Term
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Definition
-one of the most common extrarenal causes of renal failure (RF)
-25-50% of diabetics will develop end-stage renal disease within 20 years
-diabetic nephropathy is a progressive process resulting in multiple intrarenal changes including:
***intercapillary glomerulosclerosis, or scarring of the capillary loops
***progressive microangiopathy called nephrosclerosis effecting the afferent and efferent arterioles and eventually scars the glomerulus tubules and interstitium
***pyelonephritis (kidney infection)can scar the renal parenchyma and can lead to ischemia and renal papillary necrosis and sloughing of papillae
***neurogenic bladder dysfunction may lead to high incidence of UTI and back up of urine into the kidney
-silent phase-sclerosis increases renal vascular resistance, initially increasing the GFR up to 50%, however, can be diagnosed early if you look for microalbuminemia (measurable by assay)
-then, more nephrons are destroyed, leading to proteinuria (a key manifestation of RF), HTN and edema
-kidneys metabolize 30-40% of insulin, so as renal function declines, the Pt requires less insulin r/t increased levels circulating
-an increase in insulin reactions could signal a decrease in renal function
-in these patients, you should carefully control HTN, adjust insulin as needed and carefully monitor CBG's to maintain normal levels, and restrict dietary protein |
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Term
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Definition
-kidney dysfunction can cause HTN as a result of:
***renovascular hypertension (15% of cases)results from renal artery stenosis or renal infarction-this reduces renal blood flow-this activates the RAS system, increasing blood volume and increasing blood pressure
***(85% of cases)kidneys lose their ability to excrete Na and H2O and damage from glomerulonephritis, pyelonephritis, etc. can cause an increase in renin release-increase in circulating volume-increase in BP
-HTN can also cause renal failure by causing direct degenerative changes in the arterioles and interlobular arteries
-duration and degree of HTN is directly related to severity of renal vascular disease |
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Term
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Definition
-renal vasoconstriction reduces renal blood flow
-GFR remains at a functional level until the advanced shock, then ARF develops
-during the renal recovery phase p/ shock(2-8 weeks), an polyuric phase may occur and Pt's fluid and electrolyte status should be meticulously monitored |
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Term
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Definition
-disorder associated with traumatic muscle injury r/t surgery, crush injury, seizures, etc.
-also caused by heat stroke, prolonged coma, drug overdose, ar as a side effect of the prolonged use of statins
-clinical manifestations of rhabdomyolisis include fever, malaise, N/V, muscular weakness, muscle pain, and swelling, myoglobinemia and myoglobinuria (brown urine), hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia and then later hypercalcemia, and elevated creatinine
-treatments include sypmtomatic treatments like bedrest to decrease muscle metabolism, fluid volume maintenance, electrolyte maintenance, and in extreme cases, dialysis |
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Term
cardiovascular disease (CVD)
peripheral vascular disease (PVD) |
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Definition
-CVD influences kidney function primarily through cardiac output and circulating volume, hemodynamic and hormonal changes decrease the renal excretion of Na and H2O which causes a pathologic cycle of HTN
-normal aging causes a decrease in GFR, by age 70, GFR decreases 40-50%
-PVD causes complications like thromboembolic disease, causing infarctions and ischemia in the kidneys |
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Term
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Definition
-can cause things like acute tubular necrosis, defects in the tubular transport system, interstitial nephritis, vasculitis and nephrotic syndrome...acute tubular necrosis being the most common consequence
-some nephrotoxins include:
