Renal Failure Flashcards
What is RIFLE criteria?
-ARF and AKI are NOT the same
-3 graded levels of injury Risk, Injury, Failure
-2 outcome measures Loss of function and End stage renal disease
-Based on either degree of serum creatinine elevation or decrease in urine output
What are the Functions of the Kidney?
- Regulation of water, minerals and acid-base status
- Removal of metabolic waste products from the blood and their excretion in the urine
- Removal of foreign chemicals/toxins from the blood and their excretion in the urine
- Secretion of hormones (Erythropoietin, renin, Vit D)
What conditions are at a higher risk for developing AKI?
- Hypertension
- Congestive cardiac failure
- Diabetes
- Multiple myeloma
- Chronic infection
- Myeloproliferative disorder
What is Prerenal AKI Etiology?
- Once MAP <80mmhg steep decline in GFR
- Hypovolemia
- Decreased cardiac output
- Decreased effective circulating volume
- Impaired renal autoregulation
What is Pre-renal Injury?
-Most common cause of renal failure (50-80%)
-Results from poor renal perfusion
-Reversed with restoration of renal perfusion/glomerular pressure
-BUN/Creatinine ratio > 20:1
-Calculate fractional excretion of
sodium (FeNa)
-Urinalysis often reveals hyaline
casts
What are Prerenal labs?
- Volume depletion
- Decreased CO/Effective
- Urine output
What is is FeNa?
- FeNa = (UNa x PCr/PNa x UCr) X 100
- FeNa < 1% is suggestive of pre-renal azotemia
- FeNa >1% intrinsic renal failure
- FeNa >4% post-renal failure
What is Prerenal Treatment?
- Volume depletion
- Decreased CO/Effective circulating volume
- All medications cleared by renal excretion should be avoided or doses adjusted
What is the history of AKI?
Volume depletion, Cardiac failure, Radio contrast exposure, Pigment injury, Vasculitis/proliferative glomerulonephritis, Other history of hypotension, shock, exposure to nephrotoxins, new medications, vascular/cardiac surgery, anesthesia, Pertinent PMH/FH, Postrenal Sx’s
What is the AKI’s Physical Exam?
Volume depletion, Cardiac failure, Hepatorenal syndrome, Atheroembolism, Rhabdomyolysis, Interstitial nephritis, Vasculitis, Proliferative glomerulonephritis, Urine volume, Postobstructive, and Uremia
What is Intrinsic Renal Diseases?
-Acute Interstitial Nephritis (AIN)
-Acute Tubular Necrosis (ATN) 90% most
common*
-Glomerular Diseases
-Pyelonephritis
-Malignancy (MM)
-Renal artery embolism/thrombus (renal infarction)
-Vasculitis
What is Acute Interstitial Nephritis (AIN)?
-Typically allergic reaction to medication
-Post-infectious
-Autoimmune
What is the “classic presentation” of Acute Interstitial Nephritis?
- After recent new drug exposure
- Fever
- Skin rash
- Peripheral eosinophilia
- Oliguria
What is Medications associated with acute interstitial nephritis (AIN)?
-Antibiotics (B-lactams, sulfonamides, vancomycin,
erythromycin, rifampin)
-Acyclovir
-NSAIDS (can cause either direct toxicity or
allergy)
-Anticonvulsants (Phenytoin, valproate, carbamazepine)
What is Treatment of AIN?
- Discontinuation of offending agent often leads to reversal of renal injury
- Glucocorticoid therapy may accelerate renal recovery (6 week taper prednisone or IV methylprednisolone pulse 3 days)
- Damage may be permanent if long duration of exposure and high degree of tubular atrophy and interstitial fibrosis
What are Potential Nephrotoxins that cause ATN?
-NSAIDs -Chemotherapeutic agents -Aminoglycosides -Amphotericin -Vancomycin -Radiocontrast dye -Poison (ethylene glycol, heavy metals)
What is Acute Tubular Necrosis (ATN)?
acute tubular cell injury, usually reversible unless severe, prolonged
- Ischemia
- Sepsis
- Toxins
Laboratory Data for Acute Tubular Necrosis (ATN)?
- Pigmented granular casts (muddy-brown casts) on urinalysis
- Cr/BUN elevation
- FeNa >2%
- Serum hyperkalemia
- Serum hyperphosphatemia
- Serum hyperuricemia
What is Treatment for ATN?
