AKI, CKD Flashcards
CKD vs AKI
kidneys filter toxins
-controls Na, K elec therefore fluid balance
Creatinine is a chemical compound left over from energy-producing processes in your muscles. Healthy kidneys filter creatinine out of the blood. Creatinine exits your body as a waste product in urine
Chronic Kidney Disease (CKD):
-Progressive, irreversible loss of kidney function
-Greater than 3 months of eGFR <60ml/min despite attempts to try to bring it up
-risks: diabetics, untreated HTN
-when someone has CKD, it is irreversible. eGFR doesn’t return to normal
-can become AKI
-uremic syndrome
-main cause of death: CVD
-most common cause: diabetic neuropathy
vs
Acute Kidney Injury (AKI):
-potentially reversible, can lead to CKD
-Develops over hours - days
-abrupt decline in kidney function leading to increased creatinine, decreased urine output, or both
-Usually associated with other life-threatening conditions
-Follows severe, prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent
-main cause of death: infection
-most common cause: acute tubular necrosis
Who?:
-prolonged hypotension – anyone who has had volume loss dt
-trauma blood loss
-surgical blood loss,
-hypovolemic shock
-burn shock
-septic shock
-liver disease with 3rd spacing and low albumin,
Pts that don’t have enough blood going to the kidneys (hypovolemia) or something is damaging the nephrons that inhibit filtering
RIFLE Criteria
-commonly used classification systems for AKI uses serum creatinine, glomerular filtration rate (or eGFR), and urine output to identify
Risk,
Injury,
Failure,
Loss
End-Stage kidney disease.
AKI
Clinical manifestations range:
Mildly elevated serum creatinine -> anuric renal failure (when urine output is typically between 50 and 400 mL/d)
Causes leading to AKI:
Pre-renal:
-External to the kidneys that impact renal blood flow (ie hypovolemia or meds)
-renal tubular and glomerular function is preserved, just perfusion is low
-Usually, reversible
-meds that cause peripheral vasoconstriction
ex. norepinephrine, dopamine, ACE inhibitors, ARBs
-diabetic neuropathy
Post-renal:
-renal outflow obstruction caused by BPH, kidney stones, cancer, renal calculi = hydronephrosis. Fluid has nowhere to go. Need to tx that before kidney gets damaged.
-Nephrostomy tube (tube into kidney to drain urine)
-postrenal causes are usually reversible if identified before permanent kidney damage occurs
Pre & Post - treat the cause
Infrarenal:
-Conditions that cause direct damage to renal tissue (parenchyma) -> impaired nephron function (ie ATN acute tubular necrosis dt ischemia, nephrotoxins, or sepsis)
conditions:
-prolonged ischemia
-the presence of nephrotoxins (ie gentamycin or CT contrast dye),
-Hgb from hemolyzed RBC’s (ie sickle cell disease)
-myoglobin released from necrotic muscle cells
pre-renal (Tammy PPT)
Prerenal causes of AKI are factors external to the kidneys that impact renal blood flow. These factors reduce systemic circulation leading to reduced glomerular filtration. Although renal tubular and glomerular function is preserved, glomerular filtration is reduced as a result of decreased perfusion. Hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, and vascular obstruction can all decrease the effective circulating volume of the blood. With reduced circulation, autoregulatory mechanisms that increase aldosterone, angiotensin II, norepinephrine and ADH attempt to preserve blood flow to essential organs. Prerenal azotemia (or accumulation of nitrogenous waste products) result in reduced excretion of sodium, increased salt and water retention, and reduced urine output.
Another cause of prerenal AKI is vasoactive medications (ie ACE inhibitors, ARBs, Epinephrine, and/ or dopamine) that cause intrarenal vasoconstriction leading to hypoperfusion of the glomeruli.
Prolonged prerenal AKI can result in acute tubular necrosis, but if the prerenal cause is dealt with promptly, usually, renal function can be regained.
Intra-renal (TAMMY PPT)
Infrarenal causes of AKI can be due to untreated prerenal causes OR they can begin with direct damage to the renal tissue related to nephrotoxic medication administration, hemoglobin released from hemolyzed RBCs or myoglobin released from necrotic muscle cells. Nephrotoxins cause obstruction of intrarenal structures by actually damaging the epithelial cells of the tubules. Hgb and Myoglobin block the tubules and cause renal vasoconstriction. Primary renal diseases (ie SLE or acute glomerulonephritis may also cause AKI.
Post-renal (TAMMY PPT)
Postrenal causes of AKI are related entirely to mechanical obstruction of urinary outflow causing a reflux of urine into the renal pelvis, impairing kidney function. Most commonly, these causes are BPH, Prostate CA, Renal calculi, etc. Postrenal AKI is almost always treatable if identified before permanent kidney damage occurs.
AKI – Clinical Manifestations
Acute tubular necrosis (death of cells in tubules)
AKI – Clinical Manifestations
Prerenal and postrenal AKI are correctible – ADDRESS THE CAUSE
Prerenal and postrenal AKI that hasn’t caused intrarenal damage usually resolves quickly with correction of the cause.
HOWEVER, if tissue damage HAS occurred from either cause or from intrarenal causes, acute tubular necrosis results and / or the course of AKI is prolonged.
