Renal and Urology Flashcards
What do abnormal findings for the following Urine Sediment results mean?
Epithelial cells?
Red Blood Cells?
White Blood Cells?
Crystals?
Eosinophils?
Epithelial cells: Suggests contamination of the specimen d/t unhygienic meatus.
Red Blood Cells: Suggests infection, ureteral stones, glomerulonephritis, malignant hypertension
White Blood Cells: Suggests infection, acute interstitial nephritis, exudative glomerulonephritis
Crystals: Kidney stone or gout
Eosinophils: Allergic interstitial nephritis
Types of casts and what they mean:
Hyaline Casts?
Granular casts?
Red blood cell casts?
White blood cell casts?
Hyaline casts - Most common type of casts. They are solidified proteins that are presents because there was low urine flow or dehydration at one point in time and now the urine is flowing again so the hyaline casts are moving. Benign.
Granular casts - Can results as either the breakdown of cellular casts or inclusion of aggregate of plasma. Indicate chronic renal disease or “Muddy brown casts” in acute tubular necrosis
Red Blood Cell Casts: Always pathologic - indicative of glomerular damage. Something immunologic is occurring.
White Blood Cell casts: Severe inflammation or infection, pyleonephritis, nephrotic syndrome
Causes and treatment of urethritis
Frequently a sexually transmitted infection (gonorrhea or chlamydia)
Treatment: Azithromycin 1000mg PO x1 AND metronidazole 1000mg PO x1 AND ceftriaxone 250mg IM x1
A gram for the clam!
Treatment of cystitis/pyelonephritis
Simple/uncomplicated
—Bactrim 1 tab PO every 12 hours x3 days
—Macrobid 100mg PO every 12 hours x7 days
–Fosfomycin 3g PO x1
Serious/complicated
—Ciprofloxacin 200-400mg IV every 12 hours or Levofloxacin 250-500mg IV daily
—Piperacillin-tazobactam (Zosyn) 3.375 grams IV every 6 hours
For those with ESBL - producing gram negative infections: Imipenem 500mg IV every 6 hours
If they have a catheter, remove it and change it
Symptoms of nephrolithiasis
Sudden onset, severe flank pain, unrelieved by any position
Nausea, vomiting
Hematuria - gross or microscopic
Urinary urgency/frequency
Pre-renal vs Post renal: What lab results will help you determine which it is?
Pre-renal: Rise in BUN and Creatinine together (>10:1)
—The higher the BUN, the most likely that it is pre-renal
—Hyaline casts - dehydration
—Urine sodium <20
—Specific gravity >1.015
—FENa <1
Post-renal: Low BUN to creatinine ratio (BUN high but creatinine is not - 10:1)
—Urine sodium >40
—Specific gravity <1.015
—Normal urine sediment
—FENa >3
What other labs could you order to determine if acute renal failure is pre-renal, intrinsic or post-renal?
Urine osm
FENa
Urine Sodium
Pre-renal causes of acute renal failure
Hypovolemia - most common
Severe cardiac dysfunction
Loss of vascular tone - septic or neurogenic shock
Poor renal artery perfusion
Drugs that promote renal vasoconstriction (NSAIDs) or drugs that reduce glomerular filtration pressure (ACE-I)
Intrinsic causes of acute renal failure
Source of damage to the kidney itself
Most serious type of acute renal failure
Glomerulonephritis
Acute tubular necrosis
Acute interstitial nephritis
Tumor lysis syndrome - uric acid rises d/t lysis of tumor cells in chemo
Physical damage to the kidney (crush injury)
Clinical differences between nephrotic syndrome and nephritic syndrome
Glomerulonephritis can cause either nephrotic or nephritic syndrome
Nephrotic Syndrome (usually chronic) - Nephrotic is chronic
Characterized by edema (including in the face) with severe proteinuria and decreased total blood protein with hyperlipidemia
Nephritic syndrome (usually acute)
Characterized by hematuria, oliguria (decrease in urine output) and hypertension
Causes of glomerulonephritis
Non-proliferative - chronic
-Involve changes to the glomerulus where the number of cells is not changed
-Usually present in nephrotic syndrome
-Examples include: Chronic HTN, Lupus, HIV, OUD
Treatment: Long term steroid therapy
Proliferative - acute
-Involve an increased number of cells in the glomerulus
-Present with nephritic syndrome
-Frequently post-infectious, usually with Strep pyogenes
-Rapidly Progressing Glomerulophritis
—-Goodpasture’s syndrome - develops anti-glomerular basement membrane antibodies (anti-GBM) which leads to alveoli and glomeruli bleeding
——Looks like hematuria and hemoptysis at the same time
——Likely need dialysis. Treated with immunosuppression and plasmapheresis
—Granulomatosis with polyangiitis (Wegner’s) - small and medium vasculitis in the lungs and kidneys. Check a cANCA
—–Treated with immunosuppression
Acute tubular necrosis: What is it? What are the two types?
Acute tubular necrosis results from the death of tubular epithelial cells that form the renal tubules of the kidneys
Toxic:
–Rhabdomyolysis
–Aminoglycoside antibiotics (gentamicin, vancomycin)
– Cytoxic drug (cisplatin)
–Toxic alcohols
Ischemic - hypoperfusion, which overlaps perrenal causes
–Critical renal artery stenosis
–Renal artery embolism
–Shock
Treatment is large volume IVF
Causes of Acute interstitial nephritis
Infection or localized allergic reaction to medication
Characterized by sudden renal failure with eosiniphiluria
Causes of post renal acute renal failure
Obstructing renal calculi
Renal, ureteral or bladder malignancy
Prostatic hypertrophy
Obstructed urinary catheter
Acute urinary retention
This is a urologic emergency!
Treatment of hypoNa
If Na <120 there is a risk for brainstem herniation
Can develop seizures, obtundation, dilated pupils, posturing
3% NaCl (hypertonic saline) bolus over 10 minutes (100cc)
Repeat bolus 1-2 times until symptoms improve
Aim for 2-4mmol/L increase every 2 hours
Follow by continuous infusion (50-100ml/hr)
Monitor Na every 2 hours
Discontinue once symptoms free or acute rise in Na of 10mmol/L in first 5 hours
In first 48 hours, do not exceed 15-20mmol/L of correction
—Can lead to pontine myelination syndrome which is irreversible
