Nephrology Flashcards
Drugs causing a functional decrease in renal perfusion are:
NSAIDs, ACE-1, Cyclosporine, Cocaine, Contrast used in radiology
Risk factors for CIN (contrast induced nephropathy):
GFR
Prevention of CIN
Administartion of crystalloid 1-1,5 ml/kg/hour for 8 to 12 hours before this procedure
Administartion of acetylsteine in two 600 mg doses the day along with saline infusion for patients with stable chronic renal insufficiency ( Cr > 2,0 mg/dL)
Predisposing factors for NSAID induced AKI
CHF Liver Cirrhosis Atherosclerotic disease of renal artery Nephrotic syndrome Chronic renal failure Hypovolemia
Natural clinical course of ATN
Initiation Phase (hours to days) Continuous ischemic or toxic insult Evolving renal injury ATN is potentially preventable at this time Maintenance Phase (typically 1-2 wks) Maybe prolonged to 1-12 months Established renal injury GFR
Increase in creatinine without AKI
Inhibition of tubular creatinine secretion
Trimethoprim, Cimetidine, Probenecid
Interference with creatinine assays in the lab (false elevation)
glucose, acetoacetate, ascorbic acid, cefoxitin
flucytosine
Increase in BUN without AKI
Increased production GI Bleeding Catabolic states (Prolonged ICU stay) Corticosteroids Protein loads (TPN-Albumin infusion)
Prerenal azothemia
Intravascular volume depletion
bleeding, GI loss, Renal loss, Skin loss, Third space loss
Decreased cardiac output
CHF
Renal vasoconstriction
Liver Disease, Sepsis, Hypercalcemia
Pharmacologic impairment of autoregulation and GFR in specific settings
ACEi in bilateral RAS, NSAIDS in any renal hypoperfusion setting
Fenoldepam in prevention or treatment of AKI
Dopamine-1 receptor agonist, lack of Dopamine-2, and alpha-1 receptor effect, make it a potentially safer drug than Dopamine!
Reduces in hospital mortality and the need for RRT in AKI
Reverses renal hypoperfusion more effectively than renal dose Dopamine
So far so good specially in cardiothoracic ICU patients, awaiting more powered trials in other groups!
When do renal biopsy in AKI
Any evidence of glomerular disease
- nephrotic range proteinuria - sub-nephrotic range proteinuria with hematuria - RBC cast
AKI in renal allograft
Determine the prognosis and chance of recovery of renal function in dialysis dependent AKI.
Whenever potential Bx result can change the management or prognosis.
When to initiate RRT in a patient with AKI
1) Renal Replacement Therapy: Electrolytes imbalances Acid-base disturbances Uremic complications -Encephalopathy -Pericarditis -Persistant nausea, and food intolerance
Dialysis for removal of toxic agents in overdose
3) Removal of toxic agents in overdose
- Ethylene Glycol
- Methanol
- Salicylates
- Lithium
- Theophylline
- Isopropanol
Dialysis in renal/Multiorgan Support Therapy
2) Renal/Multiorgan Support Therapy
- Protects other organs by improving overall body milieu (balance of inflammatory mediators)
- Allowing therapies for other organs that pt could not otherwise tolerate
- volume resuscitation
- aggressive nutrition
Physical examination in AKI
Skin – new rashes. Livedo reticularis – atheroemboli, SLE, cryoglobulins. Petechiae – HSP. Malar rash – SLE. Eye Papilledema – malignant HTN. Roth’s spots – endocarditis. CV Rub – suggestive of uremic pericarditis, lupus. Gallop – suggesting CHF.
Assessing volume status in AKI
Is the patient intravascularly volume depleted?
Neck veins – JVP
Peripheral edema or lack of.
Orthostatic vitals.
Pt. may be edematous (low albumin) or have significant right sided heart disease.