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FP board review > Nephrology > Flashcards

Nephrology Flashcards

0
Q

What can cause a false negative microalbumin to creatinine ratio?

A

“Patients with a large muscle mass have a high rate of creatinine excretion, which may result in a falsely negative microalbumin/creatinine ratio (as the”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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1
Q

What is the best way to screen for diabetic kidney disease?

A

Get a yearly Microalbumin to creatinine ratio. “Its advantages include ease of use, relatively low cost, and good correlation with 24-hour urine collections”

“A random spot urine microalbumin/creatinine ratio is normally less than 30 mg/g. Values above 30 mg/g are consistent with 24-hour measures showing abnormal amounts of micro albumin.

“Verification by repeat urine microalbumin/creatinine ratio is sufficient for a diagnosis of microalbuminuria, so 24-hour urine collections need not be performed for confirmation.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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2
Q

What can cause a false positive microalbumin to creatinine ratio?

A

“Fever, vigorous exercise, heart failure, and poor glycemic control can cause transient microalbuminuria, potentially resulting in false-positive microalbumin/creatinine ratios.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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3
Q

What information is necessary to diagnosed diabetic nephropathy in a early diabetic patient?

A

“The combination of diabetic retinopathy (a marker for diabetic renal disease), hypertension (BP >130/80 mm Hg in a diabetic patient), and abnormal protein in the urine as measured by the urine microalbumin/creatinine ratio is sufficient to make the diagnosis of early diabetic nephropathy.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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4
Q

In addition to withholding Metformin, what procedures could be followed to avoid contrast in induced nephropathy during a procedure?

A

“patients at risk of contrast-induced nephropathy, contrast studies should be avoided if possible. If a contrast study must be done, stop aggravating medications like non-steroidal anti-inflammatory drugs (NSAIDs). Hydration, usually with IV saline, should be given if there are no contraindications (e.g., heart failure). Nonionic lower osmolality (or even iso-osmolar) contrast agents should be used.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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5
Q

At what level would a BUN to creatinine ratio suggest a prerenal cause of azotemia?

A

>

  1. “These causes include dehydration and poor renal perfusion (shock such as sepsis, CHF, and hypotension). A BUN/Cr ratio <20 is suggestive of intrinsic renal disease or urinary outlet obstruction”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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6
Q

What are the types of renal tubular acidosis?

A

“The most common cause of RTA type 4 is hyporeninemic hypoaldosteronism, which is often seen in diabetic nephropathy. The disorder is recognized by hyperkalemia and mild acidosis. RTA types 1 and 2 usually are hypokalemic and these forms of RTA are not associated with diabetes. RTA type 3 is a rare autosomal-recessive disorder. RTA type 5 does not exist”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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7
Q

What is the treatment for a potassium that is greater than 7.5?

A

“A full court press: calcium, insulin, glucose, sodium polystyrene sulfonate (Kayexalate), nebulized albuterol, etc”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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8
Q

Why would you stop Metformin when the creatinine clearance is 1.4 to 2.0?

A

This represents a nearly 50% reduction in the GFR. “When creatinine clearance decreases, patients on metformin are at higher risk of developing the rare adverse effect of lactic acidosis. There is some evidence that patients with mild CHF or slight elevations in creatinine can safely take the drug, but stopping metformin in renal failure continues to be the standard of care”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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9
Q

Given a patients serum creatinine and age, how does one estimate the creatinine clearance?

A

“Estimated creatinine clearance = (140 – age [year])(body weight [kg])/(72 × (serum creatinine [mg/dL]))
For women, multiply this figure by 0.85”

“Normal for healthy adult is 94–140 mL/min for men and 72–110 mL/min for women.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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10
Q

What’s a normal bicarb level?

A

The normal level is 20 to 29 mEq/L. Lower than normal levels can indicate diabetic ketoacidosis, lactic acidosis, alcoholic ketoacidosis, kidney disease, renal failure, diarrhoea, Addison’s disease, ethylene glycol poisoning or methanol poisoning. Greater than normal levels can be seen with excessive vomiting, hyperaldosteronism and Cushing’s syndrome.

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11
Q

In a diabetic patient with nephropathy that unfortunately responds to ACE inhibitors and ARBs with hyperkalemia, what blood pressure medication can often help kidney function?

A

“Nondihydropyridine calcium channel blockers reduce protein excretion in diabetic patients with nephropathy and slow down the progression of renal disease.”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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12
Q

Sodium restriction added to an ACE inhibitor is actually more effective than adding an ARB for proteinuria and blood pressure control. T or F

A

True

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13
Q

What are the indications for dialysis in persistent renal failure from any cause?