-Aggressive volume replacement– hydrate (If nephrotoxic agent, volume depletion)
-If Oliguria present and extracellular-volume normalized consider loop-diuretic high dose (100-200mg Lasix) to improve urine output
-Protein restriction
-If it’s due to nephrotoxic agent, remove
offending agent
-Dialysis
What is Glomerular diseases?
- Infectious Disease associated Syndromes Post-streptococcal glomerulonephritis
- Nephrotic syndrome (Minimal change disease)
- Diabetic nephropathy
- Hypertensive nephropathy
What is Post-streptococcal glomerulonephritis (PSGN)?
-Immune complex containing strep Ag deposited in
affected glomeruli
-Antihypertensives, salt restriction, diuretics
What’s the Epidemiology of PSGN?
- Most common cause of acute kidney injury in children globally
- Primarily occurs in developing countries (97%)
- In developed countries 0.3 per 100,000
- Risk is highest in children 5-12yr & adults >60yrs
What is the Urinalysis of PSGN?
+/-Red blood cell casts
How is PSGN Diagnosed?
- Hematuria, proteinuria, RBC casts
- Positive throat, skin culture (only 25% due to timing)
- Elevated titers of abs to strep products
What is the treatment for IgA nephropathy?
- ACE-/ARB
- Steroids
- Renal transplant
What are Classic clinical presentation of Henoch Schonlein Purpura?
- Rash (especially LE’s and buttocks)
- Abdominal pain/vomiting
- Arthralgias (knees, ankles)
- Edema (hands, feet, scalp, ears)
- Elevated Cr/BUN
- Urine hematuria/proteinuria
What is Nephrotic Syndrome?
- Heavy proteinuria (>3.5g/24hr)
- Hypoalbuminemia (<3 g/dL)
- Peripheral edema
What is the Etiology of Nephrotic Syndrome?
Membranous Nephropathy
- Minimal Change Disease
- Amyloidosis (secondary)
- Systemic Lupus Erythematosus (secondary)
- Membranoproliferative glomerulonephritis
- Focal segmental glomerulosclerosis (FSGS)
- IgA Nephropathy
What is Minimal Change Disease?
-70-90% of nephrotic syndrome in childhood but only 10-15% of nephrotic syndrome in adults.
-Pathophysiology uncertain
-Light microscopy is normal on renal bx or only mild
mesangial cell proliferation
-Characteristic histologic finding is diffuse
effacement of the epithelial cell foot processes on electron microscopy
-Abrupt onset edema & nephrotic syndrome
-Average urine protein – 10gm/day
-Hypoalbuminemia
-HTN
-More suceptible to infection with gram+ organisms
What are the treatments for Minimal Change Disease?
- 30% of children have spontaneous remission but all children are treated with steroids
- 90-95% of children develop complete remission after 8 weeks of steroid therapy
- 80-85% of adults develop complete remission after 8 weeks of steroid therapy
- Prednisone is first line therapy (up to 16 weeks of therapy)
- ESRD is rare but may have relapses
What is vascular AKI?
-Thrombus, embolus, dissection,
vasculitis
-TTP, HUS, DIC
What is Postrenal renal failure?
- Prostatic obstruction (hypertrophy, stricture or malignancy)
- Bladder CA, stone, clots
- Ovarian/cervical/retroperitoneal malignancy
What is Postrenal AKI Treatment?
- Bladder catheterization (Foley catheter, Suprapubic tube)
- Nephrostomy tube
What is Polycystic Kidney Disease?
- Multisystem and progressive genetic d/o with cyst formation and enlargement of the kidney (and other organs ie. Pancreas, liver, spleen)
- 50% require transplant/dialysis by 60yo
- Screen family members as autosomal dominant
- Intracranial aneurysm x2 as common as general population (10%)
- ESRD
What are signs and symptoms of Polycystic Kidney Disease?
-Pain (Abdomen, flank, back) -Enlargement of cysts -Hemorrhage into cyst or perinephric hematoma -Infectious (UTI, pyelonephritis, abscess, infected cyst) -Nephrolithiasis (20-30%)
Diagnosis of Polycystic Kidney Disease?
Urinalysis (Hematuria, 1/3 microalbuminuria)
Treatment for Polycystic Kidney Disease?
- Blood pressure management (ACE-/ARB – slows progression of disease)
- Pain control (Avoid NSAIDs, Surgical cyst decompression (can be done by IR), Nephrectomy)
- Recurrent infections (50% develop UTI (mostly women), May develop infected cysts)
- Hematuria (Hydrate and if substantial transfuse, Very suceptible to trauma (60% hemorrhage))
