Renal Disease Flashcards
Acute Renal Failure
- Lab finding
- Clinical finding
- Serum creatinine increase >0.3 over baseline
- UOP <0.5cc/kg/hr for at least 6 hours
Acute renal failure types: prerenal, renal, postrenal
- Etiology
- Diagnosis
- Treatmment
Acute Renal Failure
Prerenal
- Etiology: Perfussion deficient (volume depletion, severe liver disease, severe CHF)
- Diagnosis: FENa <1%, High urine osmolarity, BUN:creatinine ratio 20:1
- Treatmment: Fluid resuscitation
Renal
- Etiology: Tubular injury, ATN, interstitial disease, glomerular disorder
- Diagnosis: FENa >1%, BUN:creatinine ratio <10:1
- Treatment: Remove renal toxin, treat underlying disease
Postrenal
- Etiology: Urinatry tract obstruction
- Diagnosis: FENa <1% with anuria, BUN:creatinine 10-20:1
- Treatmment: remove obstruction
Chronic Renal Failure
- Diagnositic criteria: Chronicity, GFR, Albuminuria
- Etiology
- Treamtent
- Best predictor of disease progression
Chronic Renal Failure
Diagnositic criteria: Chronicity, GFR, Albuminuria
- Loss of renal function >3 months
- GFR <15
- Albuminuria >300
Etiology
- HTN, DM, Polycycstic kidney disease, Renal Artery stenosis
Treamtent
- Manage HTN with ACE-I and ARBs
Best predictor of disease progression
- Proteinuria
CRF complications
- Hematologic?
- Which electrolyte deragements?
- Anemia
- Hyperkalemia
- Acidosis
Renal Osteodystrophy
- Hypocalcemia (due to low Calcitrol)
- Hyperphosphatemia
- Hyperparathyroidism
Renal Osteodystrophy
- Describe electrolyte deragement
- Describe Endocrine deragement
- How is it treated?
- Describe disease manifestation and clinical consequences
Renal Osteodystrophy
Describe electrolyte deragement
- Kidney can’t excrete phosphate
- Kidney can’t activate Vitamin D to Calcitrol, no calcium absorption
Describe Endocrine deragement
- Increased release of parathyroid hormone
How is it treated?
- Phosphate binder
Describe disease manifestation and clinical consequences
- Bone pain
- Fractures
- Cardiovascular calcifications
Acute Renal Failure - effects
- Fatigue, anorexia, N/V, HA caused by. . ?
- Arrythmia caused by . . ?
- BUN increased or decreased?
- Creatinine increased or decreased?
Acute Renal Failure - effects
- Uremia: Fatigue, anorexia, N/V, HA
- Hyperkalemia: arrythmia
- BUN and Creatinine increased
Renal toxic drugs
- What medicine inhibits prostaglandin synthesis thereby preventing intrinsic renal vasodilitation?
- Drugs with electrolytes (Pen VK, mag citrate)
- Which inhalational anesthetic can be nephrotoxic
Renal toxic drugs
- NSAIDS inhibit prostaglandin synthesis thereby preventing intrinsic renal vasodilitation. End result is vasodilation of afferent (toward glomerulus) renal a. and decreased GFR.
- Drugs with electrolytes (Pen VK, mag citrate)
- Sevoflurane: metabolite compound A is nephrotoxic
Diabetes Insipidus
- Etiologies:
- Presentation labs:
- Presentation clinical:
- Role of DDAVP
- Tx: central
- Tx: nephrogenic
Diabetes Insipidus
- Etiologies: cranial surgery, head trauma, HELLP syndrome
- Presentation labs: hypernatremia
- Presentation clinical: Oliguria (5-10L per day), no edema, concentrated urine
- Role of DDAVP: Diagnositc test: if DDAVP decreases urine then SIADH central (pituitary). If DDAVP has no effect on UOP than renal cause.
- Tx: central: DDAVP
- Tx: nephrogenic: Thiazide, amioloride
ADH
- Life cycle: stimulated by, released from, acts on, effects are??
- What counteracts ADH?
ADH
- Stimulated by:
- hypovolemia recognized by atrial stretch recoptors
- hyperosmolarity recognized by hypothalamus
- Angiotensin II
- Sympathetic
- Released from posterior pituitary
- Acts on:
- Distal tubule and collecting duct to increase H2O permeability
- Sweat glands decrease sweating
- Blood vessels for vasoconstriction
- Effects:
- Decreased UOP
- Urine concentrated
- Intravascular volume increased
- Increased vasconstriction
- Counteracted by:
- Demeclocycline (induces nephrogenic diabetes insipidus) - no longer common tx
- Conivaptan - direct ADH antagonist
SIADH
- Etiology
- Presentation
- Management:
SIADH
- Etiology - Small cell Ca, Head trauma, stroke, meningitis, drugs
- Presentation: hyponatremia, euvolemic, urine concentrated
- Management:
- Fluid restriction
- Conivaptan (direct ADH antagonist)
- Treat underlying cause
Diuretics:
- Site of action
- Effect on K+
- Example medications
Diuretic classes
Loop Diuretic
- Ascending loop
- Lose K+
- Furosemide
Thiazide Diuretic
- DCT
- Lose K+
- HCTZ
Potassium Sparing
- Collecting duct
- Keep K+
- Sprinolactone
Nephritic vs Nephrotic
- Rate of onset
- Proteinuria
- Hematuria
- Albuminemia
- Oliguria
- HTN
- Edema
- Hyperlipidemia
Nephritic vs Nephrotic
- Nephritic is Acute
- Proteinuria = Nephrotic
- Hematuria = Nephritic
- Albuminemia = Nephrotic
- Oliguria = Nephritic
- HTN = Nephritic
- Edema = Nephrotic
- Hyperlipidemia = Nephrotic
Nephritic subtypes
Most common for each subtype
Immune complex: Endocarditis, streptococcal infection
Pauci Immune: Wegners Granulomatosis
Most common cause of primary nephrotic syndrome
Most common cause of secondary nephrotic syndrome
Primary Nephrotic Syndrome:
- Goodpasture IgG deposits
Secondary Nephrotic syndrome
- Diabetes
- Multiple Myeloma light chains
- Amyloidosis
