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116 Cards in this Set
- Front
- Back
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This is the most common kidney disease in dogs and cats |
CKD |
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What is meant by the term kidney failure? |
it is the level or organ dysfunction not a specific disease |
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What is kidney insuffiencey |
kidney dysfunction but at a level that is less severe than failure |
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What is azotemia |
abnormal concentration of BUN/Creat and other nonprotein substances. A labratory finding |
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Uremia is defined as |
1. abnormal quantities of urine in the blood by primary kidney disease 2. polysystemic toxic syndrome which results from abnormal kidney function |
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What is the best way to determine overall kidney function? |
GFR |
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Stages of Canine Chronic kidney disease Stage 1 |
Creat <1.4 mg/dL nonazotemic |
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Stages of Canine Chronic kidney disease Stage 2 |
Creat 1.4-2.0 mild azotemia |
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Stages of Canine Chronic kidney disease Stage 3 |
2.1-5.0 mg/dL moderate azotemia |
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Stages of Canine Chronic kidney disease Stage 4 |
Creatanine >5.0 mg/dL severe azotemia |
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Stages of Feline Chronic kidney disease Stage 1 |
Creatinine <1.6 mg/dL nonazotemic |
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Stages of Feline Chronic kidney disease Stage 2 |
Creat 1.6-2.8 mg/dL Mild azotemia |
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Stages of Feline Chronic kidney disease Stage 3 |
2.8-5.0 mg/dL Moderate renal azotemia |
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Stages of Feline Chronic kidney disease Stage 4 |
Creat >5.0 mg/dL Severe azotemia |
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This breed of dog has higher concentrations of creatinine. Why? |
Greyhounds athletic nature |
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What stage of CKD is considered chronic kidney failure? |
stage 4 |
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These two other tests influence prognosis and therapy with CKD |
proteinuria hypertension |
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What is the UPC ratio to be classified as proteinuric? |
>1.0 IRIS staging has it at >0.5 for dogs and >0.4 for cats |
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Minimal risk BP |
minimal risk If the systolic BP is < 150 DAP < 95 mmHg |
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moderate risk blood pressure |
moderate risk Blood pressure 160-170 mmhg Diastolic 100-110 |
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What was the most common cause via biopsy findings for dogs with CKD |
chronic tubulointerstitial nephritis (58%) glomerulonephropathy (28%) amyloidosis(6%) |
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What was the most common cause via biopsy findings for cats with CKD |
tubulointerstitial nephritis (70%) glomerulonephropathy (15%) LSA (11%) amyloidosis (2%) |
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UTI occur with CRF due to...
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UTI secondary to the immunocompromise secondary to renal failure
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What vaccines have been administered to cats that have resulted in antifeline renal tissue ABs? |
FHV-1 calicivirus panleukopenia
grown in feline tissue culture |
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How long do cats with stage 2 &3 CKD survive?
Dogs with stage 3 |
1-3 years
6-12 months |
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Increase in what test has shown to increase risk of uremic crises and death in dogs with CKD?
