Intrarenal diseases Flashcards
(83 cards)
Due to uremia or underlying cause –
Decreased urine output, fluid retention, swelling in legs, ankles, feet
Daytime drowsiness
fatigue/weakness
Excessive thirst
N/V
SOB
Irregular heartbeat
Chest pain or pressure
Confusion
Severe = seizures or coma
acute tubular necrosis
What puts someone at risk for acute tubular necrosis?
Recurrent kidney infection/recurrent nephritis
Kidney trauma (blunt/sharp injury)
Adverse reaction to transfusions
Prolonged HOTN and hypoxemia → poor circulation of blood in kidneys
Post-op phase of major surgery due to hypoperfusion
Complications following surgery
Sudden damage or death of the renal tubule/epithelial cells of tubule → acute tubular necrosis → AKI
* MCC of intrinsic kidney disease from either ischemia or nephrotoxic exposure
acute tubular necrosis
Ischemia
- Prolonged prerenal AKI (HOTN, hypovolemic, hypoxic, postop, sepsis)
Nephrotoxic exposure (exogenous, endogenous)
- Endogenous: myoglobinuria (rhabdo), Hgb, hyperuricemia, Bence-Jones
- Exogenous: AGs, amphotericin B (vanc, IV acyclovir, cephalosporins), radiologic contrast dye, calcineurin inhibitors (tacrolimus, cyclosporine)
→ destruction/apoptosis of cells → renal tubular/epithelial casts in urine (muddy brown casts)
acute tubular necrosis
What are endogenous causes of acute tubular necrosis?
myoglobinuria (rhabdo), Hgb, hyperuricemia, Bence-Jones
What are exogenous causes of acute tubular necrosis?
AGs, amphotericin B (vanc, IV acyclovir, cephalosporins), radiologic contrast dye, calcineurin inhibitors (tacrolimus, cyclosporine)
elevated BUN + Cr with BUN/Cr <20:1
Hyperkalemia, hyperphosphatemia, hypocalcemia
ABG
UO: <500mL/24 hours or nonoliguric
Urinalysis: Na>40, FeNa>2%
Muddy brown casts (granular) or renal tubular epithelial cells
Low urine specific gravity (isosthenuria = inability to concentrate urine)
Low urine osmolarity
acute tubular necrosis
What are the 3 phases of acute tubular necrosis?
Initial injury
Maintenance phase
- Oliguric (UOP<500) or nonoliguric
- Average duration 1-3 weeks
- Cellular repair + removal of debris
Recovery phase
- Diuresis
- GFR rising
- BUN+Cr falls
How do you treat acute tubular necrosis?
Fluid therapy and monitoring I&Os, removing offending agent
Widespread use of diuretics should be avoided in critically ill
Nutritional support, kidney adjustment
Dialysis
When is dialysis indicated in acute tubular necrosis?
Worsening acidosis
Life-threatening electrolyte disturbances
Worsening abnormalities or intoxication
Volume overload unresponsive to diuresis
Uremic complications
–> (AEIOU)
Acid-base
Electrolyte
Intoxications
Overload
Uremic sx
AEIOU
Acid-base
Electrolyte
Intoxications
Overload
Uremic sx
dialysis!
Triad of fever, maculopapular rash, and arthralgias
oliguria, peripheral blood eosinophilia
acute interstitial nephritis
inflammatory/allergic response in interstitium of kidney in response to drugs, infections, autoimmune diseases, idiopathic
– NSAIDs, PCNs, sulfa, cephs, rifampin, cipro, allopurinol, diuretics, phenytoin, PPIs
acute interstitial nephritis
Urinalysis: white cells, red cells, white cell casts, proteinuria (NSAID-induced)
Increased IgE, Cr, eosinophilia
Biopsy is gold standard
acute interstitial nephritis
How do you treat acute interstitial nephritis?
Supportive → remove inciting agent + steroids
If symptoms continue, IV methylprednisolone and PO prednisone
Urgent dialysis occurs in up to ⅓ of all cases
SMART NAC (nephrons are crying)
Sulfonamides
Methicillin
Ampicillin
Rifampicin
Thiazides
NSAIDs
Allopurinol
Cimetidine
Cola colored/dark/smoky urine
Edema
HTN
Fever, abdominal/flank pain
AKI = oliguria with <500ml UO
HTN + azotemia + oliguria + hematuria (RBC casts) = hallmark
nephritic syndrome
“Glomerulonephritis” - acute decrease in GFR leading to sodium retention
Inflammation → cytokine release → capillary damage → leakage of proteins and RBCs
nephritic syndrome
Proteinuria <3/day
Hematuria → red cell casts, dysmorphic RBCs
Oliguria from lowered GFR (<400)
Azotemia from insufficient filtering + excretion of urea with increased BUN
Salt retention
Blood test: increased Cr, decreased GFR
Biopsy = hypercellular; (crescent-shape means rapidly progressive glomerulonephritis)
nephritic syndrome
what can help categorize nephritic syndrome?
immune complex disease markers, ANCAs, anti-GBM antibodies, C3 glomerulopathy, monoclonal Ig mediated
How do you treat nephritic syndrome?
Supportive - anti-HTN, steroid, cytotoxic agents, plasmapheresis
Edema, hypervolemia, HTN = BBs, CCBs, loop diuretics
Onset 1-3 weeks after infection – scanty, cola-colored/dark urine, HTN
Type III hypersensitivity
commonly 2-14 year boy with facial periorbital edema up to 3 weeks after strep
Following group A strep infection, commonly pharyngitis or impetigo – deposition of immune complexes against organisms elicit acute inflammatory response
Also: staph, HIV, pneumonias, CMV, abscesses, mono, endocarditis, coccidiomycosis, shunt, malaria, hepatitis, syphilis, mycobacteria, toxoplasmosis
infection-related
infection related is
a type of glomerulonephritis
Immune complex –
Dx: increased antistreptolysin titer (ASO)
Biopsy = glomeruli appear enlarged + hypercellular
Immune complex depositions of IgG, IgM, C3 → “lumpy-bumpy appearance” → dome shaped subepithelial immune-complex deposit “humps”
infection-related glomerulonephritis