***antibiotics: aminglycosides, tetracyclines, amphtotericin B, cephalosporins, sulfanomides, bacitracin, polymyxin
***heavy metals- lead, mercury, bismuth, arsenic, copper, cadmium, gold, lithium
***poisons- mushrooms, insecticides, herbicides, snake venom
***anesthetics
***contrast dyes
***organic solvents- ethylene glycol, gasoline, kerosene, turpentine, tetrachloroethylene, carbon tetrachloride, trichlorethylene, chlorinated hydrocarbons
***analgesics- salicylates, acetaminophen, phenacetin, NSAIDS
***others- probenecid, phenytoin, heroine, dextran, mannitol, interleukin-2, cisplatin, amphetamines, and aristolochic acid
***diuretics over a long period of time can be nephrotoxic
-pre-existing renal disease, decreased renal blood flow, concurrent use of nephrotoxins, and electrolyte imbalances can all increase the toxicity of nephrotoxins
-carefully monitor renal labs on patients taking nephrotoxins and keep them weel hydrated as a high urine output keeps the medication dilute and avoids crystallization
-use nephrotoxins briefly and with as low a dose as possible to avoid complications
-ansthesia reduces the the kidney's vasoconstrictive abilities, making it more vulnerable to shock; it may also cause tubular necrosis
-contrast dyes cause tubular necrosis |
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Term
| uremia and/or uremic syndrome |
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Definition
| urine in the blood, describe a set of manisfestations that result in loss of renal function |
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Term
| sudden loss of kidney function happens with: |
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Definition
-damage from trauma
-damage from shock
-damage from toxins,
-or damage from acute glomerulonephritis |
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Term
| gradual loss of kidney function happens with: |
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Definition
-chronic glomerulonephritis
-HTN
-chronic pyelonephritis,
-or other diseases |
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Term
| minimum amount of urine output necessary for a healthy adult eating a normal diet to excrete toxins/waste products is: |
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Definition
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Term
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Definition
| daily outputs of urine between 100 ml and 400 ml |
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Term
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Definition
| daily outputs of urine less than 100 ml |
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Term
| ARF (acute renal failure) |
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Definition
process in which the kidneys abrubtly lose function (over hours to a few days, characterized by decreased GFR (glomerular filtration rate), increased BUN (blood urea nitrogen) and increased creatinine levels
-pathogenesis is unclear, but theory is that damaged tubules can't conserve sodium normally, which activates the RAS system, redistributing the renal vascular supply by increasing the tone of both afferent and efferent arterioles-the result is ischemia causing as increase in vasopressin, cellular swelling, inhibition of prostaglandin synthesis, and further stimulation of the RAS system-the resulting decreased renal flow causes decreased GFR and oliguria
-other theories involve tubular or basement membrane damage caused by various extrarenal processes |
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Term
| most common causes of ARF are: |
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Definition
| hypotension and prerenal hypovolemia |
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Term
| prerenal causes of ARF are due to decreased renal blood flow resulting from : |
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Definition
-shock
-circulatory volume depletion (diarrhea, vomiting, hemorrhage, excess diuresis, burns, renal salt-wasting conditions like traumatic brain injury, glycosuria)
-volume shifts as from 3rd spacing, vasodilation, or gram negative sepsis
-decreased cardiac output as from pericardial tompenade, acute pulmonary embolism, or cardiac pump failure
-decreased peripheral vascular resistance as from spinal anesthesia, septic shock, or anaphylaxis
-vascular obstruction as from bilateral renal artery stenosis or dissecting aneurysm |
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Term
| intrarenal causes of ARF involve parenchymal changes caused by disease or nephrotoxic substances like that which happens with: |
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Definition
-acute tubular necrosis (approx. 75% of cases of intrerenal failure, caused by nephrotoxins or impaired renal perfusion causing damage to the tubular epithelial cells)
-renal trauma
-a sudden release of large amounts of hemoglobin and myoglobin (rhabdomyolysis)due to muscle trauma (surgery, crush injury, electric shock)or severe muscle exertion