A

Persistent nausea and “vomiting, pericarditis, fluid overload, uremic encephalopathy, accelerated hypertension, bleeding due to uremia, serum creatinine greater than 12 mg/dL, and severe electrolyte abnormalities that cannot be otherwise handled”

“Counter to what you might expect, early dialysis increases mortality. Do not initiate dialysis until the GFR is 5–7 mL/min/1.73 meters squared “or the patient is having clinical problems that cannot be otherwise managed”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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14
Q

What’s the different stages of chronic kidney disease?

A 
Stage 1	≥ 90, but known kidney damage
Stage 2	60 – 89
Stage 3	30 – 59
Stage 4	15 – 29
Stage 5	< 15
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15
Q

What is milk alkali syndrome?

A

“The diagnosis should be recognized by the triad of hypercalcemia, metabolic alkalosis, and renal insufficiency in combination with the history of typical symptoms (nausea, emesis, weakness, generalized confusion) and excessive calcium carbonate ingestion”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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16
Q

What is the treatment of milk alkali syndrome?

A

“Treatment includes removal of the offending agent and treatment of the hypercalcemia with IV saline (to improve renal perfusion and metabolic alkalosis)”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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17
Q

For a patient who is anemic and has chronic kidney disease, what is the target level for hemoglobin?

A

“Target levels should be about 10–11 g/dL. Higher hemoglobin levels are associated with a greater risk of adverse events, including increased risk of mortality, need for dialysis, CHF, graft thrombosis, uncontrolled hypertension, etc”

“FDA suggests withholding erythropoietin if the Hb >12 g/dL or if the Hb increases by >1 g/dL in any 2-week period”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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18
Q

In addition to red blood cells in the urine, what additional lab findings may indicate intrinsic renal disease?

A

“Intrinsic renal disease is more likely if there is proteinuria, hypertension, elevated serum creatinine, or an active urinary sediment (e.g., nephritic, dysmorphic red cells, red cell casts).”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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19
Q

What are the recommendations for evaluating microscopic hematuria?

A

“After microscopic hematuria has been identified (2 of 3 urine samples with 3 or more RBC/hpf), the AUA recommends the following evaluation:

Infection identified → treat with antibiotics and repeat urinalysis

RBC casts, proteinuria, or elevated creatinine → begin evaluation for glomerulonephritis and consider referral to a nephrologist

No infection or primary renal disease identified in first 2 steps → urine cytology, bladder cystoscopy (if at risk for bladder cancer based on environmental exposures and/or age >40), and CT scan (helical CT if stones suspected, contrast-enhanced CT if stones not suspected)

If entire thorough diagnostic evaluation negative → follow-up urinalysis, urine cytology, blood pressure, and serum creatinine every 6–12 months”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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20
Q

Was the recommendation of urine screens to detect hematuria?

A

“The USPSTF recommends against routine screening for microscopic hematuria to detect urinary tract cancers. In one-time urine specimens in healthy adults, the presence of abnormal numbers of RBCs (≥3 RBCs/hpf) can be as high as 39%. In up to 70% of patients, even after imaging of the upper and lower urinary tract, the source of microscopic hematuria cannot be found. In a low-risk population, the false-positive rate of microscopic hematuria found on urinalysis would be unacceptably high. Also, there is no evidence that early detection of bladder cancer through screening urinalysis improves prognosis”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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21
Q

What is the recommended treatment for kidney stone less than 5 mm That is found incidentally?

A

“Most stones less than 5 mm in diameter will pass spontaneously. No further intervention is warranted in asymptomatic patients”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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22
Q

For a patient who is nauseated and vomiting frequently and is experiencing renal colic probably due to renal kidney stones, what is the appropriate office management?

A

Send him to the ER. “This patient is nauseated and vomiting frequently and may not do well at home overnight. He may not be able to tolerate oral medications and could become dehydrated. Additionally, we don’t have a UA; a postobstructive UTI is an indication for admission and possibly stenting. For these reasons, the most appropriate action is aggressive pain management, which can be accomplished in the ED”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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23
Q

What size kidneys don’t requires what intervention?

A

“Stones of 6 mm or greater will pass spontaneously only 10% of the time and those 4–6 mm 50% of the time. Those less than 4 mm pass the great majority of the time. If pain persists or the stone does not pass within 72 hours, consider urologic intervention such as nephrostomy, stent placement, and lithotripsy. Renal injury from obstruction “generally does not occur for at least 72 hours (and, amazingly enough, there is only a 20% chance of complications if a nonobstructing stone remains for 4 weeks!).”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

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Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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24
Q

What’s the most useful information regarding future stone formation and prevention in a patient with urolithiasis?

A

Stone recovery and analysis

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25
Q

What are the different types of stones from urolithiasis?

A

“Struvite stones form during bacterial infections of the urinary tract and a urine culture will help direct therapy when these stones are identified.

