Nephrology Flashcards
The best initial test in nephrology
UA
BUN
Creatinine
Tamm-Horsfall protein
The name of protein that is normally secreted by the renal tubules (very tiny amount)
Normal protein is less than 300 mg per 24 hours
Severe proteinuria means
glomerular disease
What is transient proteinuria
Protein excretion increased by standing and physical activity
Present in 2-10% of the population
Mostly benign
Urine dipstick for protein detects
only albumin
A protein-to-creatinine (P/Cr) ratio of one is equivalent to
1 g of protein on a 24-hour urine
Define microalbuminuria
The presence of tiny amounts of proteins that are too small to detect on the UA
30-300 mg/24 hours
Long-term microalbuminuria leads to worsening renal function in a diabetic patient and should be treated
Best initial therapy for any degree of proteinuria in a diabetic patient
ACEi or ARB
True/False
Bence-Jones protein in myeloma is detectable on a dipstick
False
Must use immunoelectrophoresis
WBCs in the UA means
Inflammation
Infection
Allergic interstitial nephritis
True/False
You cannot distinguish neutrophils from eosinophils on a UA
True
However, if you could:
Neutrophils indicate infection
Eosinophils indicate allergic or acute intersitial nephritis
Persistent WBC on UA with negative culture
TB
How do you detect eosinophils in the urine?
Wright and Hansel stains
Normal UA has how many RBCs
<5 RBCs per high power field
Mild recurrent hematuria
think IgA nephropathy
False positive tests for hematuria on dipstick are caused by…
hemoglobin or myoglobin in the urine
They make the dipstick positive, but no red cells will be seen on microscopic examination
Dysmorphic red cells
Glomerulonephritis
When is cystoscopy the answer?
Cystoscopy is the most accurate test of the bladder
The right answer when there is hematuria w/o infection or prior trauma and:
- renal US or CT does not show an etiology
- bladder sonography shows a mass for possible biopsy
White cell casts
Pyelonephritis
Eosinophil casts
Acute (allergic) interstitial nephritis
Hyaline cast
Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitates or concentrates into a cast
Broad, waxy casts
Chronic renal disease
Granular “muddy-brown” casts
Acute tubular necrosis (collections of dead tubular cells)
Define AKI
A decrease in creatinine clearance resulting in a sudden rise in BUN and creatinine
3 types of AKI
Prerenal azotemia (decreased perfusion)
Postrenal azotemia (obstruction)
Intrinsic renal disease (ischemia and toxins)
How do NSAIDs and ACEi effect the renal arteriole?
NSAIDs = contriction of the afferent arteriole
ACEi = dilation of the efferent arteriole
Both can lead to prerenal azotemia
With completely dead kidneys, the creatinine will rise
about 1 mg/dL a day
BUN: creatinine ratio above 20:1
Clear history of hypoperfusion or hypotension
Prerenal azotemia
BUN: creatinine ratio above 20:1
Distended bladder or massive release of urine with catheter
Hydronephrosis on sonogram
Postrenal azotemia
When the cause of AKI is not clear, the next best diagnostic step is?
UA (order first)
UNa
FENa
Urine osmolality
UNa <20
FENa <1%
Prerenal azotemia
It is normal for urine sodium to decrease when there is decreased renal perfusion because aldosterone levels rise
The urine produced in ATN is similar in osmolality to
the bood (about 300 mOsm/L)
This is called isosthenuria and the urine osmolality is inappropriately low
AKA in ATN, the body inappropriately loses sodium (UNa > 20) and water (Uosm < 300)
The only significant manifestation of sickle cell trait is a defect in renal…
renal concentration ability or isosthenuria
these patients will continue to produce inappropriately dilute, high-volume urine despite dehydration
Urine specific gravity correlates to
urine osmolality
High UOsm = high specific gravity
True/False
ATN can cause proteinuria
False
What has the most proven benefit at preventing contrast-induced nephrotoxicity?
Saline hydration
What unique labs values are found in contrast-induced renal failure (a form of ATN)
The usual finding in ATN from nephrotoxins would be UNa > 20 and
FENa > 1% and a low specific gravity
However, contrast causes spasm of the afferent arteriole leading to tremendous reabsorption of sodium and water
High specific gravity (~1.040), UNa < 20 (~5), FENa < 1%
Patient with myeloma with a plasmacytoma is admitted for combination chemo. Two days later, the creatinine rises. Why?
Tumor lysis syndrome leading to hyperuricemia
Allopurinol, hydration, and rasburicase should be given prior to chemo to prevent renal failure from tumor lysis syndrome
Ethylene glycol is associated with what type of kidney injury?