-genetic conditions (DM, malignant hypothermia)
-infectious disease
-rejection of inplanted kidney
-or metabolic conditions (hypokalemia, phosphatemia, heat stroke)
-glomerulonephritis
-microvascular and large vascular lesions as in hemolytic-urenic syndrome
-thrombosis
-vasculitis
-scleroderma
-atherosclerosis
-tumor invasion
-cortical necrosis as from prolonged vasospasms of cortical blood vessels |
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Term
| postrenal causes of ARF are due to an obstruction in the urinary tract, anywhere from the tubules to the urethral meatus, like that which happens in: |
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Definition
-prostate disease (BPH or prostate cancer)
-calculi
-invading tumors
-surgical errors
-urethral strictures or stenosis
-retroperitoneal fibrosis
-spinal chord injury leading to decreased bladder emptying resulting in a functional onstruction |
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Term
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Definition
-set of clinical manifestations caused by protein wasting secondary to to diffuse glomerular damage
-manifestations include proteinuria (> 3.5g/day), hypoalbuminemia, anemia, hyperlipidemia, and edema
-edema is usually the chief problem
-other complications include increase r/f infection, hypovolemia, thromboembolism, secondary aldosteronism, and abnormal thyroid function
-protein levels can drop 4-30g/day r/t proteinuria and albumin levels may drop as low as 1-2.5g/dl
-treat by miminizing protein loss, preventing thrombosis, maintaining F&E balance, and reducing inflammation in an effort to heal the leaking basement membrane
-give loop diuretics and albumin in an effort to decrease extracellular fluid
-check for hyperkalemia often
-skin care r/t edema is important |
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Term
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Definition
-refers to a set of clinical manifestations that include hematuria, and at least one of the following: oliguria, HTN, elevated BUN, or decreased GFR
-treatment includes management of underlying disease |
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Term
| clinical manifestations of ARF |
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Definition
-F&E imbalances (fluid overload or depletion, hyperkalemia, hyponatremia, hypocalcemia, and hypermagnasemia)
-acidosis
-increased r/f infection
-anemia
-platelet dysfunction
-GI complications (anorexia, N/V, diarrhea, constipation, and stomatitis)
-increased r/f pericarditis
-uremic encephalopathycharacterized by defective recent memory, dysarthria, tremors, convulsions and coma
-impaired wound healing |
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Term
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Definition
-(precipitating event -1wk)onset or initiating phase covers the precipitating event to the development of renal symptoms
-(1wk - 8wks) oliguric/anuric phase- the longer this phase the poorer the prognosis and may require dialysis
-urine output less than 400 ml/day
-urine has high specific gravity and osmolarity
-the BUN/creatinine ratio is significantly elevated, between 10:1 and 40:1
-(after and may be part of oliguric phase)non-oliguric/diuresis phase-gradual or abrupt return to glomerular filtration and leveling of the BUN signal this phase
-Pt's may excrete up to 2L/day
-urine is very dilute and is nearly iso-osmolar, has low specific gravity
-HTN, tachypnea, and signs of fluid overload are common
-may also show signs of extracellular fluid depletion such as dry mucous membranes, poor skin turgor, and orthostatic hypotension
-this phase has a better prognosis than does the oliguric/anuric phase
-25% of deaths occur in this phase so pay attention to fluid levels to thwart dehydration
-(3mos - 12mos)-recovery phase-slow return to activity level similar to that prior to the event
-can cause minor tubular abnormalities like glycosuria and decreased concentrating ability
-Pt is constantly at risk for F&E imbalances, especially during times of stress |
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Term
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Definition
-maintenance of F&E is key to survival in ARF
-fluid replacement volumes are typically based on a calculation/fraction of the previous day's UOP plus an amount (usually 400ml) to account for insensible losses-other losses such as those r/t vomiting and diarrhea are also added
-unles sthe Pt is on TPN, a weight loss of 0.2 - 0.5 lbs/day signifies a successful fluid replacement program
-Diuresis may be used cautiosuly with Lasix (nephrotoxic, so be careful and monitor labs) and/or mannitol.