Calcium oxalate stones are the most common and 24-hour urine collection to determine calcium and oxalate excretion can lead to diagnoses of metabolic disturbances (hyperoxaluria and hypercalciuria).

Patients with uric acid stones should be evaluated for symptoms of gout and undergo serum uric acid measurements”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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26
Q

What are the recommendations for dietary management of calcium palate stones?

A

“Restrict oxalate intake (e.g., leafy green vegetables,

Increased fluid intake to achieve a urine volume >2 L/day reduces stone formation. Water and citrus juices are traditionally recommended, but most fluids consumed are associated with a positive effect, including drinks with caffeine.

Meat, fish, and poultry are sources of purine, which is metabolized to uric acid. Auric acid crystal can form a pure uric acid stone or serve as a nidus for calcium stone formation. Therefore, a general recommendation to avoid recurrent urolithiasis is to reduce purines in the diet through reduced meat, fish, and poultry consumption”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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27
Q

What is the role of citrus fruits in urolithiasis?

A

“Urinary citrate inhibits calcium stone formation. Hypocitraturia is a common cause of recurrent urolithiasis. A nonspecific measure to decrease calcium stone formation is to increase citrus fruits in the diet. Lemonade and orange juice are excellent sources of citrate and can also be used to increase urine volume. However, the best studies suggest that lemon juice does not reduce stones from hypocitraturia and grapefruit juice increases stone formation”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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28
Q

Name 3 reasons to work up urolithiasis patients.

A

Family history of stone formation, black American, diarrhea, pending bariatric surgery.

“Patients of African ancestry are less likely to have stones. Anything that can cause malabsorption including bowel surgery, history of inflammatory bowel disease, etc., can increase the risk of stones. Thus, evaluation is indicated in these patients”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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29
Q

What is the treatment for hypercalcuria?

A

“Patients with urolithiasis and hypercalciuria benefit from long-term treatment with thiazide diuretics, such as HCTZ, which decrease calcium excretion and therefore stone formation. Furosemide increases calcium excretion and has the potential to increase stone formation.

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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30
Q

Are alpha blockers ever indicated in the treatment of stones.

A

“The use of an alpha-blocker (e.g., tamsulosin) may help speed up stone passage. However, this is true only in proximal stones (near the kidney) that are larger than 4 mm. Distal stones 4 mm or less will pass on their own anyway”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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31
Q

Concentrated urine may misrepresent what finding on UA?

A

Protein. “The urine dipstick only detects large-molecular-weight proteins like Albumin!”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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32
Q

What is orthostatic proteinuria?

A

“Orthostatic proteinuria is a common type of transient proteinuria seen in young, healthy persons. Up to 5% of adolescents have orthostatic proteinuria, and young adults may present with it as well. Protein is spilled in the urine when the patient is upright, but not when recumbent”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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33
Q

Which medication is used in the management of proteinuria?

A

“Patients with proteinuria tend to respond well to ACE inhibitors. ACE inhibitors have been shown to reduce proteinuria by 35–40%. This effect is true in nondiabetic patients with proteinuria as well as in diabetic patients. ACE inhibitors appear to be superior to other antihypertensives, including calcium channel blockers. Furosemide would be indicated if your patient develops edema, but loop diuretics should not be used primarily for treatment of hypertension or proteinuria”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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34
Q

What characterizes a nephrotic syndrome?

A

“While identifying no specific disease state, the term nephrotic syndrome refers to a constellation of signs and laboratory abnormalities. A number of diseases may lead to nephrotic syndrome (keep reading for more on this). When urine protein exceeds 3 g/day, it is often referred to as “nephrotic range” proteinuria. Complete nephrotic syndrome is characterized by nephrotic range proteinuria, edema, hypertension, hypoalbuminemia, and hyperlipidemia”

The fat, white guy with the 3 grams of protein in his urine.

“Required for the diagnosis of nephrotic syndrome:
Albuminuria >3 g/day
Hypoalbuminemia (serum albumin of <3 g/dL)
Peripheral edema
Other (nonnecessary) findings:
Hyperlipidemia
Thrombotic events”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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35
Q

What does urine sediment containing oval fat bodies indicate?

A

“Oval fat bodies and fatty casts occur in the urine of patients with heavy proteinuria and hyperlipidemia. Fat bodies reflect the increased permeability of the glomeruli and suggest some type of glomerular disease (including nephrotic syndrome) albeit not necessarily active disease. However, fat can also be seen in patients with polycystic kidney disease and fat embolism syndrome”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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36
Q

What kind of sediment cell casts is found in the glomulonephitis versus interstitial nephritis?