Acute kidney injury based on oxalic acid and oxalate precipitating within the kidney tubules causing ATN
Look for hypocalcemia (precipitates as calcium oxalate - envelope shaped crystals)
Aminoglycoside abx
Amphotericin
Cisplatin
Vancomycin
Acyclovir
Cyclosporine
Cause nonoliguric renal injury
Slow onset: 5-10 days
Low magnesium level may increase risk of aminoglycoside or cisplatin toxicity
Contrast media causes
immediate renal toxicity
UA for rhabdo
UA will be positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination
Most specific test is a urine test for myoglobin
Urine dipstick cannot tell the difference between
Hemoglobin
Myoglobin
Red blood cells
Lab findings in rhabdo
CPK markedly elevated
Hyperkalemia
Hyperuricemia (similar to tumor lysis syndrome)
Hypocalcemia (increased binding to damaged muscle)
Treatment for rhabdo
Saline hydration
Mannitol (osmotic diuretic)
Bicarbonate (drives potassium back into cells)
DO NOT TREAT HYPOCALCEMIA IF ASYMPTOMATIC
Saline and mannitol increase urine flow rates to decrease the amount of contact time between the myoglobin and the tubular cells
Why doesn’t hemolysis cause hyperuricemia?
RBCs have no nuclei
In all other cells, break down results in nucleic acids being released from the nucleus and rapidly metabolized to uric acid by xanthine oxidase
Most important intial step when someone presents with signs/symptoms of rhabdo
EKG (to detect life-threatening hyperkalemia)
Most common wrong answers for treatment of ATN
Low-dose dopamine
Diuretics
Mannitol
Steroids
Diuretics increase urine output, but do not change overall outcome
When is dialysis the right answer for ATN?
Fluid overload
Encephalopathy
Pericarditis
Metabolic acidosis
Hyperkalemia
Patient develops ATN from gentamicin. She is vigorously hydrated and treated with high dose of diuretic, low-dose dopamine, and calcium acetate as a phosphate binder. Urine output increases but she still progresses to end-stage renal failure. She also becomes deaf.
What caused the hearing loss?
Furosemide causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss (related to how fast it is injected)
What is hepatorenal syndrome?
Hepatorenal syndrome is renal failure developing secondary to liver disease (d/t splanchnic arterial vasodilation and subsequent endogenous vasoconstrictors acting on renal vessels)
Look for: cirrhosis, new-onset renal failure, very low urine sodium, FENa <1%, BUN: creatinine > 20:1
Lab values in hepatorenal syndrome fit in with prerenal azotemia
Treatment for hepatorenal syndrome
Midodrine
Octreotide
Albumin
goal = constriction of splachnic vessles and dilation of renal vasculature
Etiology of Atheroemboli
Cholesterol plaques in the aorta or near the coronary arteries are sometimes large and fragile enough that they can be “broken off” when the vessels are manipulated during catheter procedures
Cholesterol emboli lodge in the kidney, leading to AKI, look for blue/purplish skin lesions in fingers and toes, livedo reticularis, and ocular lesions
Diagnostic test for atheroemboli
Biopsy of one of the purplish skin lesions is the most accurate diagnostic test (shows cholesterol crystals)
Look for: eosinophilia, low complement levels, eosinophiluria, elevated ESR
Define Acute (Allergic) Interstitial Nephritis
A form of acute renal failure that damages the tubules occurring on an idiosyncratic (idiopathic) basis
Antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders
Fever
Rash
Arthralgias
Eosinophiluria
AIN
Differences between pyelonephritis and papillary necrosis
Pyelo: onset-few days, symptoms-dysuria, UCx-positive, CT scan-diffusely swollen kidney, Tx-abx
Papillary necrosis: onset-few hours, symptoms-necrotic material in urine, UCx-negative, CT scan-bumpy contour, Tx-none
Summary of tubular diseases
Acute
Toxins
Non nephrotic
No biopsy usually
No steroids
Never additional immunosuppressive agents
Chronic
Not from toxins/drugs
All potentially nephrotic
Biopsy sample
Steroids often
Characteristics of Glomerular Diseases
In terms of diagnostic tests, all forms of glomerulonephritis have:
- UA with hematuria
- Dysmorphic red cells
- Red cell casts
- Low UNa and FENa
- Proteinuria
Difference between glomerulonephritis and nephrotic syndrome?
The degree/amount of proteinuria
Difference between Goodpasture and Wegener granulomatosis
Goodpasture also presents with lung and kidney involvement, but unlike WG, there is no upper respiratory tract involvement
Signs of systemic vasculitis are also absent
Best initial test for Goodpasture and treatment
Antiglomerular basement membrane antibodies
Treat with plasmapheresis and steroids
The most common cause of acute glomerulonephritis in the US
IgA Nephropathy (Berger Disease)
Look for an Asian patient with recurrent episodes of gross hematuria 1-2 days after an upper respiratory tract infection (synpharynigitic)
Treatment for IgA Nephropathy
No treatment proven to reverse the disease
Severe proteinuria is treated with ACE inhibitors and steroids
Follows throat infection or skin infection (impetigo) by 1-3 weeks
PSGN
Look for dark urine, periorbital edema, HTN, and oliguria
Complement levels in PSGN
Low
How many of those with PSGN will progress to ESRD?
