Renal Flashcards
Renal Function
- Clear metabolic wastes from blood
- Conserve nutrients
- glucose
- protein
- Maintain water, electrolyte, and acid-base balance
- Hormone production
- erythropoietin
- Vitamin D
- Renin
- Hormone degredation/excretion
- Enzyme degradation / Excretion
- amylase, lipase
Healthy Glomerulus:
Stays in blood
Cells: RBC, WBC, Platelets
Plasma proteins (albumin)
Healthy Glomerulus:
Passes thru barrier
water
solutes: electrolytes, glucose, urea, small proteins
Healthy Glomerulus:
What determins what gets through
size: >68,000 not filtered
Charge: Basement membrane negatively charged, Negatively charged molecules may be repelled
Physiologic Functions of the Nephron:
Glomerular filtration
Passive:
Substances move from plasma to tubules
Physiologic Function of the nephron:
Tubular resorption
Passive and Active:
Solutes move from tubules to plasma
Physiologic Functions of Nephron:
Tubular secretion
Passive and Active:
Substances move from plasma to tubules
Physiologic function of Nephron:
Water regulation
Maintain water balance, May go to or from the plasma
Glomerular Filtration Rate (GFR)
Volume of plasma filtered form glomerular capillaries into bowman’s space per unit time
Measured by determining rate of clearance of a substance from plasma
Glomerular Filtration Rate:
Dependent on?
Renal blood flow
of functional nephrons
Hydrostatic pressure in Bowman’s capsule
Osmometer
Measures osmolality
Freezing point assay, not convenient, but more accurate
Measure depends on the number of particles in a volume of water
Refractometer
Measures Urine specific Gravity
Depends ofn particle weight and how each particle bends light
Prone to interference
Differences between how glucose, electrolytes, urea, proteins, lipids, and other substances refract light
Antidiuretic Hormone (ADH)
Synonym: Vasopressin
Synthesized in the hypothalamus
Secreted form the posterior pituitary glands
Interacts with receptors ont he cells of hte distal tubules and collecting ducts
Opens water channels via aquaporin proteins
Stimuli for ADH secretion
Plasma hyperosmolality
Decreased cardiovascular pressure
increased concentration of angiotensin
Result: Conserve body water to decrease plasma osmolality and increase blood volume
Major events of Nephron Segments:
Proximal Tubule
Revomes volume
No change in concentration
Major events of nephron segments
Descending Loop of Henle
Removes water
Increases concentration
Major Events of Nephron Segments”
Ascending Loop of Henle
removes solutes
Dilutes (decreases concentration)
Major events of Nephron segments
Distal nephron
removes water
Increases concentration
To produce conentrated Urine
Adequate number of functional nephrons
Adequate production of ADH from pituitary
Distal nephron epithelial cells must be responsive to ADH
Hypertonic interstitium in the renal medulla
Anuria
Lack of urine production
dysuria
painful or difficult urination
oliguria
production of an abnormally small amount of urine
Pollakiuria
indicating increased frequency of urination. Doesn’t indicate urine volumes
Polydipsia
increased water consumption
Polyuria
production of excessive amounts of urine
Azotemia
Increased concentration of Urea Nitrogen and/or creatinine
Urea Nitrogen
Urea diffuses readily across most cell membranes along a concentration gradient
Rapid equilibrium amont intercellular and extracellular fluid compartemnts (~90)
Whole blood urea nitrogen = serum urea nitrogen
Urea contributes to the renal medullary concentration gradient
This drives recovery of water / cocnentration of urine in the collecting ducts
Creatinine Metabolism
Creatinine is a wast product from the normal breakdown of musscle tissue
Freely filtered thru glomerular barrier into ultrafiltrate
NOT RESORBED BY TUBULES
excreted in urine
Urea Nitrogen Assay
Serum or plasma
Stable for 1 day at room temp
203 months if frozen
Creatinine Assay
Serum or plasma (NO whole blood)
Increased Creatinine (Ct)
Decreased GFR
Decreased Creatinine
May not be clinically significant
Consider:
Decreased muscle mass
Hypoproteinemia
Pre-Renal Azotemia
UN and creatinine are increased
Urine is concentrated
Pre-renal Azotemia:
Possible Causes:
- Decreased Renal Blood Flow = decreased GFR
- Dehydration
- hypovolemia / fluid maldistribution
- Severly decreased cardiac output
- Increased production of urea / creatinine
- Urea:
- high protein diet
- GI hemorrhage
- Cretinine:
- heavily muscled animals
- Urea:
Renal Azotemia
Primary causes is within the nephron
UN and creatinine are increased
Urine is NOT concentrated in the face of dehydration
decreased concentrating ability
Isothenuric urine (1.007-1.013) indicates an inability to concentrate and dilute
Post-renal Azotemia
Primary problem is after the nephron
Problem that interferes with excretion
UN and creatinine are increased
Uremia
Cliical Syndrome associated with renal failure
Azotemia plus severe physical consequences fo renal failure
- Polyuria / polydipsia
- Vomiting / diarrhea
- Ammonia odor of breath
- GI ulcers
- Nonregenerative anemia
- Weight loss
- Convulsions
- Coma
Abnormal Laboratory Results in Azotemic Animals:
Sodium and chloride
increased with prerenal azotemia
Low or WRI with renal failure due to decreased resorption
Abnormal Laboratory Results in Azotemic Animals:
Potassium
Usually high in oliguric and anuric renal failure
Low in cats and cows with polyuric renal failure
Abnormal Laboratory Results in Azotemic Animals:
Phosphate
Excretion is decreased when GFR is decreased for any reason (Prerenal, renal, postrenal)
Usually high in animals with moderates to marked azotemia
Abnormal Laboratory Results in Azotemic Animals:
Magnesium
Increased with decreased GFR
Abnormal Laboratory Results in Azotemic Animals:
Calcium:
Dogs, cats, cows
Usually WRI or slightly decreased with renal failure
Hypercalcemia in dogs and cats with azotemia is more likely to be the cuase for renal disease then the result of renal disease
Abnormal Laboratory Results in Azotemic Animals:
Calcium:
Horses
Rely on renal excretion of calcium
Calcium is high in most horses with renal failure due to decreased excretion and a species difference in calcium metabolism
Abnormal Laboratory Results in Azotemic Animals:
Hematocrit
WRI or high in pre-renal azotemia and ARF
Non-regenerative anemia in CRF
Abnormal Laboratory Results in Azotemic Animals:
Total Protein, Albumin
WRI or high in pre-renal azotemia +/- ARF
Within reference interval or low in CRF
Abnormal Laboratory Results in Azotemic Animals:
Acid/base abnormalities
Yes!
