Acute Kidney Injury And Chronic Kidney Disease Flashcards
What is acute kidney injury (AKI)?
Increase in serum creatinine +/- decrease in urine output over hours to days
What are the effects of AKI?
Electrolyte disturbances
Acid-base disturbances (metabolic acidosis)
Inability to excrete nitrogenous waste
Intravascular volume overload
20 y/o F student presents to ER after fainting. She awakened immediately after passing out. She had recurrent episodes of dizziness the past 24 hrs and has had N/V for past 2 days. No diarrhea. General body aches since GI symptoms started but no specific abdomen pain. She denies menstrual changes or vaginal drainage. LMP was 4 weeks ago. No OTC, no meds, NKDA, no tobacco/alcohol/drugs. Negative PMH, PSH, FH
Initial assessment for acute mental status change? A. Migraine Variant B. Seizure disorder C. Cardiac arrhythmia D. Drug ingestion E. Orthostatic hypotension
A. Migraine Variant - no headache, no neuro deficits
B. Seizure disorder - no apparent risk factors, immediately awakened on change in position
C. Cardiac arrhythmia - no FH or exam findings to support
D. Drug ingestion - awakened immediately, no history, neuro intact
E. Orthostatic hypotension
-dehydartion (volume contraction or extracellular volume depletion (ECVD) - due to fluid losses from N/V
20 y/o F student presents to ER after fainting. She awakened immediately after passing out. She had recurrent episodes of dizziness the past 24 hrs and has had N/V for past 2 days. No diarrhea. General body aches since GI symptoms started but no specific abdomen pain. She denies menstrual changes or vaginal drainage. LMP was 4 weeks ago. No OTC, no meds, NKDA, no tobacco/alcohol/drugs. Negative PMH, PSH, FH
In addition to urine studies, which diagnostics would help?
A. Ab xray
B. Fingerstick glucose
C. Arterial blood gases
D. ECG
E. Serum electrolytes, BUN, & creatinine
A. Ab xray - no suggestion of blockage or mass on exam
B. Fingerstick glucose - no history of diabetes, no diaphoresis or tachypnea, immediately awakened
C. Arterial blood gases - no resp distress, duration only 2 days, less likely metabolic compoment ot acid/base
D. ECG - cardiac exam normal, no chest pain, no prior histoy
E. Serum electrolytes, BUN, & creatinine
-urine (sodium, potassium, chloride levels that can be affected by dehydration)
BUN/CR will tell if retaining nitrogenous waste and retaining creatinine, indicating AKI
What is fractional excretion of sodium (FeNa)?
Calculated using a random urine sample close to time of blood draw
Helps sort between pre-renal and intrinsic renal
(Una/Pna)/(Ucr/Pcr)X100
What does 1-2% FeNa mean?
1-2% means tubular function not intact
What are the ways to categorize renal disease?
Pre-renal vs intrinsic (renal) vs post-renal
Tubular vs glomerular: based on first areas affected. Ultimately all of kidney will be affected
Underlying etiology, hypertensive nephropathy, diabetic nephropathy
What is the significance of pre-renal determination?
Pre-renal origin suggests that tubules and glomeruli were not initial location of pathology, though they will eventually become affected and possibly permanently
Describe BUN/Creatinine in AKI
Elevation in serum creatinine (Cr) by 50% (if baseline known) or by 0.5-1.0 mg/dL (affected by muscle mass available to generate Cr)
Blood urea nitrogen (BUN) also elevated due to retention of nitrogenous wastes
-elevated BUN=azotemia
-elevated BUN plus confusion = uremia
Describe GFR
Can be estimated by prediction equations that take into account not only serum creatinine but also age, gender, race, and body size
Prediction equations:
-children: Schwartz & Counahan Barrett
-adults: MDRD & Cockcroft-Gault
Describe pre-renal causes
Anything that compromises renal perfusion
- Hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
- Low cardiac output: CHF
- Altered renal/SVR ratio: sepsis, cirrhosis
- Renal hypoperfusion with impaired autoregulation: NSAIDs
- Hyperviscosity syndrome (rare): myeloma
What is effective volume depletion?
3rd spacing
Results in decreased kidney perfusion as seen in pre-renal
What is the treatment for prerenal?
