passive transfer of colostral antibodies within the first 24 to 72 hours.

187
Q

What are the pathophysiological causes of AKI in foals?

A

Isolated organ dysfunction, secondary to sepsis, periparturient hypoxia, nephrotoxicity, or a combination of these factors.

188
Q

What clinical signs indicate AKI in foals?

A

Lethargy, fluid retention resulting in subcutaneous edema, and oliguria/anuria.

189
Q

How common and severe are electrolyte derangements in foals with AKI compared to adults?

A

More common and often more severe; severe hyponatremia can lead to encephalopathy.

190
Q

How is urine output measured in foals with AKI, and what are the risks?

A

Feasible via a closed urinary collection system; catheterization can lead to ascending infection.

191
Q

What is the primary focus of treating AKI in foals?

A

: Maintaining effective circulatory volume and RBF, avoiding fluid overload while correcting acid-base and serum electrolyte abnormalities, and allowing renal tissue time to repair.

192
Q

Why is dialysis more feasible in neonates with AKI than in adult horses?

A

Cost and size

193
Q

What long-term risk do foals affected by AKI face?

A

Developing chronic kidney disease (CKD) later in life.

194
Q

What congenital abnormalities can cause oliguria and azotemia in neonates?

A

Conditions like renal agenesis or hypoplasia.

195
Q

How does uroperitoneum cause oliguria and azotemia in neonates?

A

By rupture of the bladder causing urine to leak into the abdominal cavity.

196
Q

What is spurious hypercreatininemia and its proposed new name?

A

condition reflecting placental insufficiency or maternal renal failure, leading to in-utero fetal accumulation of nitrogenous products; proposed name is “Materno-placental induced neonatal azotemia.”

197
Q

How is transabdominal ultrasonography used in diagnosing oliguria and azotemia in neonates?

A

To assess renal presence, size, structure, bladder size, and the volume of free abdominal fluid.

198
Q

What serum biochemistry and urinalysis findings are indicative of oliguria and azotemia in neonates?

A

Measuring BUN and sCr levels, identifying proteinuria, glucosuria, and other abnormalities.

199
Q

What is the prognosis for azotemia in sick foals?

A

Associated with lower survival rates, but many azotemic foals can be managed successfully with appropriate intervention.

200
Q

What is the recommended biochemical test to estimate glomerular filtration rate (GFR) in horses?

A

Serum Creatinine (sCr).

201
Q

How should serum creatinine (sCr) results be interpreted?

A

Based on laboratory reference ranges, body condition, age, breed, and sex of the horse.

202
Q

Why is blood urea nitrogen (BUN) considered unreliable for diagnosing acute kidney injury (AKI)?

A

Due to multifactorial influences, including dietary protein and protein metabolism.

203
Q

What does stall-side urinalysis in horses involve?

A

Reagent test strips and refractometer analysis for urine specific gravity (USG), and biochemical testing for protein, creatinine, gamma-glutamyl transferase, and microscopic sediment evaluation.

204
Q

How is Fractional Excretion (FE) used in diagnosing kidney function?

A

A: By assessing tubular reabsorption of electrolytes using the formula:

205
Q

What is Serum Symmetric Dimethylarginine (SDMA)?

A

: A functional biomarker highly correlated with sCr, but its superiority over sCr in supporting changes in GFR in horses is not documented.

206
Q

What is the advantage of SDMA over sCr in assessing GFR?

A

SDMA is not affected by muscle mass, potentially making it more accurate for assessing GFR in heavily muscled horses.

207
Q

What are other novel biomarkers for glomerular and tubular injury?

A

What are other novel biomarkers for glomerular and tubular injury?

208
Q

How is ultrasonography used in evaluating kidney function in horses?

A

To evaluate kidney size, structure, presence of nephroliths or cystic cavitation, and changes in echogenicity in cases of AKI and CKD/ESKD.

209
Q

What is nuclear scintigraphy, and how is it used in kidney evaluation?

A

A diagnostic imaging method using radiopharmaceuticals labeled with 99-metastable technetium (99mTc) to assess GFR and individual kidney function.

210
Q

How does computed tomography (CT) contribute to kidney evaluation in horses?

A

Provides excellent anatomical detail but is limited due to patient size and the requirement for general anesthesia.

211
Q

What is the purpose of endoscopy in diagnosing kidney issues in horses?

A

To view ureteral openings and determine the origin of hematuria or pyuria, and to permit urine sampling from each kidney through ureteral catheterization.

212
Q

What are the risks associated with renal biopsy in horses?

A

Low reported mortality (0.6%) but complications in 11.3% of cases, including colic signs (perirenal hemorrhage) and hematuria, with severe hemorrhage occasionally observed.

213
Q

When is a renal biopsy indicated in horses?

A

: Not routinely recommended for AKI or CKD evaluation unless it can change patient management or prognosis; more useful in human medicine for diagnosing glomerular diseases.

214
Q

What is the normal reference value for Urine Specific Gravity (USG) in adult horses?

A

: 1.025-1.040.

215
Q

What is indicated by hyposthenuria (USG <1.008) in horses?

A

Water excretion.

216
Q

What is isosthenuria and what does it indicate?