5%
Glomerular disease +
Sensorineural hearing loss +
Visual disturbance
Alport Syndrome
Congenital defect of type IV collagen
No specific therapy
Systemic vasculitis that commonly affects the kidneys, tends to spare the lungs, and can be associated with hepatitis B
Polyarteritis Nodosa
In addition to the presentation of glomerulonephritis, PAN presents with:
nonspecific symptoms of fever, malaise, weight loss, myalgias, and arthralgia developing over weeks to months
Stroke in a young person
Look for a vasculitis (e.g., PAN)
Best initial test for PAN
Angiography of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset HTN and characteristic symptoms
Treatment of PAN
Prednisone and cyclophosphamide
Treat hepatitis B when it is found
Why is kidney biopsy performed for lupus nephritis
To determine therapy based on the stage (not to diagnose lupus)
Mild = glucocorticoids
Severe = glucocorticoids combined with either cyclophosphamide or mycophenolate
Large kidneys on sonogram and CT scan
Amyloid
HIV nephropathy
PKD
Diabetes
Diagnosis and treatment of amyloidosis
Biopsy is the most accurate test (green birefringence with Congo red staining)
Control the underlying disease (myeloma, chronic inflammatory diseases, RA, IBD, chronic infection) and use melphalan and prednisone as a last resort
Generalized edema
Hyperlipidemia
Thrombosis
Think nephrotic syndrome
Most common causes of nephrotic syndrome
DM and HTN
- Cancer (solid organ): membranous*
- Children: MCD*
- IV drug use and AIDS: focal-segmental*
- NSAIDs: MCD and membranous*
- SLE: any*
By definition, nephrotic syndrome is:
Hyperproteinuria (>3.5 gram per 24 hours)
Hypoproteinemia
Hyperlipidemia
Edema
Uremia is defined as the presence of:
Metabolic acidosis
Fluid overload
Encephalopathy
Hyperkalemia
Pericarditis
Each of these is an indication for dialysis
Manifestations of renal failure
Anemia
Hypocalcemia and osteomalacia
Bleeding (platelets do not work in a uremic environment)
Pruritis
Hyperphosphatemia
Hypermagnesemia
Atherosclerosis
Endocrinopathy
Most common cause of death in those on dialysis
Accelerated atherosclerosis and hypertension
The immune system helps keep arteries clear of lipid accumulation; WBCs don’t work in a uremic environment
Calcium acetate
Calcium carbonate
Sevelamer
Lanthanum
Oral phosphate binders
When vitamin D is replaced to control hypocalcemia, it is critical to also give phosphate binders; otherwise vitamin D will increase GI absorption of phosphate
Why should aluminum-containing phosphate binders be avoided
Aluminum causes dementia
Intravascular hemolysis
Renal insufficiency
Thrombocytopenia
Think TTP and/or HUS
Hemolysis is visible on smear with schistocytes, helmet cells, and fragmented red cells
TTP is associated with neurological symptoms and fever (very similar to DIC, but does not have increased PT/PTT, decreased fibrinogen, or increased d-dimer)
Difference in management of HUS vs TTP
HUS from E. coli will resolve spontaneously
Plasmapheresis (exchange transfusion) is generally urgent for TTP (associated with HIV, cancer, and drugs such as cyclosporine, ticlopidine, and clopidogrel). If plasmapheresis is not one of the choices, use infusions of FFP.
Steroids DO NOT help and platelet transfusion is never the correct choice
Characteristics of a potentially malignant cyst
Mixed echogenicity
Irregular, thick
Lower density on back wall
Debris in cyst
Pain
Hematuria
Stones
Infection
HTN
PCKD
High-volume water loss from insufficient or ineffective ADH
DI
Nephrogenic is a loss of ADH effect (caused by lithium or demeclocycline, CKD, hypokalemia, or hypercalcemia)
Central is decreased production of ADH
Sodium disorders vs Potassium disorders
Sodium = CNS symptoms
Hyperkalemia = muscular and cardiac symptoms
Treatment of NDI
Correct potassium and calcium
Stop lithium or demeclocycline
Give HCTZ or NSAIDs for those still having NDI despite these interventions
How does Addison disease cause hyponatremia?
Loss of aldosterone
For every 100 mg/dL of glucose above normal, how does the sodium change
1.6 mEq/L decrease
History of bipolar disorder + hyponatremia
psychogenic polydipsia
Management of SIADH
Based on symptoms, not on sodium level
Mild = restrict fluids, Moderate = saline and loop diuretic, Severe = hypertonic saline, conivaptan, tolvaptan
Tolvaptan and conivaptan are antagonists of ADH (used for urgent treatment in the hospital). Demeclocycline treats chronic SIADH.