-electrolyte replacement is based on urine and serum levels
-hyperkalemia is the most dangerous concern due to its relation to dysrhythmias-it levels elevate due to decreased ability of the kidneys to excrete, increase in tissue catabolism, and acidosis
-EKG's show the effects of hyper/hypokalemia and is treated appropriately (kayexelate or administering potassium prn)
-hyponatremia is typically due to dilution and should be treated as a fluid replacement issue
-magnesium is excreted through the kidneys and so levels elevate in ARF-high ganesium foods dark green veggies, unrefined grains, seeds, nuts, legumes, antacids and osmotic laxatives with high magesium levels should be avoided
-metabolic acidosis is typical due to decreased ability to excrete waste products-treat with sodium bicarb, sodium lactate or sodium acetate short term...dialysis for long term treatment |
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Term
| changes in drug metabolism in ARF |
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Definition
| -drugs which are normally excreted by the kidneys can accumulate to toxic levels in ARF, so particular attention needs to be paid to the absorption, distribution, metabolism and elimination of any drug given-nephrotoxic meds should be avoided if possible |
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Term
| general diet adjustments in ARF |
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Definition
-a high-calorie, low-protein diet is typically prescribed
-diet may also be low in sodium, magnesium, phosphate, and potassium may also be required depending on electrolyte levels
-adequate carbohydrate intake reverses the process of gluconeogenesis |
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Term
| protein intake recommendations in ARF |
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Definition
-protein must be of high biologic value (complete), containing the essential amino acids to reduce nitrogenous wastes products
-during the acute phases of ARF, intake should be 135 - 150 nonprotein kilocalories for each 6.25 g of protein
-liquid supplements and TPN with lipids may be used if oral intake is inadequate
-Pt's on dialysis should take in 1.2 gm of protein per kilogram of body weight/day |
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Term
| goals of medical management of renal failure |
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Definition
-prevent ARF
***preventative measures include remaining properly hydrated, and maintaining proper electrolyte balance through diet as much as possible
-maintain F&E balance
***see "managing F&E in ARF" flashcard
-replace renal function
***dialysis is frequently required
***CRRT or continuous renal replacement therapy may also be an option-involves removal of plasma water and dissolved contents from the Pt's blood across a membrane-there are 5 types of CRRT (see box 36.1, page 814 in Black for detailed description of each)
-prevent infections
***secondary infections are a significant cause of death in people with ARF
***use meticulous clean/sterile care, especially with catheters
***avoid indwelling urinary catheters
***treat aggressively
-monitor the client
***monitor F&E closely
***monitor for the manifestations of pericarditis (pericardial friction rub, pleuritic pain which may subside in an upright position, tachycardia, and fever)
***BUN elevations decrease seizure thresholds and seizures may occur necessitating treatment with IV phenytoin or phenobarbitol
***anemia is treated with tranfusions or rerecombinant erythropoietin
***bleeding tendencies may be corredcted with vitamin K replacement and and reducing BUN levels, as elevations onterfere with platelet aggregation
-maintain nutritional status
***see "general diet adjustments in ARF" and "protein intake recommendations in ARF" flashcards |
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Term
| pharmacologic support in ARF |
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Definition
-can include things like:
***kayexelate for hyperkalemia
***sodium bicarbonate, calcium, kayexelate, sorbitol, insulin with glucose all potassium ions for other cations and excrete potassium or push into the cells-typically used for acidosis
***low doses (1 - 5mcg/kg/min) of dopamine can be given to help dilate the renal arteries, increasing renal perfusion, urine output and sodium excretion
***diureses may be achieved through Lasix and Mannitol as necessary
***electrolyte replacement therapies may be indicated per serum levels
***antihypertensives are indicated if HTN is caused by excess of renin secretion due to ARF
***phenytoin and phenobarbitol for seizures prn
***transfusions and recombitant erythropoietin for anemia prn
***Vitamin K prn for clotting issues r/t ARF |
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