AKI and CKD (Grin) Flashcards
How is AKI defined?
By the presence of any of the following:
1. increase in serum creatinine by >0.3 within 48 hrs
2. increase in serum creatinine by >1.5 within 7 days
3. urine volume <0.5mL/kg/hour for 6 hours
Define the 3 features of the ideal substance to estimate GFR.
- Freely filtered across glomerulus
- Not reabsorbed
- Not secreted
Explain the unique features of creatinine as to why we use it to estimate GFR.
It is a metabolite of creatine phosphate in muscle.
1. Freely filtered across glomerulus
2. Not reabsorbed
3. Small amount is secreted in proximal tubule
As GFR function declines, what happens to serum creatinine?
They have an inverse relationship. As GFR declines, serum creatinine will increase.
Definition of anuria
urine output <50-100 mL/day (basically no urine output)
Definition of oliguria
urine output <400-500 mL/day (very little urine output)
Definition of azotemia
elevation of BUN with NO symptoms
Definition of “pre-renal” azotemia
elevation of BUN out of proportion in serum creatinine, specifically due to poor renal perfusion
Definition of uremia
elevation of BUN with symptoms (n/v, confusion, metallic taste in mouth, fatigue, anorexia)
What is the consequence of a disruption in the maintenance of normal volume status?
Volume overload, will present with dyspnea and edema and the severe consequence of this will be pulmonary edema.
What is the consequence of a disruption in the maintenance of normal electrolyte homeostasis?
Na retention will lead to hypertension, potentially leading to a hypertensive emergency.
Decreased K+ excretion will lead to hyperkalemia which can lead to arrhythmias and sudden cardiac death.
What is the consequence of a disruption in the maintenance of normal acid-base balance?
Metabolic acidosis will lead to dyspnea (due to respiratory compensation) and can potentially lead to arrhythmias
What is the consequence of a disruption in the maintenance of waste elimination?
increase in urea will cause uremia (elevated BUN with symptoms -n/v, altered taste, fatigue, confusion) which can lead to encephalopathy, asterixis, uremic pericarditis and uremic frost
Labs for pre-renal AKI
Urine NA < 20 mEq/L; FeNa <1%
BUN/Cr ratio >20:1
Urine Osmolality >500 mosm/kg
Which medications do you want to avoid in patients with pre-renal AKI?
NSAIDs
The body produces prostaglandins to vasodilate arterioles and autoregulate the low renal blood flow, NSAIDs inhibit prostaglandins and will worsen the AKI
What typically occurs when pre-renal AKI presents for a long time?
If pre-renal AKI present long enough, Acute tubular necrosis (ATN) will develop.
What are hypovolemic causes of pre-renal AKI?
Absolute loss of fluid due to:
Bleeding
Vomiting/diarrhea
Overdiuresis
What are hypervolemic caused of pre-renal AKI?
Congestive heart failure (relative loss of fluid)
What are systemic vasodilation causes of pre-renal AKI?
Sepsis
Systemic Inflammatory Response Syndrome (SIRS)
Cirrhosis
What are causes of acute tubular necrosis (ATN)?
Prolonged pre-renal AKI (most common cause is sepsis)
Toxins: myoglobin (rhabdomyolysis), uric acid, myeloma light chains, IV contrast
What are causes of acute interstitial nephritis (AIN)?
PPIs (omprezaloe)
NSAIDs
certain Antibiotics
AIN treatment = STOP offending medications
Explain the relationship between rhabdomyolysis and intrinsic AKI.
Rhabdomyolysis is a condition when damaged skeletal muscle breaks down rapidly; symptoms - muscle pain, weakness, dark urine.
Myoglobin can cause damage to the renal tubules (cause intrinsic AKI). Diagnosis: elevated CK, dipstick positive for blood but no RBCs on sediment
What is the diagnostic test for intrinsic AKI caused by rhabdomyolysis?
elevated creatine kinase (CK) with dipstick positive for blood, but no RBCs on sediment. Myoglobin causes a false positive on dipstick.
What is the classic triad presentation for Acute Interstitial Nephritis (AIN)?
eosinophils in urine (eosinophiluria)
fever
rash
Labs for intrinsic AKI
Urine NA >40 mEq/L; FeNa >35%
BUN/Cr ratio <15:1
Urine Osmolality <350 mosm/kg
Causes of post-renal AKI
Obstruction of urinary flow because of bladder outlet obstruction (BPH most common).
Note: need either bilateral ureteral obstruction or bladder outlet obstruction
All patients with AKI should get what test done during initial workup?
basic metabolic panel (assess BUN/Cr ratio) and urinalysis (assess for blood, protein, casts, signs of infections)
Initial workup for AKI
basic metabolic panel (assess BUN/Cr ratio)
Urinalysis (blood, protein, casts, signs of infection)
Urine electrolytes (FENa and FEUrea)
Urine microalbumin/Cr ratio (assess proteinuria)
What are urinary casts an how are they formed?