A

“Red cell casts, the hallmark of glomerulonephritis, are absent in nephrotic urine. White cell casts are associated with interstitial nephritis and pyelonephritis”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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37
Q

Name three causes of nephrotic syndrome.

A 
“CAUSES OF NEPHROTIC SYNDROME:
 Diabetes
 Amyloidosis
 Systemic lupus erythematosus
 Minimal change disease (“Nil” disease)
 Diffuse glomerulonephritis
 Membranous nephropathy
 IgA nephropathy
 Postinfectious glomerulonephritis (e.g., poststreptococcal GN)
 Membranoproliferative glomerulonephritis
 Various neoplastic diseases (lymphoma, multiple myeloma, lung cancer, etc.)
 Preeclampsia
 Familial kidney disease (Alport disease, Fabry disease)
 Focal and segmental glomerulosclerosis
 Medications (NSAIDs)
 Miscellaneous”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
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38
Q

What is the work up for nephrotic syndrome?

A

“In addition to a thorough history and physical, routine evaluation of patients with nephrotic syndrome (and nephritis and glomerulonephritis) include the following:
Hepatitis B and C serology.
ANA.
Serum and urine protein electrophoresis.
ASO titer.
Cryoglobulins.
Serum complement levels.
ANCA.
Serum calcium (to rule out sarcoid).
Antiglomerular basement membrane antibodies”

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39
Q

Name two contraindications to a renal biopsy.

A

“The presence of renal or perirenal infection is a contraindication to renal biopsy. uncontrollable hypertension, irreversible coagulopathy, multiple bilateral cysts, hydronephrosis, small kidneys (indicative of chronic, irreversible disease), known renal tumor, and lack of consent are all contraindications to renal biopsy. Simply being on warfarin, which can be reversed, is not a contraindication to biopsy”

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40
Q

Name two indications for a renal biopsy.

A

“INDICATIONS FOR RENAL BIOPSY
Nephrotic syndrome without a systemic etiology found on other testing
Hematuria from a glomerular source with hypertension or increasing creatinine
Nephritis without a systemic explanation (e.g., no lupus, drug exposure)
Suspicion of Wegener granulomatosis or polyarteritis nodosum where other tissue is not available
Acute or subacute renal failure without another explanation (although history will usually result in a presumptive diagnosis)”

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41
Q

How do you determine the normal respiratory compensation based on PaCO2 and bicarb level?

A

“In order to have appropriate respiratory compensation, the PaCO2 should fall 12 points for every 10 point drop in the HCO3 below the normal level (around 24 mEq/L)”

“There is another way to do this:
The pH should change by 0.08 for every 10 change in CO2. So, if a patient’s CO2 is 50, the pH should be 7.32 if it is an uncompensated respiratory acidosis. If they are more acidotic (e.g., 7.24), they have a mixed respiratory and metabolic acidosis. If they are less acidotic (e.g., 7.39), they have a compensated respiratory acidosis”

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42
Q

Name three diseases and/or conditions that are associated with polycystic kidney disease.

A

“Liver cysts.
B) Cerebral aneurysms.
C) Colonic diverticula.
D) Cardiac valvular disease”

“Of particular importance is the possibility of cerebral aneurysms (5–20%) leading to subarachnoid hemorrhage. However, aneurysm rupture remains fairly rare (but does seem to run in families—and seems to result in a really bad day for your patient). Currently, screening for subarachnoid aneurysms in asymptomatic patients with ADPKD is not recommended.
ADPKD occurs in 1 in every 400–2000 live births and is autosomal dominant. Common “extrarenal manifestations of ADPKD include cerebral aneurysms, hepatic cysts, cardiac valve disease, colonic diverticula, and abdominal and inguinal hernias”

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43
Q

how does one calculate the water deficit in a hypernatremic patient?

A

“Water deficit = 0.6 × weight (kg) × [(plasma Na/140) – 1].”

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44
Q

What does a BUN to creatinine ratio less than 20 indicate?

A

“A BUN/Cr ratio 20 indicates a prerenal cause such as hypoperfusion (e.g., CHF, dehydration”

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45
Q

Can a patient have abnormal renal function with a normal serum creatinine?

A

“Relatively small changes in serum creatinine may reflect renal failure. A patient with a baseline creatinine of 0.7 mg/dL has lost half her renal function when her creatinine increases to 1.4 mg/dL, even though this number may still be in the normal range—thus, the need to calculate a creatinine clearance”

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46
Q

What is the significance of the fractional excretion of sodium (FENa)?