Cats? |
hypertension
No correlation has been made yet |
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This finding has been implicated in the progression of renal injury and TX may stabilize renal function in humans and dogs |
proteinuria ACEI |
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What is an anorectic factor? |
a rodent model has suggestived that uremia suppresses appetite |
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How does uremia stimulate vomiting? |
unidentified uremic toxin on the medullary emetic CRTZ and uremic gastroenteritis |
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What has been implication in development of uremic gastropathy? |
elevated gastrin levels. Gastrin indcuced gastric acid secretation by stimulating receptors located on gastric parietal cells |
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Dogs with this type of renal disease are at increased risk for hypertension |
glomerular disease |
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How common are neuromuscular diseases with uremia? (%)
Such as? Prognosis? |
65% metabolic encephalopathies (altered consciousness & seizures) - poor prognosis and peripheral neuropathies (limb weakness, ataxia & tremors) |
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Pathogenesis of uremic neurological signs? |
uncertain, possibly PTH and the uremic enviroment are suspected |
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What is an example of CKD causing a myopathy? etiology |
hypokalemia generalized muscle weakness |
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Pathogenesis of hypokalemia causing generalized muscle weakness? |
potassium influences resting cell membrane potentials hypokalemia increases the magnitue (increases electronegativity) of the resting potential. Results in hyperpolarizing of the cell membrane making it less sensitive to exciting stimuli |
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List the two common hematological consequences of CKD. |
Anemia hemorrhage due to GI bleed |
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What type of anemia occurs with CKD? Why? |
normochromic normocytic
Due to hypoplasia of the erythroid precursors in the bone marrow Severity related to the severity of CRF |
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What are some compensatory mechanisms when Hct becomes very low? |
Increased CO lowered peripheral vascular resistance |
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What is the hormonal cause of anemia with CKF (besides blood loss)?
Where is it produced? |
erythropoietin deficiency
produced in the peritubluar fibroblasts of the renal cortex |
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What stimulates erythropoietin syntheis? |
on demand in response to intrarenal hypoxemia (due to anemia or hypoxia) |
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What is thought to happen with CRF causing erythropotein defiency? |
decreased renal mass and cannot produce enough hormone |
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How dose renal failure contribute to GI bleeding? (Coagulation)
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causes platelet dysfunction
abnormalities between platelets and vessel walls abnormal platelet aggregation abnormal platelet adhesion |
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How is DDAVP (desmopressin) used for TX of GI bleeding secondary to CKF? |
stimulate release of von Willebrands factor complexes. Only works for 2-3 doses before side effects |
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What are the multifactorial effects causing hyperparathyroidism in CKD? (5)
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phospherous retention
hyperphosphatemia low circulating 1,25-dihydroxyvitamin D (calcitriol) reduced ionized calcium levels skeletal resistance to calcium action of PTH |
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Calcitriol aka |
1,25-dihydroxyvitamin D |
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Where is calcitriol formed in the body?
Enzymatic action? |
renal tubular cells
1 alpha-hydroxylation of 25-hydroxycholecalciferol |
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How dose calcitriol affect the PTH synthesis?
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negaive feedback |
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How dose CRF interfere with calcitrol synthesis? |
high phospherous in the renal tubular inhibits 1 alpha hydroxylase activity limiting calcitrol production.
Reduced calcitrol synthesis losses negative feedback, promotes renal secondary hyperparathyroidism |
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What aged animals is renal hyperparathyroidism most significant?
What happens to these animals? |
young growing animals
mandibule and skull demineralization - rubber jaw, movable teeth |
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What on physical exam maybe noted for renal hyperparathyroidism? |
paratracheal mass |
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How can renal seconday hyperparathyroidism be diagnosed?
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Plasma PTH levels
two site immunoradiometric using a two site immunoradiometric assay |
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Why do CKF have metabolic acidosis? How does the body try to compensate? |
Unable to excrete hydrogen (compensate by increasing the qty of ammonium excretion) reduced bicarbonate absorption |
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This enzyme relates well to the clinical signs of uremia |
BUN |
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How does PTH affect phospatemia? |
Increased PTH promote renal exretion of phosporous by decreasing P reabsorption in the proximal tubule, but will lose this adaption as CKF progresses |
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What is the equation for calcium phosphate product? |
Ca x Po4 (mg/dL) |
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What must the calcium product exceeded for calcium to precipitate.
Where does it precipitate? |
>70
arteries joints soft tissue
esp. prominant in proton secreting organs - stomach and kidneys |
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What is mineralization due to elevated calcium-phosphate product called? |
metastatic calcification
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Why is serum total calcium not reflective of ionized calcium concentrations? |
Get serum total hypercalcemia with normal to reduced blood ionized calcium - possibly due to increased concentrations of calcium complexed to retained organic and inorganic anions |
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If hypercalcemia is present, how can it be determined if CRF caused it or is secondary to it? |
- hypercalcemia due to malignancy or hypervitaminosis D is likely to induce renal failure. - measure ionized calcium - high ionized hypercalcemia will cause renal falure.
