Dx and Rx Flashcards
What are the two parts of urinalysis? What does each part detect/measure?
Dipstick or urine test strip - detects and measures leukocyte esterase, blood, nitrites, glucose, urobilinogen, bilirubin, ketones, specific gravity and pH.
Microanalysis - used to count WBCs (total and eosinophil count), RBCs, casts, and crystals.
What is the best initial test for any renal disease?
Urinalysis and BUN/Cr (from BMP)
What is the normal amount of protein excreted per 24 hours? What specific proteins are detected?
Protein < 300 mg per 24 hours is normal. 1+ protein means 1 gram (1000 mg) of protein excreted per 24 hours.
Urine dipstick for protein only detects albumin.
What are the two tests that can accurately measure proteinuria AFTER it is detected on urinalysis? Which test is preferred?
Transient proteinuria is present in 2-10% of the population, so the two best methods of calculating total protein per day are:
- Single protein to creatinine ratio
- 24-hour urine collection
P/Cr ratio is favored because it is faster, easier to perform, and more accurate. A P/Cr of 1 is equivalent to 1 gram of protein excreted per 24 hours, so a normal P/Cr is < 0.3.
What are the etiologies of elevated proteinuria? What confirmatory diagnostic test is done if proteinuria persists?
Elevated amounts can be associated with either tubular or glomerular disease, but may also be due to physical activity or prolonged standing (orthostatic proteinuria). Very large amounts can only be excreted with glomerular disease.
Kidney biopsy must be performed if proteinuria persists and is not related to prolonged standing.
What is microalbuminuria and why is it measured? What is the next step in management?
Microalbumin is a tiny protein that is too small to be detected by UA. Microalbuminuria = 30-300 mg per 24 hours.
It is very important to detect microalbuminuria in diabetic pts because long-term microalbuminuria leads to worsening renal function. It is found very early in the disease, long before albumin can leak out and be detected on UA in nephrotic syndrome (>3.5 protein) caused by DM.
When any degree of proteinuria, even microalbuminuria, is detected in a pt with DM, the best initial Rx is an ACEI or ARB, which decrease the progression of proteinuria and delay the development of renal insufficiency.
What do WBCs on UA indicate? Which types of leukocytes are most significant? What can persistent WBC on UA with negative culture indicate?
WBCs indicate inflammation, infection, or allergic interstitial nephritis (AIN). Urine dipstick cannot distinguish between types, but microanalysis can.
- Neutrophils indicate infection.
- Eosinophils indicate AIN.
Persistent WBC on UA with negative culture can be TB.
What are the best tests for acute (allergic) interstitial nephritis (AIN)?
Wright stain or Hansel stain will detect eosinophils in the urine.
*NSAID-induced nephropathy does not show eosinophils in urine.
Can urinalysis be used to test for multiple myeloma?
No, because the Bence-Jones protein is not detectable on urine dipstick (only albumin is). Instead, the BJ protein is detected using electrophoresis.
What test is important in a diabetic pt with kidney disease but no ophthalmic findings?
Kidney biopsy
What is the criterion for hematuria on UA? What does hematuria indicate?
Normal UA has < 5 RBCs per high power field (HPF). Hematuria (> 5 RBCs) is indicative of:
- Stones in the bladder, ureter or kidney
- Cancer of the bladder, ureter or kidney
- Hematologic disorders that cause bleeding (coagulopathy)
- Infection, e.g. cystitis or pyelonephritis
- Drugs, e.g. hemorrhagic cystitis with cyclophosphamide
- Trauma
- Glomerulonephritis
What is the best next test after a urine dipstick is positive for blood?
If blood is found on the dipstick, you must do a microscopic analysis of the urine to see if there are actually RBCs. If not, the result was a false positive.
What cause false positives on urine dipstick?
Hemoglobin or myoglobin in the urine yield false positives for hematuria. Dipstick cannot distinguish them from RBCs.
False positives are confirmed by microanalysis showing no RBCs.
After UA confirms hematuria, what is the best test if you suspect stones? When do you do IV pyelogram?
Renal CT is used to detect stones, e.g. hematuria with flank or groin pain, dysuria, Hx of stones, etc.
IVP is never used because it is slow and the contrast is renal toxic.
When is cystoscopy used?
Cystoscopy is the most accurate test of the bladder. It is done when there is hematuria without infection or prior trauma and:
- the renal US or CT does not show an etiology
- bladder sonography shows a mass for possible biopsy (bladder cancer presents with painless hematuria)
How do casts in the urine help narrow down the differential diagnosis? Are casts sensitive or specific findings?
