Lecture 20 - Renal Part 2 Flashcards
Polyuria occurs before ________
* Polyuria ~____% nephron loss
* Azotemia ~____% nephron loss
- Polyuria occurs before azotemia
- Polyuria ~66% nephron loss
- Azotemia ~75% nephron loss
How do you determine azotemia?
USG
What is the USG of a prerenal azotemia?
concentrated USG
What is the USG of a renal azotemia?
isostheniuria
What is the USG of postrenal azotemia?
variable USG
The number one cause of pre-renal azotemia is?
Dehydration
What PE findings will you see in a patient with pre-renal azotemia?
PE findings: tacky mucus membranes, skin tent, etc
What bloodwork findings, in regards to PCV, TP, and Alb, will you see in a patient with pre-renal azotemia?
Bloodwork: ↑PCV, ↑TP, ↑Alb
What conditions can cause a patient with Pre-renal azotemia to bleeed?
1. GI _______ (______, _____ therapy)
2. Bleeding _______ GI tumor
3. Coagulopathy (↓____, ___, _______, _____ failure)
What conditions can cause a patient with Pre-renal azotemia to bleeed?
1. GI ulceration (prednisone, NSAID therapy)
2. Bleeding upper GI tumor
3. Coagulopathy (↓PLTs, DIC, warfarin, liver failure)
Azotemia + Isosthenuria = ?
Renal Disease (until proven otherwise)
You are able to determine if your patient is suffering from Renal azotemia vs. other diseases
* ________ ________ is your clue
* Concentrating/diluting ability of the kidney implies functional ________
* If urine is not _______ or not appropriate for the patient’s
________ status, the cause of azotemia is probably ______
Cats can maintain some ________ capacity with renal failure
You are able to determine if your patient is suffering from Renal azotemia vs. other diseases
* Specific gravity is your clue
* Concentrating/diluting ability of the kidney implies functional nephrons
* If urine is not concentrated or not appropriate for the patient’s
hydration status the cause of azotemia is probably renal
Cats can maintain some concentrating capacity with renal failure
If you suspect your patient has Post-renal azotemia, look to your signalment and PE findings:
* _________ males (more frequent to be dx with this)
* ________ to urinate (associated with some type of flow _______ so urine is not coming out)
* ______, ______ bladder
* ________ abdomen (___-abdomen)
If you suspect your patient has Post-renal azotemia, look to your signalment and PE findings:
* Castrated males (more frequent to be dx with this)
* Straining to urinate (associated with some type of flow bloackge so urine is not coming out)
* Large turgid bladder
* Distended abdomen (uroabdomen)
If a patient is isosthenuric, but NOT azotemic, you must
Further assessment is required:
* History, Signalment, PE findings
* What is the hydration status? Appropriate?
* Is anything interfering with kidney’s concentrating ability? (calcium,
cortisol, etc)
Uroabdomen: presence of urine in the ________ cavity.
- Uroabdomen is a medical emergency, not a ______ emergency. Acute management involves stabilization of the patient with IV ______ therapy and treatment of _________.
Uroabdomen: presence of urine in the abdominal cavity. Uroabdomen is a medical emergency, not a surgical emergency. Acute management involves stabilization of the
patient with IV fluid therapy and treatment of hyperkalemia.
See
Correlate azotemia with USG, PCV, albumin, and hydration status to determine if
azotemia is prerenal, renal, or a combination. Azotemia with concentrated urine is
indicative of a prerenal azotemia. Urine is considered concentrated when the USG is
>1.030 for a dog and >1.040 for a cat. As the USG increases, confidence in the
kidney’s ability to concentrate urine increases. Postrenal azotemia is due to
obstruction of outflow (calculi) or rupture of the urinary bladder and is not part of
this algorithm. Azotemia with urine that is not adequately concentrated (≤1.030 for a
dog, ≤1.040 for a cat) suggests renal disease. It should be noted that azotemia is
often exacerbated in clinically dehydrated patients, leading to a prerenal azotemia
superimposed on a renal azotemia. Sometimes this is referred to as acute on chronic
renal disease. In these cases, kidney disease is the primary differential. Once
azotemia is identified to be caused by kidney disease, a patient’s history, body
condition, urine volume, PCV, and albumin are used to determine chronicity (acute
injury vs. chronic disease). The lesion is then localized within the kidney (glomeruli,
tubules, interstitium, pelvis) using the urinalysis and serum chemistry. There are
other differentials for a patient with azotemia and unconcentrated urine. Differentials
include decreased ADH (diabetes insipidus), substances that interfere with renal ADH
receptors (hypercalcemia, glucocorticoids, bacterial endotoxin, etc.), medullary
washout (hyponatremia secondary to hypoadrenocorticism, decreased UN in liver
8
insufficiency, prolonged IV fluids therapy), or osmotic diuresis due to substances
excreted in the urine with strong osmotic pull (glucose, ketones, mannitol, etc.). In
these cases, the classical presentation is a mild azotemia with a USG <1.013. If there
is no concurrent renal disease the azotemia is prerenal in origin, as patients are
unable to keep up with water losses. Each of these differentials may also present with
USG <1.013 and no azotemia (they are not dehydrated).