- secondary hyperparathyroidism will have normal iCa |
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Why do CRF have hypermagnesmia? |
magnesium is primarily excreted by the kidneys |
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What is the mechanism for hypokalemia for cats wtih CRF? |
mechanism unsure, but decreased intake and increased loss |
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What occurs at the glomerulus with CKD? |
- intraglomerular hypertension (secondary to systolic hypertension. - results in glomerular hyperfiltraation to maintain the total GFR as nephrons are lost |
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What occurs with the glomerulus and hypertension with glomerular disease?
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intraglomerular hypertension occurs dur to reduced permeability of the glomerular capillary walls to small solutes and water. The fall in GFR causes increase in intraglomerular pressure
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How does proteinuria occur with intraglomerular hypertension?
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impairs glomerular permeselectivity resulting in proteinuria
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What happens at the levels of the glomerular capillaries with CRF and hypertension |
reduced kidney function causes a preglomerular vasodilation that permits transmission of systemic hypertension to the glomerular capillaries |
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This has been found to progress CKF in dogs, but not yet in cats? |
proteinuria |
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How can ACEi protect the kidneys (MOI) (3)
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- enhancing interstitial O2 delivery through dilating the efferent arterioles, reducing vascular resistance, and improving microvascular flow through the interstitium.
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How are renal diets different than maintenance diets? |
reduced protein reduced Phosp reduced Na increased B -vitamin increased calorie content increased omega 3 polyunsaturated fatty acids
Feline diets have additional potassium |
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How long do kidney diets help in survival compared to maintenance diets?
Dogs? Cats? |
Dogs live 13 months longer Cats 13 months longer |
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What IRIS stage should dietary therapy be implemented? |
data supports 3 &4, but IRIS recommends stage 2. |
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Drugs that are excreted in the kidney's should have their dose _____ as renal function declines. |
reduced |
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List nephrotoxic drugs (12) |
amikacin amoxicillin amphotericin B gentamicin kanamycin neomycin streptomycin sulsoxazole tetracycline torbramycin TMS |
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These drugs should be avoided in advanced renal failure |
chloramphenicol TMS |
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How does renal secondary hyperparathyroidism occur? |
Get xs. secretion of PTH in response to a low calcium. Kidneys do not convert Vit D3 to its active form and unable to excrete xs phospherous it forms an insoluable Ca/P. Calcium is removed from ciruculation and get low calcium resulting in PTH secretion and secondary hyperparathyroidism. |
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What stage does renal hyperparathyroidism become a problem |
3 or 4 |
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Do dogs and cats have clinical signs of renal secondary hyperparathyroidism? |
rarely linked to clinical signs |
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Bottom line best way to limit secondary hyperparathyroidism and prolong survivial |
limit hyperphosphatemia |
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How do you limit Phoshorus to control secondary hyperparathryoiridism?(2) |
dietary restriction of phosphorus intestinal phosphorus binding agents |
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What is the serum phosphorus concentration goal? |
bring serum phsophorus within normal range |
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When dietary change alone cannot control phosphorus, what can be added and some examples of this |
phosphorus binding agents aluminum based exchange compounds ** OTC calcium based exchange compounds can cause hypercalcemia - monitor |
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Besides aluminum and calcium based exchange compounds, this can also be used to control hyperphosphatemia.
