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167 Cards in this Set
- Front
- Back
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Renal tight junction transport is (paracellular/transcellular), and is considered (passive/active) transport
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Paracellular; Passive
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Is the majority of the active transport component of principal cells carried out on the apical or basolateral membrane?
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Basolateral
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Approximately how much of the filtered sodium is reabsorbed by the proximal tubule?
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About 2/3
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What is the main sodium transporter in the early proximal tubule?
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Na/H exchanger (Along with various Na-solute cotransporters)
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In the late proximal tubule, what ion is sodium absorption linked to (via a complicated exchange pathway)?
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Chloride
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Does more transcellular sodium reabsorption occur in the thin or thick ascending limb of the loop of Henle? What transporter is used?
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Thick; Na/K/2Cl triporter
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Sodium-reabsorbing cells in the collecting duct are known as what?
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Principal cells
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What is the main difference in sodium reabsorption between the collecting duct and the rest of the nephron? What benefit does this serve?
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In the collecting duct (and late distal tubule), sodium is not coupled to any other ion, absorption occurs through channels rather than a transporter. This system allows for intake-dependent variations in sodium excretion (i.e. you excrete what you eat)
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What two sections of the nephron exhibit hormone-dependent sodium reabsorption (i.e. antinatriuresis)? Which hormones act on these sections?
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Proximal tubule (angiotensin II & norepinephrine receptors); Late distal tubule/Collecting duct (Aldosterone)
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Is angiotensin II considered a pronatriuretic or an antinatriuretic hormone?
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Angiotensin II stimulates sodium reabsorption, and thus is antinatriuretic.
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What effect does aldosterone have on the apical membrane of the collecting duct?
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It stimulates recruitment of sodium channels. (Also, it recruits basolateral transporters and mitochondria production)
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What hormone inhibits sodium reabsorption at the collecting duct?
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Atrial natriuretic peptide (& BNP)
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What is the target site for loop diuretics?
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Na/K/2Cl transporter on the ascending limb of the loop of Henle
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What two hormones primarily affect potassium intake into body cells?
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Insulin & Epinephrine
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Where is the majority of potassium reabsorbed in the kidney?
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Proximal tubule (~80%)
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Intercalated cells in the collecting duct have what effect on potassium concentration?
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They are responsible for potassium reabsorption
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Increasing tubular flow will have what effect on potassium secretion/excretion?
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Increase secretion due to lack of concentration gradient and increased sodium influx stimulating Na/K pump
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What two segments of the nephron are naturally water-permeable?
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Proximal tubule; Descending limb of the loop of Henle
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How does water get reabsorbed from the thin descending limb despite a lack of sodium reabsorption?
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Sodium is reabsorbed in the ascending limb, and this sodium enters the interstitium between the ascending and descending limbs, causing a gradient and promoting the absorption of water from the descending limb
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What hormone is primarily responsible for promoting water reabsorption? What sections of the kidney does it effect?
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Antidiuretic hormone; Affects the late distal tubule and collecting duct
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Which segments of the nephron are never water permeable?
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Ascending limb & early distal tubule
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How is total body water calculated?
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0.6 * body weight (kg) - 0.5 or 0.6 can be used depending on gender/source
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How much of our total body water is ICF? How much is ECF?
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ICF: 2/3; ECF: 1/3
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Where is extracellular fluid located?
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Interstitial fluid (3/4) & Plasma (1/4)
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How does approximate plasma osmolarity relate to sodium concentration?
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Plasma osmolarity ~= 2x sodium concentration (i.e. a sodium concentration of 145 will yield a plasma osmolarity of about 290). The reason it is 2x sodium is that chloride is present in equal amounts
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Plasma osmolarity is mainly governed by which two factors?
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Changes in water intake (thirst); Changes in water excretion (ADH)
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Where is ADH produced?
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Hypothalamus (released from posterior pituitary)
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330 mOsm/L
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280 mOsm/L
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In what two ways can the sympathetic nervous system affect the kidney to increase blood pressure?
