Term
| What is the normal value range for urea in blood? |
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Definition
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Term
| What can cause an increase in urea production? |
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Definition
| Fever, tissue necrosis, GI hemorrhage (RBCs release NH4 into gut), high protein diets. |
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Term
| What can cause an decrease in urea production? |
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Definition
| Chronic liver failure, portosystemic shunts, negative protein balance (anorexia/cachexia), low protein diet. |
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Term
| What is the most important factor influencing BUN levels? Why? |
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Definition
| Renal excretion. Urea is freely filtered through glomeruli, so decrease in GFR (whether due to pre-renal, renal, or post-renal disease)means increased serum BUN. |
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Term
| What happens to urea in the nephron? |
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Definition
| Freely filtered by glomerulus. In tubules, reabsorption of water results in higher concentration of urea in filtrate. Tubule is not as permeable to urea as it is to water, so only about half the urea ends up being reabsorbed back into the interstitium (although the higher the urine flow rate, the less urea is absorbed proportionally). In the interstitium urea helps create the medullary osmotic gradient which enables urine concentration. |
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Term
| How can adult ruminants maintain relatively normal BUN in the face of reduced GFR? |
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Definition
| Some circulating urea is excreted by the salivary glands and ends up in the rumen, where microbes degrade the urea into NH3 and form proteins. |
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Term
| What is the normal value of creatinine in serum? |
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Definition
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Term
| What is the major factor determining circulating creatinine levels? |
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Definition
| GFR. Creatinine production is fairly constant and minimally influenced by muscle catabolism or necrosis. It is freely filtered by the glomerulus, and no tubular reabsorption occurs (some secretion in male dogs and goats!). |
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Term
| What are causes of pre-renal azotemia? |
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Definition
1. Hypovolemia (due to dehydration, shock, acute hemorrhage)
2. Cardiac insufficiency |
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Term
| Is pre-renal azotemia associated with more or less concentrated urine? |
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Definition
| More concentrated. Hypovolemia results in ADH release, and reduced GFR due to reduced CO results in activation of renin/AT system and aldosterone release. |
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Term
| What is considered adequate urine concentration in the face of dehydration/azotemia? |
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Definition
Cow: SG > 1.026
Dog: SG > 1.030
Horse: SG > 1.030
Cat: SG > 1.035 |
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Term
| Is prerenal azotemia associated with normal or abnormal urine sediment? |
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Definition
| Usually normal. However, persistent renal ischemia can result in renal tubular damage, resulting in casts in sediment. |
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Term
| Damage to what structures can cause renal azotemia? |
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Definition
| Glomeruli, tubules, interstitium, renal blood vessels. (Vasculature and tubules are interdependent so damage to one is usually followed by dysfunction of another.) |
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Term
| Is renal azotemia associated with more or less concentrated urine? |
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Definition
| Less concentrated (isosthenuric or minimally concentrated). With renal tubular damage due to ischemia/necrosis, tubular cells may be unable to respond to ADH. Remember that concentrating ability is lost with loss of 2/3 of nephrons, but azotemia occurs with loss of 3/4 of nephrons. |
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Term
| What constitutes minimal urine concentration in face of azotemia? |
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Definition
Cow: SG < 1.026
Dog: SG < 1.030
Horse: SG < 1.030
Cat: SG < 1.035 |
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Term
| Do you expect to see normal or abnormal urine sediment in the presence of renal azotemia? |
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Definition
Abnormal. There may be:
1. Casts (due to tubular cell sloughing; renal necrosis due to persistent ischemia or toxins).
2. Inflammatory cells (due to Ag-Ab complexes in glomeruli).
3. Abnormal crystals |
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Term
| What causes concurrent pre-renal azotemia with renal azotemia? |
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Definition
| Loss of ability to concentrate urine (due to renal tubular damage in renal azotemia) results in excess water loss (polyuria) and possible dehydration...resulting in pre-renal azotemia! |
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Term
| What are some exceptions to renal azotemia being associated with minimally-concentrated urine? |
