Acute Kidney Injury And Chronic Kidney Disease Flashcards Preview

Renal II Final > Acute Kidney Injury And Chronic Kidney Disease > Flashcards

Flashcards in Acute Kidney Injury And Chronic Kidney Disease Deck (54):

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
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


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
1. Hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
2. Low cardiac output: CHF
3. Altered renal/SVR ratio: sepsis, cirrhosis
4. Renal hypoperfusion with impaired autoregulation: NSAIDs
5. 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

1. Renovascular obstruction: renal artery obstruction, eg, embolism, dissecting aortic anuerysm
(Renal artery stenosis can be pre-renal or intrinsic renal)
2. Disease of glomeruli or microvasculature: accelerated HTN
3. Acute tubular necrosis (ATN): iodinated contrast dye.
-used with CT's, vascular studies, IVP's (intravenous pyelograms)
4. Interstitial nephritis: acute pyelonephritis, NSAIDs, also can be contrast dye induced, other drugs
5. Intratubular deposition & obstruction: myeloma
6. 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

-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

1. Ureteric:
-calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis)

2. Bladder neck:
-neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot

3. Urethra
-stricture, congenital valve, phimosis


What if AKI is unresponsive to conservative measures?

Consider temporary hemodialysis in following:
Volume overload refractory to diuretics
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?

1. Kidney damage with normal or increase GFR >/= 90
2. Mild decrease in GFR 60-89
3. Moderate decrease in GFR 30-59
4. Severe decrease in GFR 15-29
5. Kidney failure (ESRD)


Describe the early stage of CKD.

Usually symptom free
Overall function intact
Reserve function diminished
BUN/Cr may even be in normal range


58 y/o F presents to clinic for ongoing care after moving. History of sarcoidosis with intermittent HTN and steroid related hyperglycemia. Lab normal. After a year, she has remained stable, on no meds, and no HTN. Her eGFR is 80. CKD stage 2

Which would you recommend?
A. Continue to monitor every 6 months
B. Beta blocker
C. Alpha blocker
D. Diuretic
E. ACE inhibitor

E. ACE inhibitor
-poses kidney protection to delay progression of CKD even if blood pressure does not need treatment


Describe later stages of CKD

Azotemia and accompanying symptoms/signs
Reserve decreases sufficiently, so sudden stress can induce further compromise
-urinary obstruction
-nephrotoxic drugs


Describe effects of uremic toxins on cellular function

Reduction in transmembrane voltage
-increased intracellular Na
-decreased intracellular K
-inhibition of Ca flux

Uremia and its effects are largely reversible with dialysis

Normal erythrocytes incubated in uremic serum demonstrate similar changes


Describe effects of uremic toxins on whole body composition

Osmotically induced overhydration of cells

Increased extracellular volume

Malaise, anorexia, N/V/D
-protein & calorie malnutrition
-negative nitrogen balance
-profound loss of lean body mass & fat deposits


Describe effects of uremic toxins on metabolism

Hypothermia (decreased active Na transport)
Intracellular deficits of K
Metabolic acidosis


Describe effects of uremic toxins on nitrogen and lipids

Protein intolerance
-increased catabolism in uremia
-decreased elimination

Hypertriglyceridemia, decreased HDL, normal cholesterol
-decreased removal by lipoprotein lipase
-increased lipogenesis
-possibly increased production by liver and intestine


Describe effects of uremic toxins on sodium and volume homeostasis

Total body content of Na and water are increased modestly: in stable CKD

Excessive salt ingestion can lead to


Describe effects of uremic toxins on Na and Water

Excessive water ingestion
-weight gain

Recommended fluid intake pre-dialysis
-urine output plus 500 ml/day


Describe potassium effects in chronic renal disease

Normal until late stages
-adaptation in renal distal tubule and colon = sites where aldosterone enhances K secretion

Increased K: cardiac arrhythmias


What are drugs that can increase serum potassium?

Antikaliuretic drugs



Describe how extrarenal fluid loss also contributes to CKD

Impaired renal mechanisms to conserve Na and water in CKD

Vomiting, diarrhea, fever: volume depletion
-dry mucous membranes, dizziness, syncope
-tachycardia, decreased JVP
-cardiovascular collapse


What is the most common complication of ESRD?

HTN as a result of primary renal disease or effects on kidney from systemic disease

Chronic dialysis pts also have a higher incidence of accelerated atherosclerosis which contributes to HTN


If no HTN on clinical exam of ESRD pt, what should you also consider?