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Renin release (RAAS activation); Norepinephrine targets on the proximal tubule increase sodium reabsorption
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Where is angiotensin converting enzyme produced?
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Lungs (and possibly the kidney)
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How does increased carbon dioxide lower pH?
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CO2 combines with water to form carbonic acid, which dissociates into hydrogen and bicarbonate.
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What is the main buffer found in extracellular fluid?
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Bicarbonate
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How is a buffer defined?
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A compound which is both a hydrogen donor and acceptor
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What is the point where equal amounts of hydrogen donor and hydrogen acceptor exist? (In a buffer solution)
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pK
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What is the Henderson-Hasselbach equation? What does it tell us?
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pH = pK + log([A-]/[HA]); Given concentrations of hydrogen donors and acceptors in a buffered solution, we can tell the pH of that solution
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What enzyme speeds the conversion of carbonic acid to CO2 + Water?
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Carbonic anhydrase
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How do you convert the partial pressure of carbon dioxide into a concentration?
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Multiply by 0.03
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How much of the filtered bicarbonate is reabsorbed by the normally-functioning kidney?
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All of it!
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Secretion of hydrogen ions in the proximal tubule allows for the reabsorption of what compound?
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Bicarbonate (Indirectly, by converting to CO2)
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Renal metabolism of glutamine results in the formation of which two compounds?
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Bicarbonate & Ammonium
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A change in PCO2 is likely due to a (respiratory/metabolic), while a change in HCO3 is likely due to a (respiratory/metabolic) cause
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PCO2: Respiratory; HCO3: Metabolic
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Is decreased pH coupled with decreased bicarbonate concentration metabolic or respiratory acidosis?
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Metabolic
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What three components make up the glomerular filtration barrier?
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Capillary endothelium; Basement membrane; Podocytes
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Are anionic solutes more readily filtered than cationic solutes at the glomerulus?
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No, cations are more regularly filtered, as the barrier has a negative charge associated with it
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What is the primary reason that albumin is not filtered across the glomerulus?
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Despite being a small protein, it is negatively charged and thus has a difficult time crossing the glomerular barrier
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Which starling force is the greatest promoter of filtration?
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Hydrostatic pressure within glomerular capillary (60 mmHg)
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Which two Starling forces promote filtration? Which two oppose filtration?
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Promote: Hydrostatic pressure within the glomerular capillary, Oncotic pressure within Bowman's capsule (though in reality this is 0); Oppose: Hydrostatic pressure within Bowman's space, Oncotic pressure within the glomerular capillary
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What is the approximate normal upper limit for creatinine in an adult male? In a female?
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Male: 113; Female: 96
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What is a normal GFR for adults?
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About 180 L/day
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What is the formula for Creatinine clearance? (Cockcroft-Gault)
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CrCl = [(140 - age) * Lean body weight (kg)]/[sCr (umol/L)]
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As kidney function declines, how does CrCl-dependent estimation of GFR change? Why?
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As renal function declines, CrCl overestimates GFR. Tubular secretion of creatinine increases as GFR decreases, and thus CrCl becomes less dependent on filtration at the glomerulus
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The presence of dysmorphic red blood cells in the urine is likely due to damage in what region of the nephron?
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Glomerulus
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Red blood cell casts in the urine are indicative of damage to what region of the nephron?
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Glomerulus
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In the presence of microscopic proteinuria, what two benign causes are important to rule out?
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Heme & Myoglobin
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What is the first thing to do once hematuria is detected in the urine?
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Repeat to ensure persistence
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What is normal daily urine protein excretion?
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< 150 mg/day
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What is the gold standard following a positive dipstick for proteinuria?
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24h urine collection
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Pathologic proteinuria is most often due to dysfunction in what region of the nephron?
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Glomerulus
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How is orthostatic proteinuria diagnosed?
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24h split urine collection (day/night)
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What are the main factors in diagnosis of nephrotic syndrome?