A

“In oliguric renal failure, the FENa is a useful tool to help differentiate prerenal causes of renal failure from intrinsic renal causes. If the FENa is less than 1%, the kidney is functioning appropriately to conserve sodium and water, and a prerenal cause of failure is more likely. If the FENa is greater than 1%, salt and water losses are excessive, suggesting intrinsic kidney dysfunction. This calculation is only useful in oliguric renal failure (urine output <400 cc/day). Also, FENa may be inaccurate in the elderly, patients receiving diuretics, and in chronic renal failure. The equation used to calculate FENa is:”

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47
Q

What is the significance of muddy brown casts in the urine of a hospitalized patient?

A

“ATN is a major cause of acute renal failure in hospitalized patients. ATN is the result of toxic and/or ischemic effects on the kidney tubules. Metabolic derangements in ATN include progressive hyponatremia, hyperkalemia, and metabolic acidosis with a high anion gap, all of which are present in this case. Typically patients with ATN have a FENa >1% (or FEUrea >50%) and a urine sodium >40 mEq/L. (Remember, the kidney should be retaining sodium to increase its perfusion. This is not happening here. So it is an intrinsic renal problem.) In this case, FENa is 9.9%. Additionally, “muddy” brown casts (renal tubular cell casts) are often found in the urinary sediment of patients with ATN”

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48
Q

What test would be of value to replace the FENa in a patient taking a diuretic?

A

“Use the FEUrea, as urea excretion is not affected by diuretics. Here’s the equation:
FEUrea (%) = (urine urea/plasma urea)/(urine Cr/plasma Cr).
If the FEUrea is 50%, acute tubular necrosis is more likely. Caveat: hyperglycemic diuresis increases excretion of urea even in hypovolemic states (e.g., 3 + glucose in the urine can give you a falsely high FEUrea).”

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49
Q

Name two causes of acute tubular process.

A

“In addition to hypoxic insult (shock, hypoperfusion, CHF, etc.), common causes of ATN include medications such as tacrolimus, various ACE inhibitors, some of the penicillin derivatives, gentamicin, tobramycin, cyclophosphamide, several antirejection drugs, and more”

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50
Q

What is the treatment for acute tubular necrosis?

A

“The treatment of acute renal failure due to ATN is largely supportive. In this oliguric patient with signs of volume overload, a trial of a loop diuretic is appropriate. Intravenous furosemide dosed at 20–100 mg every 6–12 hours is a reasonable way to start”

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51
Q

Why is early dialysis contraindicated in a patient with acute tubular necrosis?

A

“Early dialysis in ATN is associated with greater mortality and increased kidney damage from hypotension, infection, and complement activation in the kidney.”

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52
Q

What is the expected course of acute tubular necrosis?

A

“Renal failure due to ATN typically lasts 7–21 days, with renal function returning as the tubular cells regenerate. However, the course is highly variable and depends on the patient’s general health and the length and degree of the initial injury.”

“In patients with ATN who die, infection is the usual culprit. It is critical to avoid sepsis in these patients. Also, serious infection resulting in sepsis is a common cause of ATN”

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53
Q

What is the definition of hyponatremia and how does one work it up?

A

“The definition of hyponatremia is a plasma sodium concentration below 135 mEq/L. The evaluation of hyponatremia begins with the determination of the validity of the plasma sodium measurement. You must distinguish “true” hyponatremia from pseudohyponatremia, which can be the result of hyperlipidemia, hyperglycemia, or hyperproteinemia. If pseudohyponatremia is present, the calculated osmolality will be significantly lower than measured osmolality. Your patient’s calculated osmolality is determined by the formula Osm = 2 (sodium) + glucose/18 + (BUN/2.7), which for her is about 236 Osm. Her measured osmolarity is 220 mmol/kg, and the fact that measured osmolality is higher than calculated rules out pseudohyponatremia”

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54
Q

What is beer potonemia?

A

Too much beer “(or any alcohol) plus too little solute equals poor free water excretion and hyponatremia.”

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55
Q

What can urine osmolality tell you about hyponatremia?

A

“Urine osmolality can be used to distinguish between impaired water excretion, SIADH, and pathologic water intake (polydipsia). In SIADH, the urine will be inappropriately concentrated with urine osmoles of >100 mOsm/L/kg (the patient is unable to retain sodium)”

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56
Q

Name three pathological conditions and what you see how highly concentrated urine.

A

“Inappropriately concentrated urine (osmolality >100 mmol/kg) occurs when there is limited excretion of fluid and may be observed in SIADH, CHF, cirrhosis, and renal failure. This is also reflected in the urine sodium. If the kidneys respond to hyponatremia as expected, urine sodium concentration should be low, typically less than 20 mmol/L and often less than 10 mmol/L (the kidneys are attempting to retain sodium to increase the serum osmolarity). In the setting of hypovolemia, if the urine sodium concentration is inappropriately high, something is inappropriately spurring the kidney on to excrete sodium (e.g., diuretic use, hypoaldosteronism). In this patient, the elevated urine sodium is likely due to the diuretic.
Diuretic use is the most common cause of hypovolemic hypoosmolality, and thiazides are more commonly associated with hyponatremia than are loop diuretics (furosemide, etc.).”