A

USG between 1.008-1.014, indicating no excretion or concentration of urine, and the inability to concentrate urine.

217
Q

What condition is indicated by aciduria (pH <7) in horses?

A

Potassium deficiency and increased excretion of hydrogen ions in distal tubules, often due to systemic or local acid production.

218
Q

What does proteinuria indicate about kidney function?

A

Damage to the glomerular filtration membrane and reduced reabsorption in tubules, leading to protein excretion.

219
Q

What does glucosuria indicate about kidney function?

A

Hyperglycemia and tubular damage.

220
Q

What does an elevated GGT to urinary creatinine ratio indicate?

A

Leakage from proximal tubular brush border cells, suggesting tubular damage.

221
Q

What does the presence of RBCs in urine indicate?

A

Hematuria and bleeding from the urinary tract.

222
Q

What does the presence of WBCs in urine indicate?

A

Pyuria and infection or inflammation in the urinary tract.

223
Q

: What are the types of casts found in urine and what do they indicate?

A

Hyaline, myoglobin, WBC, RBC, and tubular epithelial cells; they indicate various kidney conditions such as glomerulonephritis or acute tubular necrosis.

224
Q

What does crystalluria indicate in horses?

A

The presence of crystals in urine, which is generally normal unless associated with other abnormalities.

225
Q

What is the significance of serum symmetric dimethylarginine (SDMA) in diagnosing kidney function?

A

It is a functional biomarker highly correlated with sCr, used for early detection of CKD, and is higher in azotemic than non-azotemic horses.

226
Q

What does an increase in Neutrophil Gelatinase-Associated Lipocalin (NGAL) indicate?

A

Early detection of AKI and potential to detect AKI earlier than sCr.

227
Q

Q: How is Cystatin C used in kidney diagnostics?

A

As a promising diagnostic tool for glomerular diseases, higher in horses with AKI than in healthy horses.

228
Q

What does an increase in N-acetyl-β-D-glucosaminidase (NAG) indicate?

A

Tubular damage, with higher levels in azotemic horses.

229
Q

Q: What is the role of podocin in kidney diagnostics?

A

Used in assessing kidney injury, with early detection in some nephropathies.

230
Q

Are novel biomarkers currently available for commercial or clinical use in horses?

A

no, most novel biomarkers are not commercially available for use in horses.

231
Q

What are the primary goals of IVFT in AKI patients?

A

To establish and maintain euhydration, circulatory volume, and renal blood flow (RBF), replace ongoing fluid loss, and promote diuresis.

232
Q

Under what conditions might IVFT not be necessary in CKD patients?

A

the patient drinks adequately and azotaemia is stable with established diuresis (polyuria).

233
Q

Why is 0.9% saline commonly used IN HUMANS, and what is a concern associated with it?

A

It is commonly used because it does not contain potassium, but excessive chloride from 0.9% saline can worsen glomerular filtration rate (GFR).

234
Q

What are typical maintenance rates for IVFT, and what is a potential complication of overzealous IVFT?

A

Typically 2-3 mL/kg/h, which induces increased output of dilute urine. Overzealous IVFT can lead to renal interstitial edema, worsening RBF and GFR, and cause edema formation due to a large sodium load.

235
Q

Why is avoiding fluid overload as important as providing adequate fluid support?

A

: Fluid overload can lead to complications such as renal interstitial edema.

236
Q

: Why might dosage or interval adjustments be needed in horses with AKI or CKD?

A

Impaired renal function can lead to toxic serum and tissue concentrations of drugs eliminated or metabolized by the kidneys.

237
Q

How should concentration-dependent antibiotics (aminoglycosides) be adjusted in AKI or CKD patients?

A

Prolong the interval between doses proportional to the estimated decrease in GFR.

238
Q

What is the general recommendation regarding loading doses in AKI or CKD patients?

A

A reduction in loading dose is generally not recommended.

239
Q

How can therapeutic drug monitoring help in managing drug adjustments?

A

It can help ensure plasma drug concentrations are within safe limits.

240
Q

What are the recommendations for using nephrotoxic drugs in horses with renal impairment?

A

Avoid using potentially nephrotoxic drugs if possible, select drugs with similar therapeutic effects but lower nephrotoxicity, and if necessary, do not exceed recommended dosages, use the lowest effective dose, shorten the duration of use, avoid use during hypovolemia or dehydration, and avoid simultaneous use of multiple nephrotoxic drugs.

241
Q

What recent findings about NSAID use in CKD patients should be considered?

A

NSAIDs may not worsen CKD progression and could be appropriate for treating concurrent osteoarthritis. Cyclooxygenase-2 selective NSAIDs are preferred to improve the quality of life in CKD patients.

242
Q

What is the future potential for renal replacement treatment in horses with unresponsive oliguric/anuric ARF?

A

This treatment is expected to be more widely used in the future.

243
Q

Are there any proven medical treatments to prevent the progression of renal fibrosis in CKD?

A

No, but several medications are under experimental investigation.

244
Q

What are potential future treatments for CKD in horses that are currently under evaluation?

A

Sodium glucose cotransporter 2 inhibitors, which slow the decline in GFR and decrease proteinuria in humans, and renal transplants, both natural and artificial.

ECEIM consensus statements (11 decks)

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