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>3 g/day proteinuria; Hypoalbuminermia; Edema (Also: Hyperlipidemia, thromboembolism & infection)
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Why does hyperlipidemia occur as a result of nephrotic syndrome?
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In the setting of hypoalbuminemia and decreased oncotic pressure, the liver produces both albumin and lipoproteins
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Why is thromboembolism associated with nephrotic syndrome?
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Loss of endogenous anticoagulants Antithrombin and plasminogen can occur with nephrotic syndrome (presumably through urine)
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Fatty casts with a maltese cross appearance is indicative of what kidney condition?
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Nephrotic syndrome
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What drugs have been implicated in causing nephrotic syndrome?
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NSAIDs, Gold, Penicillamine, Heroin
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Is IgA nephropathy more typically associated with a nephrotic or nephritic picture?
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Nephritic
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What is the traditional definition of acute renal failure?
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Abrupt elevation of serum creatinine (>50% rise above baseline)
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What does RIFLE stand for?
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Risk; Injury; Failure; Loss; Endstage kidney disease
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What is the first step in assessing acute kidney injury?
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Determining if it is a prerenal, intrarenal or postrenal cause
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What are some examples of pre-renal acute kidney injury?
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Decreased intravascular volume (Bleeding); Decreased cardiac output (CHF); Increased renal vascular resistance (NSAID); Vasoconstricting drugs (Cyclosporin, contrast); Decreased intraglomerular pressure (ACEi/ARB)
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What are some examples of post-renal acute kindney injury?
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Bilateral ureteric obstruction (stones, clot, cancer); Bladder neck obstruction (prostate cancer/BPH)
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Which RIFLE severity category would a 5-day abrupt increase of 100% in serum creatinine fall into?
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Injury
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How long does kidney loss/irreversible AKI have to occur for to fall into the 'loss' category of RIFLE?
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4 weeks or more
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In the setting of acute kidney injury, anuria for 14 hours coupled with a 45% decrease in GFR would fall under which RIFLE category?
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Failure. Even though a 45% decrease in GFR only falls within the 'risk' category, anuria over 12 hours falls into the 'failure' category, and the most severe category is the one chosen
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Chronic kidney disease is kidney injury which lasts for how long?
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3 months
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What are some standard blood tests to order for acute kidney injury?
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Creatinine, urea, electrolytes, calcium, phosphate, albumin, CBC (Also, serologies and special tests depending on clinical suspicion)
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What is the most common type of acute kidney injury in hospitalized patients?
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Acute tubular necrosis (50% of hospitalized patients with AKI)
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What are the two main causes of acute tubular necrosis?
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Ischemia & Toxins (Exogenous & Endogenous)
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What is the pathology of acute tubular necrosis?
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Loss of brush border, flattening of epithelium, loss of polarity, relocation of ATPase & integrins to apices, loss of tight junctions, Intratubular cast formation
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The presence of muddy brown casts in urine is pathognomonic for which condition?
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Acute tubular necrosis
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What are the three clinical phases of acute tubular necrosis?
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1. Initiation & maintenance; 2. Diuretic/polyuric; 3. Recovery
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Why does diuresis and polyuresis occur during mid-stage acute tubular necrosis?
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Regeneration of undifferentiated tubular epithelial cells and tubular debris phagocytosis encourages water excretion (i.e. self-repair)
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What percentage of patients will recover at least partially from acute tubular necrosis? If admitted to the ICU, what percentage of patients will not survive?
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90% recovery in general; 50% mortality if admitted to ICU
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What are the five most common causes of acute interstitial nephritis?
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Drugs; Malignant infiltration; Glomerulonephritis; Pyelonephritis; Autoimmune disorders
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Acute interstitial nephritis caused by drugs is known as what?
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Allergic interstitial nephritis
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A patient presents to the ER with a rash and fever. History is significant for Allopurinol and aspirin use. Urinalysis reveals WBC casts and mild proteinuria. Ultrasound is normal. What is the most likely site of injury to the kidney?
