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Flashcards in acute renal failure intro Deck (40):
1

Internal vs external balance

External balance refers to the relationship between intake from the outside and output to the outside. Internal balance refers to shifts between intra and extracellular fluid spaces.

2

1. Understand the physiologic determinants of glomerular filtration rate at a single nephron level

Starling forces: • Glomerular capillary hydrostatic pressure (PGC). • Glomerular capillary oncotic pressure (πGC). • Tubular hydrostatic pressure (PT). • Oncotic pressure in the tubule (πT). • A term that takes into account the surface area and permeability of the glomerular capillary membrane (Kf).

3

Which factor controls single nephron glomerular filtration rate the most

Hydrostatic pressure in glomerular capillary is most important, which favors glomerular filtration. Capillary oncotic pressure and tubular hydrostatic pressure oppose filtration. Tubular oncotic pressure is essentially aero because the glomerulus prevents filtration of proteins into the tubules.

4

Compare filtration at the afferent arteriole vs efferent arteriole sides of the glomerulus

Filtration decreases from the afferent arteriole to the efferent arteriole b/c glomerular oncotic pressure increases as fluid is filtered out and proteins are concentrated

5

Clinical ways to estimate GFR

Plasma based: Urea (BUN) is indirect and not used, and creatinine (most common), or Cockcroft and gault formula. Urine based: clearance formula

6

Urea in the kidney and GFR

Urea is a nitrogenous waste that is endogenously produced, is freely filtered by the glomerulus, and is not secreted. It is, however, reabsorbed at several tubular sites, and thus, its clearance tends to underestimate GFR

7

Creatinine for measurement of GFR

Creatinine is a nonenzymatic breakdown product of creatine that exists in high and fairly stable concentrations in human muscle as well as some other tissues. Creatinine production reflects muscle mass. It is freely filtered by the glomerulus, is not reabsorbed, but is secreted to a variable degree. It tends to overestimate GFR by 10-20%

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3. Understand how to calculate glomerular filtration rate based on plasma

Cockcroft and Gault formula estimates creatinine clearance which estimates GFR. Creatinine clearance = [(A) x (140 - age) x weight]/ (72 x SCr) Where:
• the creatinine clearance is in ml/min
• A=l.0 if male, 0.85 if female
• Age is in years
• Weight is in kg
• Serum creatinine is in mg/dL
Cockcroft and Gault formula estimates creatinine clearance which estimates GFR. Creatinine clearance = [(A) x (140 - age) x weight]/ (72 x SCr) Where:
• the creatinine clearance is in ml/min
• A=l.0 if male, 0.85 if female
• Age is in years
• Weight is in kg
• Serum creatinine is in mg/dL
Cockcroft and Gault formula estimates creatinine clearance which estimates GFR. Creatinine clearance = [(A) x (140 - age) x weight]/ (72 x SCr) Where:
• the creatinine clearance is in ml/min
• A=l.0 if male, 0.85 if female
• Age is in years
• Weight is in kg
• Serum creatinine is in mg/dL

9

3. Understand how to calculate glomerular filtration rate based on urine

Patient collects urine over 24 hr period and has blood draw to determine plasma creatinine. Then calculate: ClCr (ml/min) = (UCr mg/dL) V (ml/min)/ PCr (mg/dL). Where ClCr is creatinine clearance, Ucr is urine creatinine conc., V is urine flow rate (ml/min), PCr is plasma creatinine conc.

10

What causes decreased afferent arteriolar resistance and how does it affect GFR? Increased afferent?

Decreased afferent: NO, PGE2, PGI2, high protein diets cause increased GFR. Increased afferent: NSAIDS, adenosine, norepinephrine, endothelin, thromboxane decreases GFR.

11

What causes decreased efferent arteriolar resistance and how does it affect GFR? Increased efferent?

Decreased efferent: ACEI and ARBs decrease GFR. Increased efferent: angiotensin II increases GFR

12

Normal lab values for plasma: Na, K, Cl, CO2, glucose, creatinine, BUN, phosphorus, Ca, cholesterol, osmolality, plasma anion gap