Mechanisms of Polyuria
- Lack of ADH production
- central diabetes insipidus
- Phychogenic polydipsia
- Distal tubule/Collecting Duct cells cannot respond ot ADH
- nephrogenic biabetes insipidus
- Must be a conentration gradient between tubular fluid and interstitium
- solute diuresis
- Reduced medullary intersitium osmolality
Major initial/primary pathogenic mechanisms for Polyuria Chart
Decreased Renal Reserve
GFR is about 50% of normal capacity
Clinically healthy: NOT azotemic or polyuric – susceptible to insult
Chronic Renal Insufficiency
25-50% function
Azotemic, Anemia, Decreased concentrating ability, Polyuria
Chronic Renal Failure
<20-25% function
Azotemic, anemia, decreased concentrating ability,
Electrolyte imbalance, clinical signs fo uremia
End-Stage Renal disease:
<5% function
Terminal uremia signs and oliguria or anuria
Causes of Polyuria in Chronic Renal Disease?
Loos of functional nephrons
- More solute presented to remaining functional nephrons
- Increased load through nephrons
- Solute diuresis
- Medullary hypertonicity is not maintained
- medullary tissue damage or abnormal blood flow
- Decreased sodium, chloride and urea reabsorption
- Damaged cells less responsive to ADH
Acute Renal Failure
Reversible or Irreversible
Abrupt insult or disease
Marked decrease in GFR → Azotemia → Uremia
Degree of azotemia does NOT differentiate chronic vs. acute
Toxins, ischemia, infection
Vascular supply, glomerular, tubular, interstitial disease
Mechanisms of Proteinuria:
Hemorrhagic or inflammatory
This is the most common mechanism for addition of protein to urine
Hemorrhage anywhere in the urinary tract
Inflammation causing exudation of plasma proteins intohte urinary tract
Magnitide of Proteinuria varies but it DOES NOT lead to hypoalbuminemia
Mechanisms of Proteinuria:
Funcitonal
Transient mild increase in urine protein content
Exercise, fever, seizures, stress
Mechanism unclear
Mechanism of Proteinuria
Overload
Increased plasma concentration of small protiens that pass through glomerular filtration barrier and exceed capacity for tubular resorption
Hemoglobin, myoglobin, immunoglobin light chains,
Overload proteinuria DOES NOT lead ot hypoproteinemia
Mechanisms of Proteinuria:
Tubular
Proximal tubular injury causing failure to reabsorb small proteins
Usually associated with Acute renal tubule damage
Tubular damage = exposure to neprothoxins
DOES NOT result in hypoproteinemia
Mechanisms of Proteinuria:
Glomerular
- Damage/disruption of the glomerular filtration barrier
- immune complex deposition
- Amyloid deposition
- Inflammatory cells contribute - release cytokines and other mediators that can damage the glomerulus
- Increased permeability to large and or negatively charged proteins
- albumin first, globulins later with progressiive damage
- Glomerular damage often leads to sleective hypoproteinemia
- Progressive glomerular disease
- can lead to tubular damage and tubular proteinuria, loss of nephrons → azotemia, renal failure
Severe Glomerular Disease
The entire nephron may become nonfuncitonal
Severe, persistent proteinuria can lead to the nephrotic syndrome
Proteinuria
hypoproteinemia
Hypercholesterolemia
Ascited or edema
Urine Protein:
Urine Creatinine Ratio:
UPC < 0.2
Healthy dogs and cats
Urine Protein:
Urine Creatinine Ratio:
UPC 0.1-0.4, 0.1-0.5
Is borderline - not conclusive evidence of proteinuric renal disease
Urine Protein:
Urine Creatinine Ratio:
0.4-3, 0.5-3
Proteinuria is present
in this range proteinuria could result form glomerular or tubular damage
Urine Protein:
Urine Creatinine Ratio:
UPC >3
Indicative of glomerular disease
Tubular disease may also be present, but it is not the whole story
Urine Protein:
Urine Creatinine Ratio:
UPC ~15
Most indicative of amyloidosis