For hypovolemia:
- fluid replacement IV
- as always, treat underlying cause
Even with effective (rather than true) volume depletion such as pancreatitis, large quantities of IV fluids are indicated, with close monitoring for systemic volume overload
Describe causes of intrinsic renal failure
- Renovascular obstruction: renal artery obstruction, eg, embolism, dissecting aortic anuerysm
(Renal artery stenosis can be pre-renal or intrinsic renal) - Disease of glomeruli or microvasculature: accelerated HTN
- Acute tubular necrosis (ATN): iodinated contrast dye.
-used with CT’s, vascular studies, IVP’s (intravenous pyelograms) - Interstitial nephritis: acute pyelonephritis, NSAIDs, also can be contrast dye induced, other drugs
- Intratubular deposition & obstruction: myeloma
- Renal allograft rejection
72 y/o F presents to ER with midsternal chest pain that radiates into L shoulder, has lasted an hour, resting helps, worse with increased activity. No similar previous episodes. Initially cold sweats and trouble breathing. DM-2 controlled on oral agent, hyperlipidemia controlled on oral statin, HTN controlled on thiazide diuretic. NKDA.
Cardio took her for cardiac cath and was able to stent LAD artery. She tolerated procedure well and had no apparent changes through the night. BP remained controlled, but urine seems darker/more concentrated. In the morning, her BUN and creatinine are over 50% increased compared to her ER results.
In addition to dipstick, which on urine micro would point to diagnosis? A. red cell casts B. TNTC bacteria C. Transitional cells D. Urate cyrstals E. Muddy brown casts
A. red cell casts - (dysmorphic red cells) indicate glomerular damag; contrast dye poses risk of more likely tubular damage
B. TNTC bacteria - indicates infection. Pt not febrile
C. Transitional cells - line the bladder
D. Urate cyrstals - no history of gout
E. Muddy brown casts
-tubular damage is most likely initial insult to kidneys after contrast, esp larger volumes of contrast
As much as 300-400 ml for ventriculogram, instead of approx 40-75 cc to examine vessels
May have had normal lab prior to this, but her HTN & DM even though controlled still increase her risk for renal compromise
72 y/o M present with intermittent pink-tinged urine and R mid-back pain for past month. No pain, burning, or change in stream w/urination. PMH: prostatic hypertrophy, peripheral vascular disease, HTN, hyperlipidemia, controlled on current meds and follows for labs every 4 moths. NKDA. + R flank tenderness to percussion. Remainder ab exam normal.
10 months ago
-Normal dipstick and negative microscopic
4 months ago
-BUN/Cr 16/1.0
Current:
- dipstick + for blood
- micro verified few RBC’s
- BUN/Cr 18/2.5
Which would be your next step? A. Cytoscopy B. IVP (intravenous pyelogram) C. CT of pelvis D. MR angiogram E. US abdomen (attn kidneys)
A. Cytoscopy - though bladder cancer can have hematuria, other diagnostics indicated before sending to urology
B. IVP (intravenous pyelogram) - iodinated contrast involved
C. CT of pelvis - won’t show kidneys
D. MR angiogram - though peripheral vascular disease, no bruits on abdominal exam, and expensive test reserved for later if necessary
E. US abdomen (attn kidneys) - non-invasive, more affordable and accessible, and can determine kidney size, hydronephrosis, and possible masses
Describe causes of post-renal blockage
- Ureteric:
- calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis) - Bladder neck:
- neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot - Urethra
- stricture, congenital valve, phimosis
What if AKI is unresponsive to conservative measures?
Consider temporary hemodialysis in following:
Volume overload refractory to diuretics
Hyperkalemia
Encephalopathy otherwise unexplained
Pericarditis, pleuritis
Severe metabolic acidosis compromising respiratory or circulating function
What is chronic kidney disease (CKD)?
Long-standing, irreversible impairment of renal function
Uremia: clinical syndrome resulting from profound loss of renal function
-vs azotemia = elevated BUN
How can GFR be measured?
Ccr (creatinine clearance): 24 hr urine sample measured for creatinine in addition to obtaining serum creatinine
-actual measured value obtained on 24 hr urine more closely approximates actual GFR than using serum Cr alone
Can use inulin as substance to measure but has to be given IV and assay for inulin not available in most labs
What are the 5 stages of CKD?
- Kidney damage with normal or increase GFR >/= 90
- Mild decrease in GFR 60-89
- Moderate decrease in GFR 30-59
- Severe decrease in GFR 15-29
- Kidney failure (ESRD)
