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87 Cards in this Set
- Front
- Back
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What are six renal fns?
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1. regulate body fluid, electrolyte levels, and osmolality
2. excrete endogenous (urea, creatinine) and exogenous waste 3. regulate body pH 4. control blood pressure a. renin b. aldosterone c.antidiuretic hormone (ADH) (syn. vasopressin) 5. stimulate erythrocyte production (erythropoietin) 6. activate vitamin D (alpha-hydroxylase enzyme) |
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What are 3 parts of the nephron?
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1. glomerulus (filtration)
2. tubules (reabsorption and secretion) a. proximal convoluted tubule b. descending loop of Henle c. Ascending loop of Henle d. distal convoluted tubule e. collecting tubule 3. Medullary intersititium (hypertonic) |
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What are syn names for urea?
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syn blood urean nitrogen [BUN], serum urea nitrogen [SUN]
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What is the source of urea?
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break down of endogenous or dietary protein results in the production of ammonia. Ammonia is taken up from blood by liver and converted to urea thru the Cori cycle
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Describe urea filtration.
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1. Urea freely diffusible in body water and freely filtered at glomerulus
2. 1/2 filtered urea reabsorbed from tubules to help creat hypertonic intersitium in renal medulla, which is req for concentrating urine. 3. reaborption is dep on urine tubular flow--the faster the flow (high urine vol like in duresis), the less ureareabsorbed |
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Where can urea be transported besides the tubules?
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1. into GI tract where excreted or metabolized by bacteria and reabsorbed as nitrogen
-important role in nitrogen balance in cattle **means urea levels in blood affected by more than just renal fn** |
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When does one see increased urea? (2 things)
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1. increased production w/ high protein diets (minimal increase), upper GI bleeding (mild to moderate increase), rapid tissue catabolism (high fever, severe infection)
2. Decreased elimination occurs w/ decrease in GFR. Causes of decreased GFR are dehydration, renal disease, post-renal obstruction |
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When does one see decreased urea?
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decreased production during malnutrition, liver failure/portosystemic shunt (urea made in liver), hereditary deficiency in urea cycle enzymes (rare) and w/ increased elimination during diuresis (high tubular flow rate)
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What is the source of creatinine?
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by-product of muscle creatine breakdown. Happens at regular and constant rate that goes to kidney
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How is creatinine released?
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At constant rate and is freely diffusible in body water, although diffuses more slowly than urea. Freely filtered at glomerulus and undergoes no reabsorption. Dogs secrete a small amt of creatinine into tubular fluid. b/c creatinine not reabsorbed or secreted (except as noted), creatinine clearance is good est of GFR
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Why is creatinine a better measure of renal fn than urea?
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less affected by diet, tubular flow rate, or protein catabolism. Esp true w/ large animals
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When does one see increased creatinine?
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any decrease in GFR, including dehydration, post-renal obstruction, and renal disease
**creatinine only based on elimination b/c prod constantly** |
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What is azotemia?
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increased non-protein nitrogen (urea and creatinine) in serum/plasma, which often predicts a decrease in GFR.
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What is uremia?
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sp to renal failure. Refers to clin signs ass w/ sever azotemia due to renal failure. Signs include vomiting, diarrhea, ammoniacal odor of breath, convulsions, and coma
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What is isosthenuria?
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urine with a USG that is same as initial filtrate (and same as protein free plasma). Random urine samples may be isosthenuric. Urine that is repeatedly and consistently isosthenuric suggests renal disease (1.008-1.012)
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What is hyposthenuria?
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diluted urine w/ a USG less than initial filtrate. Dilution of filtrate req a fn-ing kidney
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What is hypersthenuria?
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Indicates concentrated urine w/ a USG equal to or greater than value that should be achievable for that species under cond of dehydration. Concentration of filtrate req fn-ing kidney
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What is the range of minimal concentration (ROM)?
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USG that is btwn isosthenuria and hypersthenuria
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how can USG be artifactually increased or decreased?
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increased=glucose, ketones, protein
down=administration of fluids |
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What is Prerenal azotemia?
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decreased GFR due to decreased blood flow to kidneys. low blood volume and low cardiac output
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What type of azotemia does dehydration prod? describe
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prerenal azotemia.