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57
Q

What is the reset osmostat?

A

“A reset osmostat, which is responsible for 20–30% of hyponatremia, occurs when the patient’s body “adapts” to hyponatremia and gives up trying to correct the problem: the kidneys just throw in the towel. Patients with a reset osmostat will present like SIADH (hyponatremia, euvolemia or slight hypervolemia, and inappropriately concentrated urine) but will be resistant to treatment. If a patient with apparent SIADH does not respond to usual treatment, consider a reset osmostat. Since patients with a reset osmostat generally have mild hyponatremia (125–130 mg/dL) and are generally asymptomatic, trying to correct the sodium by limiting water intake is unnecessary and futile”

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58
Q

In addition to thiazide diuretics, what other medications can cause hypovolemic hyponatremia?

A

“SSRIs and tricyclic antidepressants, among other medications, can stimulate the release of ADH from the pituitary gland, ultimately causing hyponatremia with an SIADH-type presentation. The association between SSRIs and hyponatremia is strong enough to consider measuring plasma sodium levels in elderly patients before and after starting an SSRI”

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59
Q

“In any given patient with hyponatremia, what makes SIADH likely?

A

All of the following data are used to support the diagnosis of SIADH: decreased plasma osmolality; inappropriately concentrated urine (e.g., a urine osmolality of >100 mmol/kg); clinical euvolemia or mild hypervolemia; elevated urine sodium excretion (urine sodium >20 mEq/L); and the absence of diuretic use, hypothyroidism, and adrenal dysfunction”

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60
Q

What is syndrome of inappropriate ADH and what is the mainstay of treatment?

A

“The labs and clinical picture are consistent with SIADH (euvolemia, elevated urine sodium excretion, elevated urine osmolarity). Water restriction is the mainstay of therapy in SIADH. Free water should be restricted to 1–2 L/day. Demeclocycline and lithium interfere with the activity of ADH at the collecting tubules, but these drugs are reserved for SIADH patients with severe hyponatremia unresponsive to water restriction. Saline infusion corrects hypovolemic hyponatremia, and furosemide is used in hypervolemic hyponatremia (e.g., CHF, renal insufficiency).”

“Increasing salt intake and adding a loop diuretic are other ways to treat SIADH in patients who cannot or will not maintain fluid restriction. IV urea, which causes an osmotic diuresis, is the next step to use after the sodium chloride tablets. Demeclocycline and lithium should be reserved for patients who fail the other treatments.”

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61
Q

Which urine test contributes most to the diagnosis of a metabolic alkalosis?

A

Urine chloride. “If there is NG suction or vomiting, the patient will be low on chloride and thus will have little in the urine (where it is being reabsorbed.) With mineralocorticoid excess (aldosterone or extrinsic corticosteroids), one excretes potassium causing hypokalemia. Hypokalemia prevents the kidneys from optimally reabsorbing chloride”

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62
Q

What does continued hypokalemia in the face of continued unsuccessful KCl replacement indicate?

A

“continued hypokalemia in the face of KCl repletion may indicate whole-body magnesium depletion. Serum magnesium levels may not accurately reflect whole-body magnesium stores, especially in patients with CHF. Furosemide causes further magnesium wasting”

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63
Q

What is Alport disease and how is it transmitted?

A

“Alport syndrome, also known as hereditary nephritis, typically presents with microscopic hematuria and progresses to complete renal failure. Alport syndrome has a heterogeneous inheritance pattern: 80% of cases are due to X-linked disease, about 15% are autosomal recessive, and about 5% are autosomal dominant. Since most cases are X-linked, males are affected more severely and earlier than females. If your medical student’s father had Alport syndrome, it was most likely X-linked, and the patient could not possibly have inherited it. However, there is a 5% chance that the father had autosomal-dominant disease and then a 5% chance that the trait was passed on to the patient”

64
Q

What are the signs and symptoms of hypocalcemia?

A

“Symptoms are mostly neurological—generalized seizures, perioral paresthesias, and carpopedal spasms. The two best-known signs of hypocalcemia are Chvostek and Trousseau sign. Chvostek sign is present if a grimace occurs in response to tapping the facial nerve. Trousseau sign is evoked by inflating a blood pressure cuff above the systolic pressure for 3 minutes and observing for hand spasms”

65
Q

What’s the formula to correct calcium for decreased albumin?

A

To correct total calcium for decreased albumin, use the following formula: corrected calcium = measured calcium + [0.8 × (normal albumin—measured albumin)].”