When looking at Biochemical profile in Renal disease, want to look at other markers in addition to BUN and CK
Our patient has a renal azotemia, what should
we look for?
- The first tier of evaluating a renal patient:
* BUN, Creatinine (CREA), USG - Once renal azotemia is confirmed, there are some key analytes to
check out (i.e. “second tier”)
a. Phosphorus (Phos)
b. Calcium (Ca)
c. Potassium (K)
d. Sodium (Na) and Chloride (Cl)
e. Bicarbonate (HCO3) and the Anion Gap (AG)
- How are phosphate levels affected in a case of renal azotemia?
- Mechanism: when GFR drops below ____% of normal, phosphorus _____ is impaired –> Phosphorous ________
- What happens as phosphorous levels change?
- Kidneys excrete _____% of phosphorous load while GI excretes the other ___%. Not significantly bound to _______, so filtered at _______.
- Which hormones control phosphorous homeostasis?
- What happens in cases of renal azotemia in horses and cows?
- Hyperphosphatemia (↑PHOS)
- Mechanism: when GFR drops below 25% of normal, phosphorus excretion is impaired –> Phosphorous accumulation
- As phosphorus increases, there is a risk for mineralization of soft tissues: Ca x Phos > 70
- Kidneys excrete 90% of phosphorous load while GI excretes the other 10%. Not significantly bound to albumin, so filtered at glomerulus.
- Phosphorous homeostasis under direct hormone control of calictrol, PTH, others. Ca + phosphorous product is > 70 –> possibility of soft tissue mineralization. More than 100% –> tissue mineralization is really happening at that time.
* Species variation: - Horses and cattle may or may not have hyperphosphatemia
* Horses lose phosphorus from the gut
* Cattle secrete phosphorus in the saliva
Why do we look at calcium?
b. Calcium
* Ranges from ______- to ______- to ______-calemia
* Depends on:
* _______
* the ________ cause
* the ________ of renal failure
* Must measure an ________ calcium (iCa2+)
* In 10-20% of dogs the total calcium will be _________, but the ionized
calcium will be ______ or ________
b. Calcium
* Ranges from hypo- to normo- to hypercalemia
* Depends on:
* species
* the underlying cause
* the stage of renal failure
* Must measure an ionized calcium (iCa2+)
* In 10-20% of dogs the total calcium will be increased, but the ionized
calcium will be normal or decreased
Most animals with renal failure are __________. This applies to ______, _______ and ________. The only exception is the ______ (has to do with how their body manages calcium and how it is excreted)
* _____/______ stages of renal failure
- Most animals with renal failure are NORMOCALCEMIC
- Applies Dogs, cats, ruminants; only exception is the horse (has to do with how their body manages calcium and how it is excreted)
- Early/mild stages of renal failure
As renal failure progresses, __________ develops.
–> Mechanisms:
1. Decreased renal tubular _______ resorption
2. Decreased renal tubular production of Vitamin ____
3. _______phosphatemia:
- A physiologic response is _________ calcium
- Calcium mineral _______ on tissues
- As renal failure progresses, HYPOCALCEMIA develops.
- Mechanisms:
- Decreased renal tubular calcium resorption
- Decreased renal tubular production of Vitamin D
- Hyperphosphatemia:
- A physiologic response is decreasing calcium
- Calcium mineral deposition on tissues
- Mechanisms:
Hypocalcemia leads to?
