Renal Flashcards
What is AKI (definition)
acute kidney injury - sudden decline in kidney function with or without oliguria
what is the criteria for AKI
increased serum creatinine (SCr) by 50% in 7 days or >0.3mg/dL in 48 hrs
Likely also increased serum BUN, K, uremia, and fluid/electrolyte imbalances
what is uremia
build up of toxins in the blood (BUN & Cr) that manifests as symptoms in multiple body systems
what are the four phases of AKI
initiation, extension, maintenance, and recovery/polyurea
what is the initiation phase of AKI
hypoperfusion/toxicity leading to acute cell injury and dysfunction; characterized by:
1. increased SCr
2. increased BUN
3. oliguria
what is extension phase of AKI
progressive ischemia and inflammation
what is the maintenance phase of AKI
established kidney injury after initial event, body unable to excrete waste
–>changes in urine output, fluid & electrolyte imbalance, uremia
what is the recovery phase
osmotic diuresis from high urea concentration in the glomerular filtrate & inability of tubules to concentrate urine (due to damage) –> causes polyurea which may lead to loss of Na, K & water
what is the cause of pre-renal AKI
renal hypoperfusion (due to hypovolemia, reduced cardiac output, increased vascular resistance, shunting, vasodilation); if prolonged leads to acute tubular necrosis
what labs would be elevated in pre-renal AKI
serum urea and serum creatinine (not being filtered due to low pressure), low urine Na (Na & water retention due to RAAS)
*tubules are still intact and can reabsorb urea and excrete creatinine further leading to serum urea +++
what are the clinical manifestations of pre-renal AKI
oliguria (30cc/hr or less), salt and water retention, low urine Na, high urine osmolality, high BUN/Plasma creatinine ratio (20:1)
what is the cause of intra-renal AKI
intrinsic disorders involving renal parenchymal or interstitial tissue damage (vascular infarctions, HTN/preeclampsia, glomerulonephritis, drug toxicity, or tubulointerstitium causes like ATN or rhabdo)
necrotic cells block tubules and cause them to become dysfunctional (cannot reabsorb urea or excrete creatinine)
what labs are elevated in intra-renal AKI
plasma urea and plasma creatinine +++, high urine sodium
what is the most common type of intra renal AKI
acute tubular necrosis (ATN)
what are the clinical manifestations of intra-renal AKI
nonoliguria, high urine Na, casts (muddy brown), dilute urine (low osmolality)
what is the cause of post-renal aki
obstructions - causes increase in hydrostatic pressure upstream and gradually decreases GFR
what are the clinical manifestations of post-renal AKI
anuria, flank pain, followed by polyurea
what is glomerulonephritis
inflammation of the glomerulus caused by primary injury (infection, ischemia, drugs/toxins, vascular disorder) or secondary injury (systemic disease: DM, CHF, HIV)
*epithelial or podocyte layer to glomerular capillary membrane is disturbed, changing it’s permeability so some proteins can escape into the urine
what is nephrotic syndrome
glomerular injury leads to increased permeability leading to protein (esp albumin) to escape in the urine –> 3.5g more more per day (more than glomerulonephritis)
what is creatinine
a waste product that comes from energy production in the muscle - normally filtered by glomerulus and excreted by kidneys
how is creatinine clearance altered in pre-renal AKI
less Cr filtered due to low perfusion pressure - tubular excretion remains intact
–> serum Cr slightly elevated
what is tubular Cr excretion
moving Cr from plasma directly into renal tubules for excretion into the urine
how is Cr clearance altered in intra-renal AKI
less Cr filtered at clomerulus AND tubular secretion impaired
–>serum Cr ++ elevated
what is eGFR
estimated glomerular filtration rate
what is the eGFR and serum Cr in kidney injury
reduced eGFR and elevated SCr
what are the stages of kidney disease
- GFR normal >90ml/min, no CM
- GFR 60-89, mild HTN, increasing SCr & urea
- GFR 30-59, same as 2
- GFR 15-29, worsening as above, EPO deficiency anemia, hyperphosphatemia, metabolic acidosis, hyperkalemia
- ESKD GFR<15, as 4
what is the goal of treatment for AKI
prevent progression of injury, resolve any complications (hemodynamics, fluid/electrolytes etc)
what is the treatment goal for CKD
dialysis, renal transplant, slow progression
what is the treatment for AKI
-lab evaluation (SCr & urea, lytes, CBC, LFTs, glucose, bone profile, urinalysis, renal US, chest x-ray
-manage hemodynamics & electrolytes, prevent infection, correct metabolic acidosis, maintain nutrition and glucose control, avoid nephrotoxic agents, renal replacement therapy
-no pharm
what is management of CKD
early screening/detection: lab tests (eGFR, SCr, BUN, urinalysis) and imaging (CT, xray, US, biopsy)
nutrition (adequate calories & vit D, restriction of protein, Na, K, and Ph)
manage dyslipidemia (CV risk) HTN, and glucose control
what is the MOA of thiazide diuretics
block reabsorption of Na and Cl in the DISTAL convoluted tubule to promote excretion fo Na, CL, K, and water –> leads to mild diuresis
what are indications for thiazide diuretics
HTN, edema, postmenopausal osteoporosis
–> first line in community “go to” diuretic
what is the MOA for Loop diuretics
blocks reabsorption of Na and CL in the ascending LOOP of Henle to prevent reabsorption of water–> substantial diuresis (most effective)
what is an example of a loop diuretic
furosemide/Lasix
what is the black box for loop diuretics
profound diuresis with water and electrolyte depletion
what is a side effect unique to loop diuretics
ototoxicity, transient deafness with furosemide
what is an indication for loop diuretics
urgent diuresis needed, pulmonary edema related to CHF, uncontrolled HTN, not used in primary care often
MOA for K-sparing diuretics
promotes mild excretion of Na and water while decreasing K excretion, some directly inhibit aldosterone while others work in distal nephron
what are Black Box warnings for K-sparing diuretics
spironolactone = tumorigenic in rats
triamterene = hyperK
indications for K-sparing diuretics
combo use with thiazide or loop to prevent hypoK
what is azotemia
elevation of SCr adn BUN as a result of decreased renal filtration
what are the three most common clinical manifestations of AKI
- anemia (EPO deficiency)
- neurological (confusion, drowsiness, seizures)
- derm (pruritis, inflammation)
prerenal azotemia is associated with: (3 things)
- decreased excretion of Na
- increased salf & water retention
- oliguria
which medications are associated with PRErenal AKI
- ACEi, ARBs, epi, dopamine –> cause efferent arteriole vasodilation
- NSAID - cause afferent arteriole vasoconstriction
both lead to hypoperfusion
are pre-renal AKIs reversible?
yes, but can progress to intra-renal if not corrected
what are the two main causes of ATN
ischemia & nephrotoxins
what is the pathology of AKI
hypovolemia and decreased renal blood flow stimulates release of renin, which triggers RAAS, leads to constriction of afferent arteriole and decrease in glomerular pressure, further decreasing GFR
ischemia damages tubules, which leads to necrosis
necrotic cells build up within tubules and cause obstructions, and glomerular filtrate leads into the blood
ultimately leads to oliguria
when can AKI be reversed?
when ischemia is not prolonged, basement membrane not destroyed, tubular epithelium regenerates
what are the most common causes of post-renal AKI (5)
- prostatic hyperplasia
- prostate cancer
- renal calculi (kidney stones)
- trauma
- extrarenal tumors
what kind of renal injury are associated with casts?
intra-renal
what is the best indicator of kidney function
GFR - provides an approximate measurement of number of functional nephrons