66
Q

Why is giving a UREMIC patient platelets to correct platelet dysfunction an inappropriate treatment?

A

“The cause of bleeding dysfunction in uremia appears to be the effect of uremic toxins on platelet function. Giving a uremic patient more platelets—especially when there is no thrombocytopenia—will not improve the situation, as the platelet dysfunction due to uremia will occur with the new platelets as well”

67
Q

What is renal osteodystrophy?

A

“Renal osteodystrophy occurs when parathyroid hormone levels are elevated and bone is mobilized. This occurs because patients with renal failure cannot clear phosphate. The body tries to compensate by increasing parathyroid hormone secretion, which reduces phosphate and increases serum calcium. However, it also is detrimental to bone and leads to demineralization.”

68
Q

How does one treat renal osteodystrophy an uremic patient?

A

“Gastrointestinal binding of phosphate requires large doses of a cation such as calcium (2 g/day). Calcium carbonate is associated with the least potential toxicity; therefore, it is the initial choice for treating hyperphosphatemia to reduce the risk of renal osteodystrophy. Also, you may consider calcium acetate, which is as safe as calcium carbonate and is a more potent phosphate binder but more expensive. Avoid aluminum and magnesium products in renal failure as these ions accumulate and can cause toxicity.”

69
Q

Name two renal diseases that present with nephritic symptoms and “active” urinary sediments.

A

“associated with hematuria, either microscopic or gross. Henoch-Schönlein purpura, poststreptococcal glomerulonephritis, IgA nephropathy, and membranoproliferative glomerulonephritis all have more “nephritic” features with “active” urinary sediments (dysmorphic red cells, red cell casts, granular casts, white cells, and protein in the urine). Also, these diseases have a similar pathologic process in which immune complexes deposit in the glomeruli, resulting in glomerulonephritis”

70
Q

Tell me about post-streptococcal glomulonephritis.

A

“Poststreptococcal glomerulonephritis, characterized by immune complex deposition in the glomeruli, is a self-limited disease in most patients. There is a latent period, averaging 10 days, between pharyngitis and the development of hematuria. Recovery is expected in 1–2 weeks. Unlike IgA nephropathy, recurrent episodes of gross hematuria are rare in poststreptococcal glomerulonephritis. Poststreptococcal glomerulonephritis is more common in children and tends to be more severe when it affects adults. Hypertension and uremia resolve relatively quickly, but microscopic hematuria may persist for 6 months”

71
Q

How does interstitial cystitis usually present?

A

Interstitial cystitis, or bladder pain syndrome (also IC/BPS), is a chronic inflammatory condition of the submucosal and muscular layers of the bladder. The cause of IC is currently unknown and the condition is regarded as a diagnosis of exclusion. IC may be associated with urinary urgency, urinary frequency, waking at night to urinate (nocturia), and sterile urine cultures. Those with interstitial cystitis may have symptoms that overlap with other urinary bladder disorders such as: urinary tract infection (UTI), overactive bladder, urethritis, urethral syndrome, and prostatitis. IC can result in a quality of life comparable to that of a patient with rheumatoid arthritis, chronic cancer pain, or a patient on kidney dialysis.

72
Q

How does one diagnose interstitial cystitis?

A

“Cystoscopy and hyperdistention are NOT required in order to make the diagnosis of interstitial cystitis. It is a clinical diagnosis of exclusion: Is there anything else causing the symptoms? If not, as Sherlock Holmes said, “Once you eliminate the impossible, whatever remains, no matter how improbable, must be the truth.” It is important to rule out tumor (if indicated), stones, neurogenic bladder (thus the postvoid residual). There are biomarkers in the works for this disease, but they have not yet entered the clinical arena”

73
Q

Schistocytes are indicative of which anemia?

A

Microangiopathic hemolytic anemia

74
Q

What is the classic pentad of TTP?

A

“classic pentad: thrombocytopenia, fever, mental status changes, renal insufficiency, and hemolytic anemia. Usually, there is a prodrome viral illness with TTP but diarrhea occurs only rarely”

75
Q

What is TTP?

A

a rare disorder of the blood-coagulation system, causing extensive microscopic clots to form in the small blood vessels throughout the body.[2][3] These small blood clots, called thrombi, can damage many organs including the kidneys, heart and brain. In the era before effective treatment with plasma exchange, the fatality rate was about 90%. With plasma exchange, this has dropped to 10% at six months. Immunosuppressants, such as glucocorticoids, rituximab, cyclophosphamide, vincristine, or cyclosporine, may also be used if a relapse or recurrence follows plasma exchange

76
Q

What does one expect from a blood culture in a patient with hemolytic uremic syndrome?