Renal Secondary Hyperparathyroidism
* Hypocalcemia stimulates the parathyroid glands to release
parathyroid hormone (PTH)
* PTH increases calcium (mostly from bone resorption)
Biochem changes: Azotemia, ↑Phos, N-↓Ca, ↑PTH
Some patients with renal azotemia may become hypercalcemic. Explain how?
- Some patients may have HYPERCALCEMIA (↑Ca)
- Horses and renal failure
- Diet and excretion
- Cats, and some dogs
- Usually chronic renal failure
- Mechanisms:
- Unknown, probably involves a receptor abnormality
- Called “TERTIARY HYPERPARATHYROIDISM”
- Horses and renal failure
- Patients with HYPERCALCEMIA and renal failure are expected to be
hyposthenuric. Calcium interferes with ADH receptors.
- Sometimes renal failure causes hypercalcemia.
- Many times, other diseases causes hypercalcemia;
and hypercalcemia leads to renal disease.
Hypokalemia is seen in cases of in _______ renal Failure
- Occurs in cats, –? “_____ nephropathy”
* ________ mechanism
- Also seen in _____
* Mechanisms (multifactorial):
* _____ loss
* ______ loss
* _______
* Metabolic _______
- HYPOKALEMIA in Chronic renal Failure
* Occurs in cats, “hypokalemic nephropathy”
* Unknown mechanism
* Also seen in cattle
* Mechanisms (multifactorial):
* Renal loss
* Salivary loss
* Anorexia
* Metabolic alkalosis
Why do we see hyperkalemia in cases of renal azotemia?
• Associated with ______/______
- Kidney are _______ to excrete
potassium
- _____-stage chronic renal failure
- ______ renal failure
• Metabolic ________
- Hydrogen ions move __________;
potassium ions move ___________
• Associated with oliguria/anuria
- Kidney are unable to excrete
potassium
- End-stage chronic renal failure
- Acute renal failure
• Metabolic acidosis
- Hydrogen ions move intracellularly;
potassium ions move extracellularly
Sodium and chloride levels in horses and cattle with renal azotemia are normal. However, sometimes it can lead to _________ and _________. This is also sometimes seen in cases of _______ renal failure, especially in horses and cattle. This happens if they ____ less, _______ Na/Cl intake. Can sometimes be seen in ____ and ____
You will Always find in a ________.
Sodium and chloride levels in horses and cattle with renal azotemia are normal. However, sometimes it can lead to HYPONATREMIA and HYPOCHLOREMIA. This is also sometimes seen in cases of seen in chronic renal failure
§ Especially in horses and cattle
* Eat less, decreased Na/Cl intake
§ Sometimes in dogs and cats
* Always a finding in uroabdomen
Metabolic acidosis occurs in cases of severe renal disease (either _____ or _____) via one of the following mechanisms:
1. Increased urinary loss of ____ (_____)
2. Decreased tubular secretion of ___ ions
3. Production of ______ and _______
- unmeasured _____
- contribute to an ________ anion gap
Metabolic acidosis occurs in cases of severe renal disease (either acute or chronic) via one of the following mechanisms:
1. Increased urinary loss of bicarbonate (HCO3)
2. Decreased tubular secretion of H+ ions
3. Production of sulfates and phosphates
- unmeasured anions
- contribute to an increased anion gap
The glomerulus filters proteins based on:
1. ______ (<___ kDa)
2. Electrical ______: ________ charge along podocytes
The glomerulus filters proteins based on:
1. Size (<68 kDa)
2. Electrical charge: negative charge along podocytes
In the process of filtration, _____ proteins with ______ or _______ charge pass. Most are resorbed in the _________ renal tubules.
- Not _______ in urine samples
In the process of filtration, small proteins with positive or neutral charge pass. Most are resorbed in the proximal renal tubules.
- Not detected in urine samples
Protein in the urine is measured by ________ ______. Changes in the color of the pad correlate with an estimated [protein]:
Negative, Trace, +, ++, +++, ++++ (1+ –> 4+)
* Best at detecting _______
Protein in the urine is measured by reagent strip. Changes in the color of the pad correlate with an estimated [protein]:
Negative, Trace, +, ++, +++, ++++ (1+ –> 4+)
* Best at detecting albumin
In order to to have measurable protein (albumin) in the urine:
* Get past the _________
and/or
* Enter after the _______
In order to to have measurable protein (albumin) in the urine:
* Get past the glomerulus
and/or
* Enter after the glomerulus
How do we categorize proteinuria ?
a. Prerenal
b. Renal, glomerular
c. Renal, tubular
d. Post-renal
In what cases do we see pre-renal proteinuria?