Untreated prerenal and postrenal causes +/ or intrarenal causes => ATN
Acute Tubular Necrosis (ATN) has 3 phases:
- Initiation
- Maintenance
- Recovery
NOTE: In some situations, the patient does not recover from AKI and CKD develops
1: Initiation Phase
ATN
1: Initiation Phase
INCREASE serum creatinine + BUN
DECREASE urine output
eGFR is not affected here because it is a later responder to kidney injury
BUN and creatinine are more sensitive
Prime indicator: Urine output is the most early responder – pt is bolused, catheterized, and monitored output
2: Maintenance Phase
ATN
2: Maintenance Phase
days-weeks
Changes in urinary output
Fluid and electrolyte abnormalities
Uremia
urine output changes:
-May be anuric, oliguric, or nonoliguric
Anuric: NO URINE. This is RARE in AKI which is why we won’t talk about it
oliguric: produces LESS THAN 400mL/day or 20mL/ hr
Nonoliguric: dilute urine but uremic toxins present (low specific gravity) (10-14 days). Non-oliguric means the urine output remains unchanged or relatively normal, but the kidneys are unable to filter out urea toxins into the urine.
We will discuss primarily oliguric AKI.
Fluid volume excess: JVD, edema, hypertension -> pulmonary edema, pericardial and/ or pleural effusions
Metabolic acidosis: Kussmaul’s resps (deep rapid) to increase blowing off CO2, lethargy/ stupor (if prolonged)
Sodium Balance: Hyponatremia
Potassium Excess: Hyperkalemia, tall, peaked T waves (ECG)
Calcium and Phosphate: Hypocalemia + hyperphosphatemia
Hematological Disorders: Anemia, bleeding, decreased WBCs.
Waste Product Accumulation: increased creatinine, BUN, decreased eGFR
Neurological Disorders: Fatigue/ difficulty concentrating-> seizures, stupor, coma
explanations for above manifestations
Metabolic acidosis: Kidneys can’t synthesize ammonia, which is needed for hydrogen ion excretion or to excrete acid products of metabolism. Serum bicarb level decreases b/c bicarb is used up buffering H+ ions.
Sodium Balance: Damaged tubules cannot conserve sodium, therefore, the urinary excretion of sodium may increase resulting in hyponatremia.
Potassium Excess: Occurs b/c the normal ability of the kidneys to regulate and excrete potassium is impaired. May be precipitated by a number of causes: massive tissue trauma; bleeding and blood transfusions may cause cellular destruction; acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid. Prompt treatment is essential.
Hematological Conditions: Anemia r/t impaired erythropoietin production. Uremia reduces platelet adhesiveness, leading to bleeding. WBC’s are altered leading to immune deficiency. Infection in association with AKI is associated with double the mortality rate.
Calcium and PO4: Activated Vit D must be present for GI absorption of calcium. Only functioning kidneys can activate Vitamin D, therefore, in damaged kidneys, serum calcium decreases. In response, the parathyroid gland releases PTH, stimulating bone demineralization. Phosphate is released as well, leading to hyperphosphatemia, worsened by the reduced excretion of PO4 by the kidneys. Metabolic acidosis also causes more calcium to be in its ionized state (vs bound to protein). An ionized calcium level that decreases significantly can lead to tetany
Waste Product Accumulation: Kidneys are the primary excretors for urea, the end product of protein metabolism and creatinine, and end product of endogenous muscle metabolism. BUN results have to be interpreted with caution b/c dehydration, corticosteroid use, catabolism d/t infection, severe injury, and GI bleeding can also increase BUN. BUN is non-specific. So Clinically, the recommended method to evaluate kidney function is with an eGFR.
Neurological Disorders: related to accumulation of nitrogenous waste products in the brain and nervous tissue.
3: Recovery Phase
Diuresis: The high urine output occurs d/t osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine.
In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine.
Hypovolemia and hypotension can occur from massive fluid losses.
ATN
3: Recovery Phase
Marked by return of BUN, Creatinine and GFR towards normal states
Diuresis–> fluid & electrolyte abnormalities
-Begins 1-3 L/ 24h –> 3-5 L/ 24h
-Pts must be monitored for hyponatremia, hypokalemia and dehydration
-May last 1-3 weeks
-Patient’s acid-base, electrolyte and waste product values begin to normalize
-Renal function may take up to 12 months to stabilize.
-eGFR returns to normal last
AKI Dx
*CT can see a cause of obstruction but introduces more damage risk to kidneys
MRI and MRA are NOT recommended
Dx
Urinalysis:
-muddy brown Sediment WITH casts (cells wrapped in proteins) -> intrarenal disorders
Urine:
-specific gravity, sodium content, osmolality: helps differentiate different types of AKI
Renal ultrasound:
-anatomy and function
Renal CT:
-can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk
Collaborative Care
Collaborative Care
GOALS of CARE:
Eliminate the cause(s)
Manage S/s
Prevent complications
IMPORTANT: Is there sufficient _Intravascular volume _____ and __cardiac output _____ to perfuse the kidneys?
Intravascular volume and cardiac output = end organ profusion
Diuretic Therapy:
Loop diuretics (ie Lasix)
Osmotic diuretic (ie mannitol)
-Diuretic therapy not helpful in dehydrated pts. Like Prerenal pts with hypovolemia and Postrenal pts with obstruction.
-More for intra-renal tx
Fluid Restriction: 600mL (insensible losses) + previous 24h losses
-more for intrarenal
-Don’t fluid restrict a prerenal hypovolemic pt
Treatment of Electrolyte imbalances
-PPO
Renal Replacement Therapy (RRT) – Usually, hemodialysis (HD)
-HD rather than peritoneal dialysis for AKI because can insert a central line faster and more accurate to reverse AKI than to insert a catheter in peritoneal
If AKI is already established, fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications.
Nutritional Therapy
Nutritional Therapy
Main challenge: Balancing adequate calories to prevent catabolism despite restrictions required to prevent electrolyte and fluid disorders
Energy from fat and carb sources prioritized to prevent ketosis
25-35kCal/kg
Electrolyte replacement in accordance with serum levels
-Sodium is restricted
-Hyperphosphatemia, hypermagnesemia and hypocalcemia
Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)