• Na- 140 ± 3 mEq/L
• K- 4.5 ± 0.6 mEq/L
• Cl- 104 ± 3 mEq/L.
• Total CO2 (tCO2)- 27 ± 2 mEq/L
• Glucose (Fasting)- 90 ± 30 mg/dL
• Creatinine- 1.0 ± 0.3 mg/dL
• BUN- 12 ± 4 mg/dL
• Phosphorus- 4.0 ± 1.0 mg/dL
• Calcium- 9.5 ± 1.0 mg/dL
• Cholesterol- 140-200 mg/dL
• Osmolality- 285 ± 3 mosm/kg H2O
• Plasma Anion Gap = Na – (Cl + tCO2) = 9 ± 2 mEq/L • Na- 140 ± 3 mEq/L
• K- 4.5 ± 0.6 mEq/L
• Cl- 104 ± 3 mEq/L.
• Total CO2 (tCO2)- 27 ± 2 mEq/L
• Glucose (Fasting)- 90 ± 30 mg/dL
• Creatinine- 1.0 ± 0.3 mg/dL
• BUN- 12 ± 4 mg/dL
• Phosphorus- 4.0 ± 1.0 mg/dL
• Calcium- 9.5 ± 1.0 mg/dL
• Cholesterol- 140-200 mg/dL
• Osmolality- 285 ± 3 mosm/kg H2O
• Plasma Anion Gap = Na – (Cl + tCO2) = 9 ± 2 mEq/L • Na- 140 ± 3 mEq/L
• K- 4.5 ± 0.6 mEq/L
• Cl- 104 ± 3 mEq/L.
• Total CO2 (tCO2)- 27 ± 2 mEq/L
• Glucose (Fasting)- 90 ± 30 mg/dL
• Creatinine- 1.0 ± 0.3 mg/dL
• BUN- 12 ± 4 mg/dL
• Phosphorus- 4.0 ± 1.0 mg/dL
• Calcium- 9.5 ± 1.0 mg/dL
• Cholesterol- 140-200 mg/dL
• Osmolality- 285 ± 3 mosm/kg H2O
• Plasma Anion Gap = Na – (Cl + tCO2) = 9 ± 2 mEq/L

13

Normal lab values for urine: Na, K, creatinine, osmolality, specific gravity, pH

• Na- low < 10 mEq/L, high> 40 mEq/L
• K- must be considered in light of plasma potassium.
• Creatinine- usually viewed in concert with plasma creatinine; a UCr/PCr value greater than 20 suggests avid tubular water reabsorption, a value less than 10 suggests less avid water reabsorption.
• Osmolality (again, no "normal range) 285 is isotonic -normally can dilute to less than 50-100 mosm/kg H2O, -normally can concentrate to greater than 1000 mosm/ kg H2O
• Specific gravity- 1.010 is isotonic (< this is dilute, > this is concentrated)
• pH- normally, when faced with an acid load, can decrease urine pH to < 5.2• Na- low < 10 mEq/L, high> 40 mEq/L
• K- must be considered in light of plasma potassium.
• Creatinine- usually viewed in concert with plasma creatinine; a UCr/PCr value greater than 20 suggests avid tubular water reabsorption, a value less than 10 suggests less avid water reabsorption.
• Osmolality (again, no "normal range) 285 is isotonic -normally can dilute to less than 50-100 mosm/kg H2O, -normally can concentrate to greater than 1000 mosm/ kg H2O
• Specific gravity- 1.010 is isotonic (< this is dilute, > this is concentrated)
• pH- normally, when faced with an acid load, can decrease urine pH to < 5.2• Na- low < 10 mEq/L, high> 40 mEq/L
• K- must be considered in light of plasma potassium.
• Creatinine- usually viewed in concert with plasma creatinine; a UCr/PCr value greater than 20 suggests avid tubular water reabsorption, a value less than 10 suggests less avid water reabsorption.
• Osmolality (again, no "normal range) 285 is isotonic -normally can dilute to less than 50-100 mosm/kg H2O, -normally can concentrate to greater than 1000 mosm/ kg H2O
• Specific gravity- 1.010 is isotonic (< this is dilute, > this is concentrated)
• pH- normally, when faced with an acid load, can decrease urine pH to < 5.2

14

Define acute kidney injury

rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine (Pcr) concentration, urea and other nitrogenous waste products. Azotemia is the state where clearance of nitrogenous wastes is reduced

15

Broad categories of disorders that cause acute kidney injury

1. Pre-renal azotemia: a decrease in GFR due to decreases in renal plasma flow and/or renal perfusion pressure. 2. Post-renal azotemia or obstructive nephropathy: a decrease in GFR due to obstruction of urine flow. 3. Intrinsic renal disease: a decrease in GFR due to direct injury to the kidneys (may be due to a variety of insults).

16

Define uremia

constellation of signs and symptoms of multiple organ dysfunction caused by retention of "uremic toxins" and lack of renal hormones due to acute or chronic kidney injury. Symptoms include nausea, vomiting, abdominal pain, diarrhea, weakness and fatigue.

17

Define oliguria and anuria

Oliguria Urine volume is < 400 ml/24 hours in a normal sized adult. Anuria Urine volume is < 50 ml/24 hours in a normal sized adult.