Physiologic:
* Hypertension
* Fevers
* Seizures
* Strenuous exercise
Increase in small proteins in the blood occurs due to changes in the:
* Hemoglobin
* Myoglobin
* Paraproteins (Bence-Jones)
In cases of renal proteinuria, protein in urine can be due to?
inflammation of the glomerulus or tubular changes
What occurs in a case of glomerulonephritis?
Damaged barrier
* Antigen-Antibody
* Amyloid
Tubular proteinuria is usually associated with _____ renal disease
- Fanconi’s Syndrome: Defective _______ tubules; filtered proteins are not ________
- Usually associated with acute renal disease
- Fanconi’s Syndrome
- Defective proximal tubules; filtered proteins are not resorbed
Animals with hemorrhage or inflammation will present with?
______-renal proteinuria
1. Hemorrhage: RBCs in _____ (________)
* Blood ____ damage from inflammation
* ______
* ______
* _________
2. Inflammation: _____ in urine (_____)
* _______ tract infections
* _______
Post-renal proteinuria
1. Hemorrhage: RBCs in urine (hematuria)
* Blood vessel damage from inflammation
* Trauma
* Neoplasia
* Coagulopathy
2. Inflammation: WBCs in urine (pyuria)
* Urinary tract infections
* Cystitis
We quantify the protein in the urine by looking at the?
Urine protein:creatinine ratio (UPCR)
The Urine protein: creatinine ratio _________ proteinuria
1. Normal __ _______
2. Tubular or Glomerular __ ____
3. Glomerular __ ____
The Urine protein: creatinine ratio quantifies proteinuria
1. Normal <0.5
2. Tubular or Glomerular >0.5
3. Glomerular >1.0
Which form of proteinuria is the most severe? What do you also concurrently see?
- Glomerular proteinuria is the most severe!
- This is the only time you will also see decreased serum albumin:
HYPOALBUMINEMIA
Glomerulnephropathy occurs?
ØSignalment
* ________ (many breeds); often manifests ______
* Secondary; _____-aged to _______ dogs
- _______ infectious diseases
- noninfectious ________ diseases
- ________
ØHistory
* Many are ________
* Some are sick with ________ disease
ØSignalment
* Familial (many breeds); often manifests young
* Secondary; middle-aged to older dogs
* chronic infectious diseases
* noninfectious inflammatory diseases
* neoplasms
ØHistory
* Many are asymptomatic
* Some are sick with underlying disease
What is the pathogenesis of Glomerulonephropathy?
- Pathogenesis: Renal ______ damage
- Damage to the ______
- ______-_______ complex deposition
- ________ deposition
- Pathogenesis: Renal glomerular damage
- Damage to the podocytes
- Antigen-antibody complex deposition
- Amyloid depositio
Glomerular structure is thickened with deposition of amyloid –> aters filter –> glomerulars are strained and podocytes are altered too.
Glomerulonephropathy allows filtration of _________, _________ charged proteins
- Protein _____ exceeds protein _______
- Albumin → _____albuminemia
- Antithrombin → ______coagulability
Glomerulonephropathy allows filtration of larger, negatively charged proteins
* Protein loss exceeds protein production
* Albumin → hypoalbuminemia
* Antithrombin → hypercoagulability
In cases of glomerulonephropathy you should look for?
Look for:
* Moderate to marked hypoalbuminemia
* Moderate to marked proteinuria
* +/- Evidence of renal insufficiency
Nephrotic syndrome is a protein-_______ nephropathy (PLN) that leads to abdominal ________
* Requires 5 things:
1. __________ (________ disease)
2. ______albuminemia (_____ of albumin)
3. Abdominal _______ (loss of ______ pressure due to low levels of ______)
4. _____cholesterolemia (______ mechanism)
5. ______coagulable state (loss of ________)
- Protein-losing nephropathy (PLN) that leads to abdominal effusion
- Requires 5 things:
1. Proteinuria (glomerular disease)
2. Hypoalbuminemia (loss of albumin)
3. Abdominal effusion (loss of oncotic pressure due to low levels of albumin)
4. Hypercholesterolemia (unknown mechanism)
5. Hypercoagulable state (loss of antithrombin)
What are the alternative names for acute renal failure?