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Likely allergic interstitial nephritis (caused by drug exposure)
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How do NSAIDS reduce glomerular filtration? How do ACE inhibitors affect it?
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NSAIDs impair the function of vasodilatory prostaglandins in the afferent arteriole; ACEi's inhibit angiontensin II-dependent vasoconstriction of the efferent arteriole
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The clinical triad of AKI, eosinophilia and livedo reticularis is classic for which renal vascular condition?
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Cholesterol emboli (Atheroembolic renal disease)
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One of the definitions for chronic kidney disease is defined as a glomerular filtration rate less than what?
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< 60 ml/min (~90 L/d)
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What is the serum creatinine rule of thumb for estimating GFR?
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GFR falls by 50% as sCr doubles
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Do creatinine-based methods of estimating GFR overestimate or underestimate GFR in someone with a large amount of muscle mass?
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Underestimates (due to intrinsically high Creatinine)
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What is an ultrasound hallmark of chronic medical renal disease?
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Loss of corticomedullary differentiation
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What two factors are considered when staging chronic kidney disease according to the national kidney foundation?
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eGFR & Proteinuria/structural disease
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Stage 3 CKD is defined as an eGFR of below what?
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60
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Is an eGFR of 65 with no evidence of proteinuria or structural disease considered chronic renal failure?
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No, this is possibly normal in some people. The presence of proteinuria would put the patient in stage 2
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What are the four most common modifiable risk factors for developing chronic kidney disease?
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Hypertension; Diabetes; Obesity; Smoking
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Aside from diabetes, hypertension, heart failure and vascular disease, what four groups of patients should be tested for CKD?
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Patients with unexplained anemia; FHx of ESRD; First nations peoples; Inflammatory diseases (RA, etc)
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What is the target blood pressure for people with chronic kidney disease?
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130/80
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Which class of antihypertensive agent is also useful for reducing proteinuria?
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ACE inhibitors
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Why can anemia occur with renal failure?
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Reduced erythropoietin production in the kidney limits red blood cell formation
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What calcium/phosphate abnormalities can you get with chronic renal disease? What problems can this cause?
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Low serum calcium (due to reduced active vitamin D); High serum phosphate (due to decreased renal excretion) - This put the patient at risk for secondary hyperparathyroidism and osteomalacia. Calcification of the blood vessels can also occur
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How can you help prevent progression of metabolic bone disease secondary to renal failure?
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Phosphate binders; Calcium (Calcium carbonate can affect both of these issues); Vitamin D
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The constellation of signs and symptoms found with endstage renal disease is collectively known as what?
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Uremia
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What are two access routes for hemodialysis?
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AV fistula; Central tunneled catheter line
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What are some complications of hemodialysis?
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Infection; Access thrombosis; Central venous stasis; Bleeding; Hypotension
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What is used as a filter in peritoneal dialysis?
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Peritoneal membrane
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What are the two categories/uses of drugs used post-renal transplant?
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Induction & Maintenance agents
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What are some complications post-renal transplant?
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Graft loss; Infection; Cardiovascular disease; Malignancy
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How do you assess internal consistency in an approach to acid-base disorders?
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Henderson equation: [H+] = 24*(PCO2/HCO3). If > 10% error, something is incorrect
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What is the pH range for which the rule of thumb for estimating [H+] will work?
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7.25 - 7.55
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What is the rule of thumb for calculating [H+] from pH?
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Drop the 7 and decimal point, subtract remainder from 80. Gives the answer in nM
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Overproduction of acids leads to a (normal/elevated) anion gap metabolic acidosis, while loss of NaHCO3 leads to a (normal/elevated) MA.
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Overproduction of acids: Elevated; Loss of NaHCO3: Normal
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What is the formula for calculating anion gap (ignoring potassium)
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[Na+] - [Cl-] - [HCO3-] = 12 +/- 2 mM
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How do you correct anion gap calculations for changes in albumin?