1.Physical exam: skin tent w/ sticky mucous membranes 2. PCV and TP are increased above expected norm 3. increased urea and creatiine due to decreased GFR; urea may be proportionally higher than creatinine 4. increased phosphorus (P) due to decreased GFR (hyperphosphatemia) 5. hypersthenuria in animals w/ normal renal fn |
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What is postrenal azotemia?
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urinary bladder obstruction leads to increased back pressure in Blowman's capsule w/ subsequent vasoconstriction and a decrease in GFR. Repture or any part of urinary tract w/ leakage of urine and absorption of urine consituents from peritonea cavity also results in azotemia
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How does one detect postrenal azotemia in physical exam?
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1. firm, distended bladder (obstruction)w/ stranguria (staining to urinate, distended abdomen (uroabdomen), absence of normal urination
2. physcial signs of dehydration 3. increased urea and creatinine-goes from high concentration to low concentration, so goes to blood 4. increased P-equilibrates w/ blood 5. Increased K-increased in urine, so equilibrates w/ blood, slow heart rate is concern w/ this 6. uroabdomen also results in low plasma sodium (na) and chloride (Cl) as result of equilibration of plasma sodium and chloride w/ high volume of urine w/ low concentrations of Na and Cl in abdomen 7. USG can be any value |
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What is renal azotemia?
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decrease in number of fn-ing nephrons resulting in decreased GFR
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How does one detect renal azotemia?
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1. signs of illness typicaly seen (may have signs o dehydration)
2. increased urea and creatinine 3. increased phosphorus in cats and dogs. Hypophosphatemia and normophosphatemia may be seen w/ renal failure in horses and cattle, respectively 4. USG isosthenuric or in ROM 5. may have mild proteinuria from lack of protein reabsorption (damaged tubules) 6. decreased secretion of waste acids result in high anion gap metabolic acidosis of varying severity. Exception: cattle often have metabolic alkalosis due to chloride retention in abomasum and rumen resulting from abomasal atony |
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How does one det renal failure?
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1. loss of renal concentrating ability occurs when >66% nephrons lost
-animals polyuric (increased urine) -animals polydipsic (increased drinking) 2. Loss of excretory fn and appearance of azotemia occurs when >75% nephrons lost 3. end-stage renal failure occurs when >90% nephrons lost and patient dev signs of uremia |
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What is acute renal failure (ARF)?
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results from acute infection, toxic insult, or loss of blood flow to kidney. increased urea, increased creatinine, increased P
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What are signs of ARF?
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1. anuric (produce no urine) or oliguric (produce less urine than expected), but some polyuric
2. USG typically isosthenuria or ROM, but can be any value 3. often concurrently dehydrated d. Hyperkalemia from decreased elimination 5. hypercalcemia from decreased elimination 6. PCV normal or increased (dehydration) 7. Tenal damage may be reversible |
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What is isosthenuria?
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urine with a USG that is same as initial filtrate (and same as protein free plasma). Random urine samples may be isosthenuric. Urine that is repeatedly and consistently isosthenuric suggests renal disease (1.008-1.012)
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What is hyposthenuria?
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diluted urine w/ a USG less than initial filtrate. Dilution of filtrate req a fn-ing kidney
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What is hypersthenuria?
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Indicates concentrated urine w/ a USG equal to or greater than value that should be achievable for that species under cond of dehydration. Concentration of filtrate req fn-ing kidney
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What is the range of minimal concentration (ROM)?
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USG that is btwn isosthenuria and hypersthenuria
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how can USG be artifactually increased or decreased?
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increased=glucose, ketones, protein
down=administration of fluids |
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What is Prerenal azotemia?
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decreased GFR due to decreased blood flow to kidneys. low blood volume and low cardiac output
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What type of azotemia does dehydration prod? describe
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prerenal azotemia.
1.Physical exam: skin tent w/ sticky mucous membranes 2. PCV and TP are increased above expected norm 3. increased urea and creatiine due to decreased GFR; urea may be proportionally higher than creatinine 4. increased phosphorus (P) due to decreased GFR (hyperphosphatemia) 5. hypersthenuria in animals w/ normal renal fn |
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What is postrenal azotemia?
