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
Glomerular structure is thickened with deposition of amyloid –> aters filter –> glomerulars are strained and podocytes are altered too.
Uroabdomen
?
Answer the q below
D
Answer the question below
B
Answer the question below
A