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For each decrease of albumin of 10, the normal AG decreases by 4
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How should the change in anion gap relate to the change in HCO3 in anion gap metabolic acidosis?
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The Gap/Gap ratio should be 1:1
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How do you calculate the osmol gap?
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Calculated osm = (2*Na) + urea + glucose
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What can cause an increased osmol gap with acidosis?
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Methanol, Ethylene glycol, Diabetic ketoacidosis, Alcoholic ketoacidosis, Lactic acidosis
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What does the presence of HCO3 in the urine in the setting of metabolic acidosis imply?
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There is something wrong with the kidney - renal tubular acidosis
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What is the formula for calculating expected NH4+ excretion?
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NH4+ = 0.5 (measured Uosm - Calculated Uosm)
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Outline a basic approach to diagnosing acid-base disturbances
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1: Is there internal consistency?; 2: What is the major/primary disturbance?; 3: Is there appropriate compensation for the major disturbance?; 4: What is the anion gap?; 5: Additional tests (urine net charge, osmol gap)
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What are the two possible disruptions in the generation phase of metabolic alkalosis?
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Loss of acid or gain of HCO3-
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How can vomiting cause metabolic alkalosis?
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Vomiting of hydrochloric acid prevents the later elimination of HCO3-, and thus it builds up in the body
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What is an approach to metabolic alkalosis?
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ECF volume assessment; Labs (ABG, Lytes, RAAS)
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Recent vomiting will have what effect on urine sodium, potassium and chloride?
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Increased sodium and potassium (due to HCO3- buildup in blood), decreased chloride (HCl is vomited out)
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Recent diuretic use will have what effect on urine sodium, potassium and chloride?
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It will cause an increase in all three electrolytes
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How does acetozolamide help in removing HCO3- from the body in cases of metabolic alkalosis?
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It inhibits carbonic anhydrase in the kidney, and causes you to lose HCO3- in the urine
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Which is better, PC or Mac?
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PC, obviously.
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What are four things to think about when evaluating etiologies for potassium disorders?
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Pseudo; Intake; Shift (ECF/ICF); Excretion
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What effect does insulin have on ECF/ICF potassium concentrations?
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Insulin will shift potassium from the ECF to the ICF
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What effect does alpha-adrenergic stimulation have on ECF/ICF potassium concentrations?
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Alpha agonists will inhibit the Na/K ATPase and shift potassium out of the ICF
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How can we decrease potassium secretion?
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Amiloride (closes luminal sodium channels); Spironolactone (aldosterone competitive antagonist); Digitalis; NSAIDs
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What is the formula for transtubular potassium gradient? What is its use?
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[Uk/{Uosm/Posm}]/Pk
It is used to estimate the driving force for K excretion at the level of the collecting duct - to assess appropriate aldosterone activity at the principal cells |
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What is an appropriate TTKG for hyperkalemia? For hypokalemia?
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Hyperkalemia: >8; Hypokalemia: <3
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What are some ECG findings for hyperkalemia?
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Early: Arrhythmias, conduction defects, peaked T waves; Mid: loss of P-waves; Late: QRS prolongation and conduction blocks
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Are catabolic states associated with hyper or hypokalemia? What are some examples?
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Hyperkalemia; Tumor lysis syndrome, burns, rhabdomyolysis, GI bleed
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How can you protect the heart from damage in acute hyperkalemia? What is its mechanism of action?
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Give calcium gluconate/chloride; calcium will increase the threshold potential and help prevent arrhythmias
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What are three pharmacological ways to shift potassium into cells?
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Bicarbonate; Glucose & insulin; Beta agonists (ventolin, albuterol)
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What are some options for promoting excretion of potassium from the body?
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Diuretics (Loop/Thiazide); Kayexalate; Dialysis
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What effect does metabolic alkalosis have on shifting potassium into/out of cells?
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There is a shift of potassium into the ICF, and thus can induce hypokalemia
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Will hyperaldosteronism cause increased or decrease serum potassium?
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It will cause decreased serum potassium due to increased sodium retention (I think?)