Side effects? |
cationic polymer agent sevelamer hydrochloride (Renagel)
Vit K deficiency |
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What is the suspected MOI of how low potassium exacerbates kidney disease |
- low potassium may result in reduced renal blood flow and GFR secondary to ANG II causing renal vasoconstiriction - promotes polyuria by impairing renal response to ADH - low potassium may result in increased ANG II release |
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How long until resolution of muscle weakness with postassium supplementation? |
1-5 days |
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During TX of renal disease and diuresis, what needs to be monitored in cats? |
postassium supplement |
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When should TX be instituted for metabolic acidosis and list the TX options. |
Plamsma bicarbonate levels remaine below 15 mmol on more than 1 occasion
diet sodium bicarbonate postassium citrate |
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Although there are no conclusive studies in dog about arterial hypertension TX ( will prevent or amerolate renal or extra renal complications), what has been found in cats?
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elevated blood pressure promotes renal injury in cats
TX is warrented |
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What blood pressure number should TX be started? HOw whould it be obtained? |
>160/100 mmHg after 3 clinic visits then should be started on TX |
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What is the goal of hypertensive therapy?
How long may it take to achieve this? |
get BP below 160/100 mmHg
weeks to months |
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How much does amlodipine reduce systolic blood pressure by? |
30-50 mmHg |
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What are some TX options for GI blood loss secondary to CRF? |
H2 receptor antagonists sucralfate |
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This is a common cause problem in dogs and cats with CRF and can be due to inadequate intake or loss due to GI bleed |
iron defiency |
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Why is it important to determine iron deficency (Gi bleed) vs. anemia of chronic disease |
ACD will not improve in response to iron supplementation |
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TX for iron defiecency anemia What other condition can it be used to TX? |
oral ferrous sulfate iron-deficient erythropoetiesis in patients starting erythropoietin replacement TX
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How can iron defiency be diagnosed? |
difficult serum iron levels stainable iron content in bone marrow (normal w/ ACD and low with Fe anemia) |
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What changes in chemisty/CBC may be indicative of occult GI blood loss? |
iron defiency microcytosis elevation in BUN/Creat ratio |
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What happens to RBCs life span with advanced CKF? |
decreased |
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TX options for anemia secondary to CRF?(3) pros and cons TX of choice |
anabolic steriods (work in a small % of patients) blood transution hormone replacement therapy - rHuEPO |
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At what Hct level is rHuEPO instituted? |
20% or when C/S are attributable to anemia |
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How long does it take rHuEPO to take effect? |
2-8 weeks |
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What can occur if the dosage of rHuEPO continually needs to be increased/axed out? |
erythropoietin resistance |
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Why must iron be supplemented for rHuEPO TX? |
high demand for iron |
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Adverse affects to rHuEPO TX? |
hypertension seizures local reactions at injection site developement of Ab |
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What is the most important complication of rHuEPO? |
refractory anemia and hypoplasia of the bone marrow due to Antibodies probably reversable when stop rHuEPO |
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This medication is the primary TX for renal secondary hyperparathyroidism |
calcitriol |
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What serum concentration must be reduced prior to calcitriol TX? Why? |
serum phosphorus
high phosphorus may inhibit the effectiveness of calcitriol TX and enhance renal mineralization |
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This RX rapidly and effectively suppresses renal secondary hyperparathyroidism |
calcitriol |
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How are ACEi renoprotective (2) |
- blood pressure -suppressing renal ANG1-ANG2 (ANG2 may have detramental effects on the kidneys) |
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Selective blockade of this hormone in addition to renine-angiotension system helps reduce proteinuria and glomerular disease. |
Aldosterone |
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This is a aldosterone-receptor antagonists |
eplernone |
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Hypertensive with no complications is defined as HNC
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BP > 160 with no C/S
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Hypertension with complications is defined as HC
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BP>150 with C/S
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Hypertension with complications is defined as HC
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BP>150 with C/S
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Borderline hypertension is defined as BH
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150-180 with no C/S
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Hypertension with complications is defined as HC
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BP>150 with C/S
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Borderline hypertension is defined as BH
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150-180 with no C/S
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No hypertensive is defined as
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BP < 150
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