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urinary bladder obstruction leads to increased back pressure in Blowman's capsule w/ subsequent vasoconstriction and a decrease in GFR. Repture or any part of urinary tract w/ leakage of urine and absorption of urine consituents from peritonea cavity also results in azotemia
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How does one detect postrenal azotemia in physical exam?
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1. firm, distended bladder (obstruction)w/ stranguria (staining to urinate, distended abdomen (uroabdomen), absence of normal urination
2. physcial signs of dehydration 3. increased urea and creatinine-goes from high concentration to low concentration, so goes to blood 4. increased P-equilibrates w/ blood 5. Increased K-increased in urine, so equilibrates w/ blood, slow heart rate is concern w/ this 6. uroabdomen also results in low plasma sodium (na) and chloride (Cl) as result of equilibration of plasma sodium and chloride w/ high volume of urine w/ low concentrations of Na and Cl in abdomen 7. USG can be any value |
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What is renal azotemia?
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decrease in number of fn-ing nephrons resulting in decreased GFR
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How does one detect renal azotemia?
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1. signs of illness typicaly seen (may have signs o dehydration)
2. increased urea and creatinine 3. increased phosphorus in cats and dogs. Hypophosphatemia and normophosphatemia may be seen w/ renal failure in horses and cattle, respectively 4. USG isosthenuric or in ROM 5. may have mild proteinuria from lack of protein reabsorption (damaged tubules) 6. decreased secretion of waste acids result in high anion gap metabolic acidosis of varying severity. Exception: cattle often have metabolic alkalosis due to chloride retention in abomasum and rumen resulting from abomasal atony |
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How does one det renal failure?
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1. loss of renal concentrating ability occurs when >66% nephrons lost
-animals polyuric (increased urine) -animals polydipsic (increased drinking) 2. Loss of excretory fn and appearance of azotemia occurs when >75% nephrons lost 3. end-stage renal failure occurs when >90% nephrons lost and patient dev signs of uremia |
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What is acute renal failure (ARF)?
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results from acute infection, toxic insult, or loss of blood flow to kidney. increased urea, increased creatinine, increased P
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What are signs of ARF?
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1. anuric (produce no urine) or oliguric (produce less urine than expected), but some polyuric
2. USG typically isosthenuria or ROM, but can be any value 3. often concurrently dehydrated d. Hyperkalemia from decreased elimination 5. hypercalcemia from decreased elimination 6. PCV normal or increased (dehydration) 7. Tenal damage may be reversible |
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What is chronic renal failure (CRF)?
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Progressive loss of nephrons often due to self-perpetuating desease; signs of superimposed ARF may occur intermittently and/or terminally. Increased urea, increased creatinine, increased phosphorus. Small nubby kidneys
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Is urine from chronic renal failure concentrated or dilute?
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moderate columes of dilute urine (polyuria)
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Is urine from chronic renal failure isothenuric, hypersthenuric, or hyposthenuric?
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isothenuric or in the ROM concentration
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Describe calcium and potassium levels w/ CRF.
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-Hypokalemia due to polyuria (decreased level potassium)
-Hypocalcemia (ionized calcium) due to decreased activation of vitamin D. Horses, which do not activate vitamin D in the kidney, are an exception and typically have hypercalcemia w/ CRF due to decreased urinary excretion of calcium |
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What kind of anemia do you get w/ CRF?
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non-regen due to decreased erythropoietin prod
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What happens w/ PTH (parathyroid hormone) w/ CRF?
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high. Low Ca++ and increased phos stimulates PTH. Causes lots of damage in late stage renal failure
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Is CRF reversible or not?
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non-reversible
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What are some specific causes of acute renal failure?
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ethylene glycol, leptospirosis, inadequate perfusion during anesthesia in geriatric patients w/ marginal renal fn, endotoxemia (esp large animals), phenylbutazone toxicity (equine), prolonged hypercalcemia esp w/ concurrent hyperphosphatemia; chronic renal failure may be sequela to ARF and interstitial nephritis often noted histologically
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How can one assess GFR?
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measure plasma concentration at steady state and urine concentration (24 hr pooled urine) of substance that is freely filtered (not protein bound) and neither secreted or reabsorbed. Urine volume measured over a defined time period (usually 24 hours) is determined in order to calculate urine flow rate
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What are 3 ways GFR can be measured or extimated?