Casts in the urine indicate the pathology originated in the kidneys. They are often not present, but are very useful if found because they are a specific finding and thus can be used to answer “most likely diagnosis” questions.
What diseases are associated with the following types of cast:
- RBC
- WBC
- Eosinophil
- Hyaline
- Broad, waxy
- Granular, “muddy brown”
- RBC casts indicate glomerulonephritis
- WBC casts indicate pyelonephritis
- Eosinophil casts indicate acute (allergic) interstitial nephritis
- Hyaline casts indicate dehydration*
- Broad, waxy casts indicate acute tubular necrosis; they are collections of dead tubular cells
*Dehydration concentrates urine and the normal Tamm-Horsfall protein precipitates into a hyaline cast.
What is the best initial test for acute kidney injury (AKI) aka acute renal failure? How does it help distinguish between prerenal, intrinsic renal, and postrenal disease?
BUN and Cr is the best initial test. Their ratio is most important.
BUN:Cr is above 20:1 in prerenal and postrenal disease.
BUN:Cr is closer to 10:1 in intrinsic renal disease.
In postrenal azotemia, how many kidneys need to be obstructed for Cr to increase?
Both kidneys must be obstructed for Cr to rise; this is why stones can present without elevated Cr.
For BUN:Cr > 20:1, how do you distinguish between prerenal and postrenal disease?
Prerenal azotemia is usually the clear diagnosis when BUN:Cr > 20:1 AND the pt has a Hx of hypoperfusion or hypotension
Postrenal azotemia is usually the clear diagnosis when BUN:Cr > 20:1 AND the pt has a distended bladder or massive release of urine with catheter placement AND bilateral or unilateral hydronephrosis on sonogram (US).
How much does creatinine rise with completely dead kidneys?
About one point (1 mg/dL) per day
What is the best initial imaging test for AKI?
Renal sonogram is the best initial test because it does not require contrast, which should be avoided in renal insufficiency.
When the cause of AKI is unclear, what is the next best diagnostic step?
Urinalysis is the next best step.
*If urinalysis is not one of the choices then urine sodium, fractional excretion of sodium, and urine osmolality can be used.
How can urine sodium, fractional excretion of sodium, and urine osmolality be used to determine the etiology of AKI?
Urine sodium and fractional excretion of sodium give you the same info. Urine osmolality is inversely proportional to them.
Prerenal azotemia:
- low UNa (500 mOsm/kg)
Postrenal or interstitial azotemia:
- high UNa (>20%) = high FeNa (>1-2%)
- low urine osmolality (<300 mOsm/kg)
Does urine specific gravity correlate with UNa, FeNa, and/or osmolality?
Specific gravity is correlated with osmolality; thus, they are directly proportional.
Can a kidney be transplanted from a pt with prerenal, intrinsic, or postrenal disease?
A kidney in prerenal and postrenal disease would function normally if transplanted into another person.
Explain the findings for UNa, FeNa, and urine osmolality in prerenal disease
In prerenal disease:
- low BP or low intravascular volume –> increased aldosterone release –> increased Na reabsorption –> decreased UNa and FeNa.
- low intravascular volume –> increased ADH release –> increased water reabsorption –> increased urine osmolality.
Explain the findings of UNa, FeNa, and osmolality in interstitial renal disease
In ATN, for example:
- tubule cell damage –> decreased Na reabsorption –> inappropriate Na loss –> increased UNa and FeNa
- tubule cell damage –> decreased water reabsorption –> inability to concentrate urine –> decreased osmolality
Why is dehydration a problem in a pt with ATN?
In a healthy pt with dehydration, urine osmolality is increased (urine is concentrated) because water is reabsorbed.
In ATN, tubule cells die and lose the ability to reabsorb water; thus, the pt cannot concentrate their urine, so water that is necessary to maintain blood pressure and volume is lost via dilute, high-volume urine.
What is the treatment for ATN?
There is no specific therapy proven to benefit ATN. Treating the underlying cause is always the best method.
Patients should be managed with hydration (if they are volume depleted) and correction of electrolyte abnormalities.
Common incorrect answers are low-dose dopamine, diuretics, mannitol, and steroids.
Why is it critical to know the causes of ATN in order to diagnose it?
There is no specific diagnostic test to confirm the etiology of ATN or distinguish ATN from other causes of intrinsic renal disease. You cannot do a blood level of a drug or a biopsy to prove that a particular toxin caused the renal failure.
The clues to answer “What is the most likely diagnosis” questions are simply acute renal failure and a toxin in the pt’s history; diagnosis can be assumed and treatment can be initiated based on this info alone. A confirmatory diagnostic test is unnecessary because there isn’t one.
How is rhabdomyolysis diagnosed?