Salt wasting form of renal disease causing CKD
-polycystic or medullary cystic disease
-chronic tubulointerstitial disease
-papillary necrosis

Volume depletion

On antihypertensive therapy at the time


Describe pulmonary congested associated with CKD

Unique form, even in absence of volume overload
-normal or mildly elevated intracardiac or pulmonary capillary wedge pressures
-chest x-ray: butterfly wing distribution (peripheral vascular congestion)
--increased permeability of alveolar capillary membranes


Describe pericarditis associated with CKD

Less frequent with early dialysis
-thought to be secondary to metabolic toxins

If occurs in well dialyzed, likely viral infection or systemic disease

Effusion often hemorrhagic

TX: pericardiocentesis, pericardiectomy


Describe hematologic anemia associated with CKD

Normocytic, normochromic anemia
Hemolysis: uremic pts
GI, chronic dialyzer blood loss
Hyperspenism: occasional


Describe hematologic abnormal hemostasis associated with CKD

Prolonged bleeding time
Decreased platelet factor III activity
Abnormal platelet aggregation and adhesiveness
Impaired prothrombin consumption


Describe enhanced susceptibility to infection associated with CKD

Atrophy of lymphoid structures
Neutrophil production relatively unimpaired
Uremia impairs function of all leukocytes


Describe bone changes with uremia

Renal rickets: widened osteoid seams at growth margins

Osteitis fibrosis cystica: due to secondary hyperparathyroidism
-osteoclastic bone resorption
-subperiosteal erosions
-terminal phalanges, long bones, and distal clavicles



Describe bone changes in long term dialysis

Adynamic or aplastic bone disease

Aluminum-induced osteomalacia

Dialysis-related amyloidosis (DRA)
-carpal tunnel syndrome
-tenosynovitis of hands
-shoulder arthropathy
-bone cysts
-cervical spondyloarthropathy
-cervical pseudotumors


42 y/o F presents with increasing fatigue, dyspnea, and poor appetite. Developing elevated BP, lipids, and swelling of extremities.
Lab showed hematuria, RBC casts, increased potassium, low albumin, and eGFR of 20
FH positive for multiple members with kidney problems and several on dialysis (most diabetics with 2 sisters already deceased)

What is your initial diagnosis?

Idiopathic nephrotic syndrome since no diabetes and no prior HTN

However renal biopsy showed FSGS which comprises 15% of nephrotic syndromes
Progresses to CKD in 5-10 yrs.
No proven therapy.


What are signs and symptoms of CKD?

Severity depends on
-magnitude of loss in renal function
-rapidity of loss

Weight loss
Sleep & taste disturbance
Confusion, possibly other forms of encephalopathy


What will PE show with CKD?

Pericardial +/- pleural friction rub
Muscle wasting
Excoriations & ecchymoses


What will labs show with CKD?

Potassium phosphate, uric acid all high
Calcium, albumin, and hemoglobin all low
Metabolic acidosis


What are treatments for CKD?

Aggressive control of HTN
Eliminate volume overload (diuretics, volume intake restriction)
EPO (rHuEPO): recombinant human erythropoietin
Phosphate binders: Ca carbonate or acetate
Restrict dietary potassium
Sodium polystyrene sulfonate binds potassium
ACEIs: diabetes, signficant proteinuria (>1 gm/d)
Dietary protein restriction


What are indications for dialysis?

Unresponsive to conservative measures
Volume overload refractory to diuretics
Encephalopathy otherwise unexplained
Pericarditis, pleuritis
Severe metabolic acidosis compromising respiratory or circulatory function
Need for fluids/drugs also consideration


Describe dialysis methods

PD (peritoneal dialysis) cycler vs dwell time then drain

IHD (intermittent hemodialysis)
-most common type used for AKI
-many CKD pts maintained on 3x/wk

Night-time dialysis
-in-center hemodialysis
-in-home hemodialysis

CCRT (continuous renal replacement therapy)
-if intolerant to IHD
-may see in extremely unstable ICU pts


Describe complications of peritoneal dialysis

Dialysis-related amyloidosis
Insufficient clearance due to vascular disease or other factors


What are complications of hemodialysis?

Accelerated vascular disease
Rapid loss of residual renal function
Access thrombosis
Access or catheter sepsis
Dialysis-related amyloidosis
Protein-calorie malnutrition


Describe absolute contraindication for renal transplant

Active glomerulonephritis
Active bacterial or other infection
Active or very recent malignancy
Hep B surface antigenemia
Severe comorbidity (vascular disease)


What are relative contraindications of renal transplant?

Age>70 yrs
Severe psychiatric disease
Moderately severe degrees of comorbidity
Hep C w/chronic hepatitis or cirrhosis
Noncompliance with dialysis or other tx

Primary renal diseases:
-primary focal sclerosis with prior recurrence in transplant
-multiple myeloma


What are complications of renal transplant?