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Glycyrrhizic acid is found in what food? What electrolyte disorder can it cause?
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Licorice; Hypokalemia
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Why can administration of KCl for hypokalemia cause hypernatremia?
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K moves into cells, osmolality in cells moves up, water moves into cells and thus you get a mild hypernatremic state in serum
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Why is rapid fluid shift out of the brain dangerous?
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Fixing osmolar disorders too quickly can cause demyelination syndrome
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Hypernatremia will activate which two systems?
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Thirst center; ADH secretion
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Why can high blood sugar cause hyponatremia?
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Serum glucose can pull water from cells and cause hyponatremia, but not necessarily hypoosmolality
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What should you assess first in a patient with hyponatremia?
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Volume status
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What four conditions are associated with high-volume hyponatremia?
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Heart failure; Cirrhosis; Nephrotic syndrome; Advanced renal failure
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If hyponatremia occurs during pregnancy, what is usually the volume status?
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Typically normal volume status
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Profound hyponatremia in the setting of non-maximally dilute urine implies the presence of what compound?
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It is suggestive of the presence of ADH
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Gentamicin is notorious for causing what kidney condition?
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Acute tubular necrosis
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What are two forms of toxicity with aminoglycosides?
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Acute tubular necrosis (nephrotoxicity) & Ototoxicity (balance issues)
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Rhabdomyolysis is a side effect of what very common class of drugs?
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Statins
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If someone is going to be needing radiocontrast dye, what medications should be stopped temporarily?
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ACEi/ARB & NSAID
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What are some common medications (8) which can cause allergic interstitial nephritis?
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Beta-lactams; Sulfonamides; Quinolones; NSAIDs; Diuretics; PPI; Anticonvulsants; Allopurinol
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The release of what substance has been associated with cough in ACE inhibitor use?
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Bradykinins
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Daily use of combined analgesics (NSAID/Acetaminophen + codeine/caffeine) has been associated with what condition?
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Analgesic nephropathy
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Papillary necrosis has been associated with high medullary concentrations of what medication?
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Acetaminophen
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Lithium toxicity has been associated with what two glomerular conditions? (pathology)
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Minimal change disease& Focal segmental glomerulosclerosis
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Administration of which medication has been associated with nephrogenic diabetes insipidus?
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Lithium (Competes with ADH collecting tubules, decreases ADH response)
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What four biological factors should you consider when dosing drugs?
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Absorption; Distribution; Metabolism; Excretion
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What 11(!) drugs can accumulate in renal failure?
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Allourinol; Benzodiazepines; Chlorpropamide; Gabapentin; Gentamicine; Glyburide; Insulin; Lithium; Meperidine; Metformin; Morphine
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What is required for a diagnosis of hypertension?
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Persistent BP elevation on several office visits (2-5, depending on averaged BP and presence of other conditions). Also, an obvious hypertensive crisis requires only one visit
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What are some vascular changes present in chronic hypertension?
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Strucutral vascular change (increased total peripheral resistance, dysfunctional endothelium); Blunted baroreceptor response to HTN
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Obstructive sleep apnea has been associated with what cardiorenal condition?
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Hypertension
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What is renovascular hypertension? What are the two main causes?
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Hypertension secondary to renal artery stenosis - Causes: Atherosclerosis; Fibromuscular dysplasia (in young women)
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A 65-year old presents with sudden onset of hypertension, which is resistant to ACE inhibitors, diuretics and beta-blockade therapy. They have a 50 pack-year history of smoking, and an abdominal bruit on auscultation. What secondary cause of hypertension should we consider investigating?
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Renovascular hypertension (Technically, only two of these would suffice for suspicion, as well as pulmonary edema and a rise in creatinine with ACEi)
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What is a possible secondary cause of hypertension in someone who also has headaches, sweating and palpitations?
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Possible pheochromocytoma - do a 24-hour urine catecholamine metabolites screen
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What are typically first-line agents for treatment of hypertension?
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ACEi/ARB
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