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inulin, expogenous creatinine, and endogenous creatinine
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What is the formula to measure GFR?
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GFR= (urine [x] X urine flow rate)/plasma [x]
x=concentration of inulin or creatinine |
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What is protein-losing nephropathy (PLN)?
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Glomerular injury results from deposition or antigen-antibody complexes in glomerular filtration barrier w/ activation of complement and subsequent inflammation.
-podocytes keep protein in -antigen-antibody complexes may accumulate secondary to chronic infections or autoimmune disease -amyloid deposition is either acquired (chronic infection or inflammation) or inherited -terms for glomerular diseased include glomerulonephritis, glomerulonephropthay, or GN |
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What are the consequences of protein-losing nephropahty (PLN)?
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1. Damage to filtration barrier results in loss of small (<69,000 Da), negatively charged proteins into filtrate.
-large proteins and positively charged proteins retained in blood -increased amt of protein in filtrate overwhelms resorptive capacity of prox tubule transporters resulting in protein loss in urine (proteinuria) -most clinically sig proteins lost are albumin and antithrombin |
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What do you see in urine w/ PLN?
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proteinuria in absence of pyuria or hematuria
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What do you see in serum/plasma w/ PLN?
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hypoalbuminemia w/ normal/increased globulins, total protein may be low or w/in reference interval
-loss of albumin, major contributor to oncotic pressure, impairs retention of fluid w/in vasculature OR albumin holds fluids in vasculature |
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What happens w/ hemostasis when have PLN?
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Low levels of antithrombin predispose patients to hypercoagulability and thromboembolic disease
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How do you qualify protein loss in PLN?
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evaluate protein reaction in context of USG
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how do you quantify proteinuria in PLN?
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The amt of protein (mg/dL) in the urine is divided by the amt of creatinine (mg/dL) in the urine to create a urine protein:creatinine ratio (UPC). Both are measured on chemistry analyzer. Comparing protein to creatinine normalizes the amt of protein to urine concentration.
**Looks at glomerular and tubular defects** |
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What is a result of increased globulins?
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infection or inflammation
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What is nephrotic syndrome?
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an advanced form of protein losing nephropathy.
-proteinuria as a result of GN -hypoalbuminemia -ascites or edema (decreased oncotic pressure due to low albumin) -hypercholesterolemia (loss of small protein in urine that regulates cholesterol) -hypercoagulation due to loss of antithrombin |
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What are common causes of GN-PLN?
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heartworm disease, chronic bacterial infections, systemic lupus erythematosus (autoimmune disease), amyloidosis (acquired of familial)
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What happens w/ lack of or dysfunctional ADH/ADH receptors (syn for ADH is vasopressin)
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-cause of polyuria
1. congenital: diabeses insipidus a. central: lack of ADH synthesis in hypothalamus b. nephrogenic: lack of fn-al ADH receptors on renal tubules 2. Acquired (dysfn occurs at renal tubules) a. hypercalcemia b. endotoxemia (canine pyometra) c. hypercortisolemia |
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What is chronic renal failure a cause for?
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polyuria
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What is osmotic diuresis (diabetes mellitus) a cause for?
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polyuria
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What can fluid intake in excess of need cause (pyschogenic or behavioral polydipsia)?
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polyuria
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What can renal medullary washout (insufficient sodium and/or urea) cause?
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-polyruria
-liver failure (low urea) -hypoadrenocorticism (some) -prolonged polydipsia |
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What is total protein?
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1. albumin + globulins
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How do you measure TP?
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serum proteins, can mearue w/ refractometry or spectrophotmetry
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Describe albumin and its fn.
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small and negatively charged; major contributor to oncotic pressure, 'carries' Ca2+, Mg2+, unconjugated bilirubin, thyroxine, drugs and many other substances; source of amino acis
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What is the source of albumin?
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liver
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How does one analyze albumin?
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dye-binding spectrophotometry (BCG most common); serum protein eletrophoresis (SPE); some methods don't measure animal proteins equally; spectrophotometric assys are notoriously inaccurate in birds and rabbits
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Describe globulins:
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more than 1000 diff globulins of diff sizes and charges; globulin=TP-albumin; fibrinogen and immunoglobulins are greatest proportion of total globulins
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Describ fibrinogen and give fn.