Correction of sodium must occur slowly: 0.5-1 mEq per hour or 12-24 mEq per day
True/False
Hyperkalemia causes seizures
False
Life-threatening management of hyperkalemia
- Calcium chloride or calcium gluconate
- Insulin and glucose
- Bicarbonate
Kayexalate and loop diuretics can be used to lower potassium when no EKG changes are present
When replacing potassium, what should you keep in mind?
There is no maximum rate or oral potassium replacement (GI cannot absorb faster than the kidneys can excrete)
IV potassium replacement, however, can cause a fatal arrhythmia
How does magnesium effect potassium?
Hypomagnesemia can lead to increased urinary loss of potassium (via magnesium-dependent potassium channels)
2 most important caued of a metabolic acidosis with a normal anion gap
- RTA
- Diarrhea
The anion gap is normal in both of these because the chloride level rises
Define RTA Type 1
AKA Distal RTA
The distal tubule is responsible for generating new bicarbonate under the influence of aldosterone. Drugs such as amphotericin and autoimmune diseases (SLE and Sjogren syndrome) can damage the distal tubule.
Result = acid cannot be excreted into the tubule, raising the pH of the urine
Best test for RTA Type 1
Best initial = UA looking for high pH (> 5.5)
Most accurate = infuse acid into the blood with ammonium chloride (those with distal RTA cannot excrete acid and the urine pH will remain basic)
Define RTA Type II
AKA Proximal RTA
Normally 85-90% of filtered bicarbonate is reabsorbed at the proximal tubule. Damage to the proximal tubule from amyloidosis, myeloma, Fanconi syndrome, acetazolamide, or heavy metals decreases the ability of the kidney to reabsorb most of filtered bicarbonate
Result = bicarbonate is lost in the urine until the body is so depleted that the distal tubule can absorb the rest
Most accurate test for diagnosing RTA II
Give bicarbonate and test the urine
Because the kidney cannot absorb bicarb, the urine pH will rise
Treatment for RTA II
Thiazide diuretics
Volume depletion will enhance bicarbonate reabsorption
What type of RTA occurs most often in diabetics?
Hyporeninemia, Hypoaldosteronism (Type IV RTA)
Test by finding a persistently high urine sodium despite a sodium-depleted diet
For RTA I, II, and IV describe the following:
Urine pH
Blood potassium
Nephrolithiasis
Diagnostic Test
Treatment
I: pH >5.5, low potassium, (+) nephrolithiasis d/t alkaline urine, administer acid to diagnose, treat with bicarb
II: variable pH, low potassium, (-) stones, administer bicarb to diagnose, treat with thiazides
IV: pH <5.5, high potassium, (-) stone, diagnose with urine salt loss, treat with fludrocortisone (steroid with the highest mineralocorticoid effect)
How is the urine anion gap (UAG) used to distinguish RTA from diarrhea?
UAG = Na - Cl
Positive = RTA Negative = diarrhea
The more acid excreted, the greater amount of chloride found in the urine
Causes of metabolic acidosis with an increased anion gap
Lactate
Ketoacids (test acetone level)
Oxalic acids (crystals on UA d/t ethylene glycol overdose)
Formic acid (inflamed retina d/t methanol overdose)
Uremia
Salicylates
COPD/emphysema
Drowning
Opiate overdose
Alpha 1-antitrypsin deficiency
Kyphoscoliosis
Sleep apnea/morbid obesity
Common causes of respiratory acidosis
When the presentation of nephrolithiasis is clear, it is important to…
provide relief from pain (usually with ketorolac, an NSAID that is available orally and IV, that provides a similar level of analgesia to opiates)
Treatment for stones 5-7 mm
Give nifedipine and tamsulosin
Management for stones 0.5-2 cm
Lithotripsy
Long term management of stones
HCTZ
Removes calcium from the urine by increasing distal tubular reabsorption of calcium
Pregnancy safe HTN drugs
Labetalol (first line)
Nifedipine
Alpha methyldopa
Hydralazine
The best initial therapy for HTN with:
CAD
DM
BPH
Depression
Hyperthyroidism
Osteoporosis
CAD - BB, ACEi/ARB
DM - ACEi/ARB (goal <140/90)
BPH - Alpha blockers
Depression - Avoid BBs
Hyperthyroidism - BB first
Osteoporosis - Thiazides
Best initial therapy for hypertensive crisis
Labetolol or nitroprusside (nitroprusside needs monitoring with an arterial line)
Hypertensive crisis is defined as high BP in association with: confusion, blurry vision, dyspnea, or chest pain (not defined as a specific level of BP)