The best initial test is UA showing blood on dipstick but no RBCs on microscopic analysis. CPK levels will be markedly elevated, but it isn’t necessary to do them after the UA indicates myoglobin in the urine.
The most specific test is urine test for myoglobin; it may not be necessary if the history and UA were enough to go on.
Other findings are hyperkalemia, hypocalcemia, and hyperuricemia.
How does the onset of ATN help you determine the cause?
Contrast media cause immediate renal toxicity.
Drugs such as aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir, and cyclosporine have a slower onset of 5-10 days.
Hyperuricemia (e.g. from tumor lysis syndrome) takes about 2 days (e.g. after treatment is started).
How is ATN from tumor lysis syndrome prevented?
Allopurinol, hydration, and rasburicase should be given prior to chemotherapy to prevent renal failure from tumor lysis syndrome.
How does contrast-induced ATN differ from the other etiologies?
Contrast causes spasm of the afferent arteriole that leads to renal tubular dysfunction. There is tremendous reabsorption of sodium and water, leading to profoundly low urine sodium.
Contrast ATN results in very high specific gravity and osmolality and very low UNa and FeNa. The usual findings of ATN are the opposite.
Contrast media also has a very rapid onset of injury.
What is the treatment for contrast-induced ATN?
Only saline hydration has proven benefit.
Describe the lab values in hepatorenal syndrome
The lab values in HR syndrome are the same as prerenal syndrome:
- Very low UNa ( 20:1
What is the treatment for hepatorenal syndrome
- Midodrine
- Octreotide
- Albumin (albumin is less clear)
What is the treatment for rhabdomyolysis?
Rhabdomyolysis is treated with saline hydration, mannitol, and bicarbonate.
- Saline hydration and mannitol (as an osmotic diuretic) increase urine flow rates to decrease the amount of contact time between myoglobin and the tubular cells. Myoglobin is a severe oxidant stress on these cells.
- Bicarbonate - drives potassium back into cells and may prevent precipitation of myoglobin in the kidney tubule
*Don’t treat hypocalcemia in rhabdomyolysis unless it is symptomatic. In recovery, the calcium and will come back out of the muscles.
When is dialysis used for ATN?
Initiating dialysis is not based on a specific level of BUN or Cr; it is based on the development of life-threatening conditions that cannot be corrected another way, including:
- Fluid overload
- Encephalopathy
- Pericarditis
- Metabolic acidosis
- Hyperkalemia (symptomatic)
When is kidney biopsy done for AKI?
Kidney biopsy is the most accurate test for AIN or poststreptococcal glomerulonephritis, but it is rare for either of these to actually require biopsy for diagnosis.
What is the renal manifestation of sickle cell trait? What is the best advice for pts?
A defect in renal concentrating ability, or isothenuria, is actually the only significant manifestation of sickle cell trait. The pts will continue to produce inappropriately dilute, high-volume urine despite dehydration. As such, they must avoid becoming dehydrated.
What are the physical findings in atheroemboli? What are the important diagnostic findings?
PE shows:
- Blue/purplish skin lesions in fingers and toes
- Livedo ritcularis
- Ocular lesions
- Peripheral pulses are normal
Diagnostic tests show:
- Eosinophilia
- Eosinophiluria
- Low complement levels
- Elevated ESR
What is the most accurate test for atheroemboli? What does it show? What is the Rx for atheroemboli?
Biopsy of one of the purplish skin lesions is the most accurate diagnostic test. It shows cholesterol crystals, but this does not change management because there is no specific therapy to reverse atheroembolic disease.
What do UA and BUN/Cr show for AIN? What is the most accurate test for AIN?
Initial labs show:
- WBCs and RBCs in the urine
- Eosinophilia on CBC
- Elevated BUN and Cr with a ratio below 20:1 (intrinsic renal disease)
The most accurate test is either the Hansel stain or the Wright stain, which show eosinophils in the urine. Microanalysis is not sufficiently accurate to prove there are eosinophils in the urine.
What is the treatment for AIN?
AIN usually resolves spontaneously with stopping the drug or controlling the infection. If the creatinine continues to rise after stopping the drug, giving glucocorticoids (prednisone, hydrocortisone, methylprednisone) is the best answer.
Severe disease is managed with dialysis, which may be temporary.
What are the findings for UNa, FeNa, and osmolality in AIN?
Variable - they cannot help establish the diagnosis.
How is analgesic nephropathy from NSAIDs diagnosed? What is the Rx?
There is no specific diagnostic test to determine NSAIDs caused the disease. Exclude other causes and look for NSAIDs in the Hx.
Stop NSAIDs and correct hypoperfusion.
