Therapeutic Discussion – Acute Kidney Injury

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Therapeutic Discussion – Acute Kidney Injury
Basic Pathophysiology
Kidneys involved in acid/base balance, hormone regulation, filtering/waste products, BP regulation, water balance
Results in retention of nitrogenous (urea & Cr) & non-nitrogenous waste products, which is accompanied by metabolic
acidosis & hyperK, changes in body fluid balance.
Myoglobin from muscle is toxic to kidney itself
What are the types of acute kidney injury?
Pre-renal – reversible increase in SrCr & [urea]; resulting from decreased renal perfusion = reduction in GFR
- BP falls = dilation of pre-glomerular arterioles via PGI2 & NO
- Concomitant vasoconstriction of post-glomerular arterioles via Ang II
- Both stabilize GFR & fluid delivery to distal nephron
Intrinsic Renal – structures of nephron affected due to tubular necrosis from ischemic or nephrotoxic injury
- Acute tubular necrosis due to sepsis, after surgery or acute radio-contrast nephropathy – will resolve on its own
o Vascular component: intrarenal vasoconstriction w/ fall in GF pressure, vascular congestion, activation of
tubuloglomerular feedback
o Tubular component: tubular obstruction, transtubular backleak of filtrate, interstitial inflammation
o Sepsis – arterial vasodilation w/ decrease in systemic vascular resistance
o Kidneys receive 25% of CO – most of supply is directed to renal cortex -- Blood flow decreased by 3050% w/ a selective reduction in blood supply to outer medulla
- Ischemia – inflammation major pathophysiological finding
o Rapid loss of cytoskeletal integrity & cell polarity w/ shedding of proximal tubule brush border,
mislocalization of adhesion molecules & other membrane proteins, apoptosis & necrosis
 Apoptotic cell death is active process requiring participation of dying cell & changes in cellular
biochem  doesn’t lead to release of intracellular material  doesn’t result in inflammatory
response
Post-renal – obstruction of urinary collection system
**see below for chart
CC. HPI,
Subjective
findings
PMHx
Meds PTA
Objective
 What are the symptoms of acute kidney injury?
Symptoms are related to cause of kidney injury
 What are the risk factors?
Pre-renal: volume depletion (hypoV: decreased effective circulating volume) – acute blood loss, cirrhosis, nephrotic
syndrome, CHF; bilateral renal artery stenosis; sepsis (blood vessels become leaky and volume moves to interstitial
space); hemodynamic changes
Renal: acute tubular necrosis – pre-existing renal impairment, HTN, cardiac disease, PVD, DM, jaundice, advanced age
Post-renal: older men with prostatic disease; pts w/ single kidney/intra-abdominal cancer esp. in pelvic cavity; kidney
stones in ureter
 Are there any medications that may cause acute kidney injury?
NSAIDs in non-healthy – reduce GFR & renal blood flow (pre-renal)
ACEI/ARBs – in pts w/ stenosis of renal artery in solitary kidney or bilateral stenosis (pre-renal) – no pressure to force
blood into tubules; especially bad in hypovolemic patients, liver disease and heart failure patients .. therefore assess
hypovolemia (SBP, HR, SrCr/BUN <10-12, JVP, mucous membranes, urine output <0.5mL/hr)
Nephrotoxic agents – AMG
Acyclovir IV can cause crystallization in urethra causing post-renal failure
 How do we diagnose acute kidney injury?
Acute and sustained increase in [SrCr] of 44.2 mcmol/L (baseline < 221 mcmol/L) OR increase of >20%
(baseline > 221)
Vitals
Physical Exam
Investigations
Vitals, CNS, HEENT: if hypovolemic
GU: acute anuria/severe oliguria (pre-renal: oliguria <400 mL/day; post-renal/renal: any);
renal U/S will show hydronephrosis in post-renal failure
Lab
SrCr – depends on urinary Cl of Cr & on rate of production & Vd – doesn’t accurately reflect
GFR in non-SS condition of acute renal failure; best marker is urine output!
Tubular necrosis w/ intact tubular function: fractional excretion of filtered Na <1%
- If not: fractional excretion > 2-3%
Acute allergic interstitial nephritis: hypersensitivity rxn (fever, rash, arthralgias); urine
contains WBC, RBC, white cell casts; fractional excretion of Na >1%; eosinophilia (except
NSAIDs); mostly caused by B-lactam abx and Septra
Pre-renal: fractional excretion of uric acid & lithium <7% (more specific than Na for prerenal); urine volume & Na excretion are low
Goals of therapy
D/C the offending agent
Prevent pre-renal failure to progress to ischemic acute tubular necrosis
1. Look at post-renal causes first
2. Then look at pre-renal causes (i.e. volume status)
3. Then lastly look at intrinsic causes
Treatment alternatives and duration
Prevention & treatment of associated complications
- HyperK: IV Ca; NaHCO3, glucose & insulin (drives K into
cells)  don’t remove K from body
o Additional tx w/ Na-K exchange resin (ie.
Kayexalate) or dialysis
- Oliguric – daily fluid intake limited to 400 mL + prev.
urinary output
- Dietary Na restricted to 2g/day
- Acidosis – NaHCO3 if conc < 15-19 mmol/L
- HyperP – CaCO3 or other phosphate binders
o Severe – treat w/ dialysis
Dialysis: (cont. > intermittent HD)
Non-oliguric: >450 mL/day
Oliguria: urine output <200 mL/12 hr (50-450 mL/day)
Anuria: urine output <50 mL/12 hr
HyperK: K >6.5 mmol/L
Severe acidemia: pH <7
Azotemia: urea conc >30 mmol/L
Uremic encephalopathy, neuropathy/myopathy, pericarditis
Plasma Na: >155 mmol/L or <120 mmol/L
Hyperthermia
Drug overdose w/ dialyzable toxin
Post-renal – BPH & crystallization  put catheter in
Pre-renal – STOP DRUG; replace intravascular space with NS (250mL will go into space), but caveat is that in
cirrhosis/HF you are also increasing their interstitial volume; should see a decrease in SrCr within 1 day
Post-renal – treat the underlying cause; ensure volume is restored; allow kidneys to recover on their own
Acute allergic interstitial nephritis – stop offending agent, and then may try steroid therapy x 4-6 weeks, then try
cyclophosphamide
Mannitol – prevented acute renal fx only in rhabdomyolysis & kidney-transplant surgey
Low-dose dopamine – renal vasodilator; doesn’t reduce mortality/promote recovery of renal fx; option in septic shock
Acetylcysteine PO – w/ hydration lowers risk of contrast nephropathy in chronic renal insufficiency; also affects tubular
handling of Cr (so decrease in SrCr conc. doesn’t lead to protective effect on GFR)
CCB – no evidence
Monitoring Parameters: Efficacy and toxicity
Efficacy: SrCr, BUN, lytes, urine output
Acute glomerulonephritis – protein leakage
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