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)
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 -infection -urinary obstruction -dehydration -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 CHF HTN Ascites Edema
Describe effects of uremic toxins on Na and Water
Excessive water ingestion
- hyponatremia
- 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
- spironolactone
- triamterene
- amiloride
- trimethoprim
- pentamidine
Others:
- ACEIs
- beta-blockers
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
- orthostasis
- 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
Lymphocytopenia
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
Osteosclerosis
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
Anorexia Weight loss Dyspnea Fatigue Pruritus Sleep & taste disturbance Confusion, possibly other forms of encephalopathy
What will PE show with CKD?
HTN JVD Pericardial +/- pleural friction rub Muscle wasting Asterixis 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 Hyperkalemia 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
Peritonitis Hyperglycemia Hypertriglyceridemia Obesity Hypoproteinemia Dialysis-related amyloidosis Insufficient clearance due to vascular disease or other factors
What are complications of hemodialysis?
Hypotension Accelerated vascular disease Rapid loss of residual renal function Access thrombosis Access or catheter sepsis Dialysis-related amyloidosis Protein-calorie malnutrition Hemorrhage Dyspnea/hypoxemia Leukopenia
Describe absolute contraindication for renal transplant
Active glomerulonephritis Active bacterial or other infection Active or very recent malignancy HIV 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
- amyloid
- oxalosis
What are complications of renal transplant?
Rejection
Immunosuppression
-infection
-neoplasm