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Beta-globulin.
source is liver. fn important coagulation protein and an acute phase protein. tell if have inflammation |
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How does one analyze fibrinogen?
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refractometry-heat precipitation of fibrinogen (only detects increased concentration); thrombin time coagulation assay (detects on both increased and decreased concentrations)
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Describe immunoglobulins and give fn
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synonyms: gamma-globulins, Ig, antibodies)
-generally large and positively charged -source: plasma cells fn: humoral immunity |
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How can one measure Ig?
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precipitation/turbidity tests (tests for failure of passive transfer), serum protein electrophoresis (SPE), radioimmunodiffusion, immunoelectrophoresis
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What are the 'other globulins' of the course? How do you analyze?
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alpha-globulins and beta-globulins: lipoportein, macroglobulin, transferrin
-soure: liver fn: many fn (inflammation, carrier proteins, actue phase proteins) Analysis: SPE or individual assays |
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Describe 5 steps of serum protein electrophoresis.
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a. migration of proteins in electrical field depends upon charge, size, and shape
b. separates proteins into several bands, each band representing one or more proteins c. albuin travels the farthest and fastest, while gamma-globlins hardly mve from site of application d. tall, skinny peaks are single proteins (albumin, monoclonal immunoglobulin), while short, fat peaks are mult proteins e. used primarily to differentiate btwn polyclonal (inflammatory/infectious) and monoclonal (usually neoplastic) gammopathies and in birds for more accurate protein assessment |
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What causes hypoalbuminemia w/ hypoglobulinemia (TP decreased to normal) PANHYPOPROTEINEMIA
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decreased proteins caused by:
-hemorrhage -Protein losing enteropathy (PLE): leakage or poteins into GI tract thru infiltrated mucosa e.g. intestinal pymphoma, inflammatory bowel diease, lymphangiectasia -dermatologic lesions (i.e. excessive burns) -exudative effusion: sequestration of inflammatory fluid in thoracic or abdominal cavity |
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what causes hypoalbuminemia w/ normal to increased globulins (TP decreased to increased) SELECTIVE HYPOALBUMINEMIA
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decreased proteins from:
a. decreased prod of albumin via -liver failure -cachexia/starvation: hypoalbuminemia occurs late -GI parasitism: competition for nutrients and hemorrhage -Intestinal malabsorption: failure to absorb amino acids; history of chronic diarrhea -exocrine pancreatic sufficiency: failure to digest proteins to absorbable amino acids; history of chronic diarrhea b. increased loss of albumin from the gody -glomerulonehropathy/protein-losing nephropathy (PLN): selective loss of albumin into urine; maybe associated w/ chronic inflammatory disease and increased globulin c. several diseases may be ass w/ increased globulin prod as result of inflammation. if globulins increased, total protein may be normal or even increased |
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What causeshypoglobulinemia w/ normal to increased albumin? SELECTIVE HYPOGLOBULINEMIA
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decreased proteins by:
-failure of passive transfer -acquired or inherited immunodefieciency |
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What causes hyperalbuminemia (relative)?
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increased proteins by dehydration
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What causes hyperalbuminemia and hyperglobulinemia (relative)?
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increased proteins by dehydration
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What causes hyperglobulinemia w/ normal albumin:
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a. increased alpha and beta globulins usually as result of acute inflammatory response, rarely are increases solely in alpha and beta proteins sufficient to increase TP or globulin
b. increased gamma-globulins GAMMOPATHY: 1. polyclonal:immunoglobulins prod by many diff plasma cells which is result of chronic inflammatory disease 2. monoclongal immunoglobins prod by single plasma cell clone, usually prod by neoplastic plasma cells (mult myeloma) or lymphocytes-lymphoblasts (lymphoma/leukemia); rarely ass w/ chronic inflammatory response c. hyperfibrinogenemia: inflammation, dehydration (relative) |
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What is sig of albumin:globulin ratio and plasma protein:fibrinogen ratio?
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-useful in determining whether proteins are changing in relation to one another e.g.w/ dehydration, both albumin and globulin increase so A:G doesn't change
-if ratio increases, either numerator increased or denominator decreased; therefore, in the end, you need to look at the individual values to determine the problem SAME FOR IF RATIO DECREASES |