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Definition
1. Cats can sometimes retain concentrating ability in face of renal azotemia.
2. When glomerular lesions haven't resulted in severe enough tubular lesions to impair concentrating ability ("glomerulotubular imbalance"). |
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Term
| If azotemia is not present, can you rule out kidney disease? |
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Definition
| No. It takes the loss of 3/4 of nephrons to result in (renal) azotemia. |
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Term
| What situations can result in post-renal azotemia? |
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Definition
"Plumbing" problems, including:
1. Urolithiasis
2. Neoplasm of bladder/urethra
3. Enlarged prostate
4. Uterine stump granuloma (impinging on UT)
OR
5. Neurologic deficit
Also, urinary tract rupture. |
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Term
| Do you typically see more or less concentrated urine with post-renal azotemia? |
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Definition
| Neither, necessarily - urine SG can be widely variable with post-renal azotemia. |
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Term
| Is azotemia usually seen with a unilateral ureteric or pelvic obstruction? |
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Definition
| No - the unobstructed kidney can increase urine output to maintain normal BUN/creatinine levels. |
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Term
| What other serum chemistry changes are you likely to see with azotemia if it's post-renal? |
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Definition
-Increased serum K+ and P- due to decreased filtration (hyperkalemia -> bradycardia)...mitigated in ruminants by excretion of K+ and P- in saliva.
- Hypocalcemia can be seen: possibly resulting from increased P-, which complexes with Ca++ (reducing free Ca++) and eventually precipitates into soft tissues (reducing total Ca++). |
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Term
| What serum abnormalities are you likely to see with uroabdomen? |
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Definition
1. Azotemia
2. Hyponatremia
3. Hypochloremia
4. Hyperphosphatemia
5. Hyperkalemia
Azotemia, hyperkalemia, and hyperphoshatemia are due to the fact that urea, K+, and P- diffuse from area of high concentration (in urine in peritoneal cavity) across peritoneum into blood. Hyponatremia and hypochloremia are due to the fact that Na+ and Cl- are usually reabsorbed from urine to a great extent, so are at low concentration in urine...so diffuse from blood INTO the peritoneal cavity. |
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Term
| In the case of uroabdomen, does BUN or creatinine increase faster? |
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Definition
| BUN, since urea is a smaller molecule and diffuses across peritoneum faster. Creatinine diffuses more slowly, taking about 4 hrs to reach equilibration (but continuous leak of urine means full equilibration is not likely to be reached). |
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Term
| What ratio of creatinine in abdominocentesis effusion to serum is diagnostic of uroabdomen? |
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Definition
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Term
| What serum chemistry and urinalysis findings are consistent with extravascular hemolysis? |
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Definition
1. Anemia
2. Bilirubinemia and bilirubinuria
3. Plasma often icteric (yellow) |
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Term
| What serum chemistry and urinalysis findings are consistent with intravascular hemolysis? |
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Definition
1. Anemia
2. Bilirubinemia & bilirubinuria
3. Pink-red plasma/serum
4. red-brown urine
5. positive urine heme reaction
6. no RBCs in urine sediment |
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Term
| What serum chemistry and urinalysis findings are consistent with myoglobinuria (muscle necrosis)? |
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Definition
1. NO anemia
2. Normal plasma/serum appearance (usually)
3. red-brown urine
4. positive heme reaction
5. no RBCs in urine sediment |
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Term
| What is nephrotic syndrome? |
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Definition
Collection of lab and clinical signs indicating presence of protein-losing nephropathy:
1. Proteinuria (renal)
2. Hypoalbuminemia
3. Hypercholesterolemia
4. Edema and/or ascites |
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Term
| Why might serum creatinine be a less valuable measure of GFR in a very thin, geriatric cat? |
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Definition
| In animals with severe muscle wasting, less creatine may be produced. |
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Term
| What are the unique serum abnormalities with horses with CKD? |
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Definition
| Hypercalcemia, normo- to hypophosphatemia (opposite from most species). |
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