Microscopic clusters of urinary particles wrapped in a protein matrix and found in urine.
Tamm-Horsfall protein (secreted by tubules) aggregates into protein matrix and attracts other tubular particles.
Can provide clues to renal pathology.
Tamm-Horsfall protein
Tamm-Horsfall protein (secreted by tubules) aggregates into protein matrix and attracts other tubular particles. Forms urinary casts and can provide clues to renal pathology.
Hyaline cast
Nonspecific cast found in urine, but can indicate pre-renal azotemia
Renal tubular epithelial cells or granular cast (‘muddy brown”)
Can indicate acute tubular necrosis (ATN)
WBC, WBC cast, or urine eosinophils
Can indicate acute interstitial nephritis (AIN)
Proteinuria (<3.5 g/day), hematuria, dysmorphic RBC and RBC casts
Can indicate Nephritic syndrome
Heavy proteinuria (>3.5 g/day), fatty cast, oval fat bodies, minimal hematuria
Can indicate Nephrotic syndrome
FENa indications
FENa <1% = suggests pre-renal (trying not to excrete Na)
FENa >2% = suggests intrinsic AKI (ATN/AIN)
When should you be concerned FENa will be inaccurate?
In patients on diuretics. Consider FEUrea instead.
FEUrea indications
FEUrea < 35% suggests pre-renal
FEUrea > 50% suggests intrinsic AKI: ATN/AIN (we are not excreting urea because the tubules are damaged)
When should we consider a post-void residual test
if concerned for bladder outlet syndrome
When should we consider a renal ultrasound?
if concerned for ureteral obstruction or other post-renal process
When should we consider to test for urine eosinophils?
to assess acute interstitial nephritis (AIN) but sensitivity and specificity is poor
When should we consider a renal biopsy?
reserved for severe AKI of unclear etiology
Indications for dialysis
AEIOU
A- acidosis (metabolic) pH <7.1
E- electrolytes (hyperkalemia) tall peaked t wave on ECG
I- intoxication of methanol, ethylene glycol, lithium
O- overload (volume overload)
U- uremia (encephalopathy or pericarditis)
Chronic Kidney Disease
decreased kidney function or presence of kidney damage (eGFR <60 or markers - albuminuria, urine sediment abnormalities) for 3 or more months
CKD Stage 1
Normal to high CKD
GFR >90 (something else has to be going on)
CKD Stage 2
Mild decrease CKD
GFR 60-89 (something else has to be going on)
CKD Stage 3a
Mild to moderate decrease
GFR 45-59
CKD Stage 3b
Moderate to severe decrease
GFR 30-44
CKD Stage 4
Severe decrease
GFR 15-29
CKD Stage 5
Kidney Failure/End Stage Renal Disease (ESRD)
GFR < 15
What is markers are included when calculating eGFR?
Gender, age and race
What are the top 2 causes of CKD?
Diabetes and hypertension
CKD pathophysiology
Damage to the nephrons from diabetes or HTN (most common) and the nephrons die. There is hyperfiltration and hypertrophy of the remaining nephrons (adaptation) and then there is glomerular damage from increased pressure and flow.
What is the consequence of a disruption in normal erythropoietin (EPO) production as seen in CKD?
Decreased EPO will lead to anemia (inability to compensate) and anemia can potentially lead to requiring a transfusion
What is the consequence of a disruption in the regulation of calcium and phosphate as seen in CKD ?
Secondary hyperparathyroidism, the patient can present with bone pain and fragility and potentially have fractures.
How can CKD lead to iron deficiency?
- chronic blood loss from hemodialysis
- decrease in GI iron absorption
How can CKD lead to bone disease?
- Kidneys cannot excrete phosphate, lead to phosphate retention, increased serum phosphorus will lead to hypocalcemia
- Kidneys cannot produce 1,25(OH); decreased gut Ca reabsorption, hypocalcemia.
Hypocalcemia will cause secondary parathyroidism, increase PTH will increase osteoclast activity which will then lead to chronic bone turnover
Labs for secondary hyperparathyroidism
Decreased calcium
Increased PTH
Increased phosphorus
Labs for tertiary hyperparathyroidism
Increased calcium
Increased PTH
Increased phosphorus
Osteitis fibrosis cystica
CKD leads to decrease calcium, increased PTH, osteoclast activation, bony breakdown.
Bone cyst formation and “brown tumors” -microhemorrhages in bone
All patients with CKD should get what set of tests done?
Basic metabolic panel (creatinine, potassium, bicarb)
eGFR (CKD-EPI equation)
Urinalysis with microscopy
Urine microalbumin/creatinine ratio or urine protein/creatinine ratio