A

“Although HUS is the result of bacterial enteritis, patients are not bacteremic. Instead, the endothelial damage and hemolysis are caused by Shiga toxin, released from E. coli and Shigella dysenteriae”

77
Q

Our antibiotics indicated in hemolytic uremic syndrome?

A

“The idea is that bacterial death from antibiotics releases more Shiga toxin leading to HUS. Remember that most cases of bacterial gastroenteritis—E. coli O157:H7 included—will clear without antibiotic therapy”

78
Q

Does one expect to sign with a salicylate overdose in regards to the pH?

A

Normal pH offer results as a result of the mixed picture from the metabolic acidosis and the respiratory alkalosis. “In salicylate overdoses, a high anion gap metabolic acidosis is often observed. Since salicylates directly stimulate the CNS respiratory center, there is usually a concurrent respiratory alkalosis”

79
Q

How does one treat salicylate overdose?

A

“Proper treatment of salicylate overdoses includes supportive therapy, urine alkalinization with sodium bicarbonate. Dialysis may also be necessary.”

80
Q

That woman complains of urinary symptoms, based on these complaints alone, what is the probability that she has a urinary tract infection?

A

“If a woman complains of dysuria and increased frequency without vaginal discharge, the likelihood ratio of UTI is about 25 and “posttest” probability is greater than 90% that she has a urinary tract infection”

“If her urinalysis were completely normal, she may still have an infection and have a false-negative dipstick urine. Using urine dipstick alone in a woman with urinary symptoms only increases the posttest probability to 81%. Thus, certain symptoms and historical elements are more useful than urinalysis”

81
Q

Name three diagnoses to consider with a patient who has typical UTI symptoms and a negative urine culture.

A

“With typical UTI symptoms (e.g., dysuria, frequency) and a negative urine culture or no response to antibiotics, consider other causes: interstitial cystitis, chlamydia urethritis, prostatitis (in men), pelvic inflammatory disease (in women), pelvic mass, herpes genitalis, and drugs (e.g., diuretics, caffeine, and theophylline”

82
Q

The patient presents with fever, rash, mild eosinophilia, a history of starting a new drug (methicillin) and white cell casts in the urine. What is the diagnosis?

A

“The combination of fever, rash, mild eosinophilia, exposure to a new drug (methicillin) and white cell casts in the urine essentially makes the diagnosis of interstitial nephritis.
The patient with ATN may have the same FENa and urine sodium as this patient but should have renal tubular cells and/or granular casts in the urine. Also, ATN does not cause fever, eosinophilia, or rash”

83
Q

How long after drug exposure does a patient typically develop interstitial nephritis

A

“Patients can develop interstitial nephritis anywhere from 1 day to several months after beginning a drug”

84
Q

What is the treatment of interstitial nephritis caused by a drug?

A

“Patients with interstitial nephritis will often have eosinophils in the urine and peripheral smear, but eosinophils may be absent especially in those with NSAID-induced interstitial nephritis. Treatment is to stop the offending drug. If this doesn’t work, steroids or cytotoxic drugs may be needed”

85
Q

A Patient presents with an elevated creatinine and hypertension, what medication would be useful to start with the thoughts of preserving kidney function?

A

“ACE inhibitors have been shown to be useful in reducing progression of renal disease even when the patient’s creatinine is 5.0 mg/dL. But, be very careful in this group.”

“ACE inhibitors can be used safely in patients with stage 4 CKD. Due to the risk of rising creatinine and potassium, ACE inhibitors should be started at a low dose and increased slowly, checking creatinine and potassium levels within a week or 2 after making a dose adjustment”

86
Q

What is minimal change disease?

A

It is the most common cause of nephrotic syndrome in pediatric patients. It is associated with edema and proteinuria and hypoalbumenia. For years pathologists found no changes when viewing specimens under light microscopy; hence the name minimal change disease. With the advent of electron microscopy, the changes now known as the hallmarks for the disease were discovered. These are diffuse loss of visceral epithelial cells foot processes (podocyte effacement),[4] vacuolation, and growth of microvilli on the visceral epithelial cells.

The pathology of minimal change disease is unclear and is currently considered idiopathic. The pathology does not appear to involve complement, immunoglobulins, or immune complex deposition. Rather, an altered cell-mediated immunologic response with abnormal secretion of lymphokines by T cells is thought to reduce the production of anions in the glomerular basement membrane, thereby increasing the glomerular permeability to serum albumin[5] through a reduction of electrostatic repulsion.[6] The loss of anionic charges is also thought to favor foot process fusion.[1] The etiological agent is somewhat of a mystery but viruses such as EBV, and food allergies have been implicated. Also, the exact cytokine responsible has yet to be elucidated, with IL-12, IL-18 and IL-13 having been most studied in this regard, yet never conclusively implicated.

FP board review (15 decks)

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