- Many names: Acute Renal/Kidney Failure/Insufficiency
What are the abbreviations for acute renal failure?
- Many abbreviations: ARF, AKF, ARI, AKI
How do patients with ARF present?
- Patient: Any signalment
- History: Acute onset of clinical signs (i.e. GET SICK FAST!)
Speed of development, not severity, differentiates
acute from chronic renal failure
Physical exam for ARF patient
Physical Exam:
* Patients usually have a good BCS (vs. CRF patients)
1. GI:
* anorexia
* vomiting
* diarrhea
* halitosis (NH 3 )
2. Renal:
* oliguric to anuric
3. Neuro:
* depressed to obtunded to non-responsive
* seizures
Acute Renal Failure (ARF)
–> Etiologies… There are many! Commonly associated with:
* __________ (i.e. lily toxicity in cats)
* renal _________
* _________ (i.e. leptospirosis)
i.e., things that damage the kidneys _______!
–> Features
* Marked _________ in GFR leading to azotemia
* May be _______ or _________
Acute Renal Failure (ARF)
* Etiologies… There are many! Commonly associated with:
* toxicants (i.e. lily toxicity in cats)
* renal ischemia
* infection (i.e. leptospirosis)
i.e., things that damage the kidneys swiftly!
* Features
* Marked decrease in GFR leading to azotemia
* May be reversible or irreversible
What are the alternate name for chronic renal failure?
Chronic Renal/Kidney Failure/Insufficiency
What are the abbreviations for chronic renal failure?
RF, CKF, CRI, CKI
How do CRF patients typically present?
- Usually ________ (but not _______)
- Frequently _____
- History: ______ onset of clinical signs
______ of development, not severity, differentiates acute from chronic renal failure
- Usually geriatric (but not always)
- Frequently cats
- History: Slow onset of clinical signs
Speed of development, not severity, differentiates acute from chronic renal failure
What is the etiology of CRF in cats?
In cats, irreversible chronic interstitial fibrosis
PE - CRF?
- Patients usually have a ___ BCS (______, _______)
- ________
- GI: (4?)
- Renal: ______
- Neuro: _________
- Cardiovascular: ________
- Patients usually have a poor BCS (thin, cachexic)
- Dehydration
- GI: anorexia, vomiting, diarrhea, halitosis (NH3)
- Renal: polyuric
- Neuro: depressed Cardiovascular: hypertension
Uroabdomen
Of male and female animals, which suffer more from uroabdomens?
More common in males than females
List the causes of a uroabdomen.
- Trauma: birth (foals), hit-by-car (dogs), etc.
- Chronic urethral obstruction
How do uroabdomen patients typically present?
- Abdominal Effusion
- Serum electrolyte imbalances
- Hyperkalemia
- Hyponatremia, hypochloremia
IMPORTANT:
An ↑K and ↓Na occurs with several diseases.
★ Uroabdomen = one ddx
In a healthy dog, the kidney ___________ sodium (Na) and chloride (Cl); and ________ creatinine (Cr), urea, and potassium (K).
conserves, excretes
?
Uroabdomen
Diffusion!
§ _______ molecules move quickly…
* ____, ____ move into urine
ØAppear _______ in plasma
- _____natremia
- _____chloremia
* _______, _____ move into plasma
ØAppear ________ in plasma
* ________
* _____________
§ Large molecules move slowly…
* ___________ remains in the urine
Uroabdomen
Diffusion!
§ Small molecules move quickly…
* Na, Cl move into urine
ØAppear decreased in plasma
- Hyponatremia
- Hypochloremia
* Urea, K move into plasma
ØAppear increased in plasma
* Azotemia
* Hyperkalemia
§ Large molecules move slowly…
* Creatinine remains in the urine
What would you typically see for the following parameters in a patient suffering from a Uroabdomen?
- Hyponatremia (↓Na)
- Hyperkalemia (↑K)
- Hypochloremia (↓Cl)
- Azotemia (↑BUN) …
- +/- ↑Crea from previous post-renal disease
Peritoneal Effusion: - Modified transudate
- High Crea concentration
- Diagnostic when the creatinine concentration of the effusion is more than 2x
the creatinine concentration of the plasma
Dx = [Crea] effusion»_space; [Crea] plasma
Answer the q below
D
Answer the question below
B
Answer the question below
A