18

Most common cause of abrupt fall in GFR in hospitalized patient

Prerenal azotemia

19

Causes of pre-renal azotemia

1) Decreased ECF volume: renal losses, third space losses, GI losses, hemorrhage. 2) Increased ECF volume (hypervolemia) with decreased cardiac output: CHF, MI, valvular disease, pericardial tamponade. 3) Increased ECF volume with systemic arterial vasodilation: cirrhosis, sepsis, medication, autonomic neuropathy

20

Urine Na and creatinine in pre renal azotemia

Urine sodium concentration will be low (less than 20 mEq/L) because of high reabsorption and urine creatinine concentration will be high (Ucr/Pcr ratio > 20) because of the high water reabsorption which concentrates the urine

21

Equation for fractional excretion of sodium

Ratio of clearance of sodium to creatinine: FENa = (UNa/PNa) ÷ (UCr/Pcr ) X 100 (expressed in %)

22

Pre-renal azotemia vs other pathologies using FEMa

In general, the FENa is < 1% when AKI is caused by prerenal azotemia and > 2% when AKI is caused by other pathologies

23

Causes of post-renal azotemia

• Obstruction of ureters: o Extraureteral (e.g. carcinoma of the cervix, endometriosis, retroperitoneal fibrosis, ureteral ligation)
o Intraureteral (e.g. stones, blood clots, sloughed papilla). • Bladder outlet obstruction (e.g. bladder carcinoma, urinary infection, neuropathy). • Urethral obstruction (e.g. posterior urethral valves, prostatic hypertrophy or carcinoma).• Obstruction of ureters: o Extraureteral (e.g. carcinoma of the cervix, endometriosis, retroperitoneal fibrosis, ureteral ligation)
o Intraureteral (e.g. stones, blood clots, sloughed papilla). • Bladder outlet obstruction (e.g. bladder carcinoma, urinary infection, neuropathy). • Urethral obstruction (e.g. posterior urethral valves, prostatic hypertrophy or carcinoma).

24

Urine Na and creatinine levels in post-renal azotemia

In general there is an impairment of tubular sodium reabsorption that is reflected by high urinary sodium concentrations (> 40 mEq/L) and an impairment of water reabsorption that results in low urine creatinine concentrations (Ucr/Pcr, ratio < 10).

25

Compare acute vs prolonged post-renal obstructions

Prompt relief of acute obstruction is usually associated with complete return of renal function, but prolonged obstruction is often accompanied by incomplete return of renal function after relief of the obstruction

26

Intrinsic renal disease causes

• Vascular diseases: e.g. cholesterol emboli, renal vein thrombosis • Glomerular diseases: e.g. acute glomerulonephritis, hemolytic uremic syndrome • Interstitial diseases: Acute interstitial nephritis (e.g. allergic interstitial nephritis (AIN)), infection, myeloma kidney. • Tubular diseases: Ischemic or nephrotoxic acute tubular necrosis (ATN).

27

Mechanism of acute tubular necrosis

Vascular factors include decreases in renal blood flow and decreases in glomerular permeability (Kf), whereas the tubular factors include tubular obstruction (by cellular debris) and backleak of glomerular filtrate. The primary event may be reduced renal blood flow causing ischemia and injury to proximal tubular epithelial cells which break away exposing bare sections of tubule and allowing backleak. Those cells clog up the tubule causing obstruction

28

Complications of acute tubular necrosis

Infections due to decreased leukocyte function and gastrointestinal tract hemorrhage due to increased acid secretion

29

Components of urine analysis

Macroscopic: visual observation- clear, pale to dark yellow, etc. Dipstick analysis: glucose, protein, heme, bilirubin, ketones, leukocytes. Microscopic: cells (WBCs, RBCs, bacteria, epithelial), casts (cylindrical gel of proteins from renal tubules which are normal if no cells, but abnormal if containing cells)

30

Where are urinary casts formed?

Distal convoluted tubule or collecting duct

31

UA patterns for prerenal azotemia

Relatively high specific gravity, no heme pigment, normal sediment (i.e. any casts are waxy or finely granular).

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glomerulonephritis UA pattern

Variable tonicity, + heme pigment, sediment exam reveals RBC and RBC casts.

33

Acute interstiitial nephritis UA pattern

Isotonic urine, +/- heme pigment, white blood cell casts, eosinophils (with allergic interstitial nephritis)

34

Vascular UA pattern

Variable tonicity, ± hematuria

35

Acute tubular necrosis UA patterns

Typically isotonic, variable heme pigment (+ if from hemolysis or rhabdomyolysis). Sediment exam will show pigmented coarsely granular casts and renal tubular epithelial cells (RTEs).

36

Obsruction UA pattern

Tonicity usually isotonic or hypotonic, usually heme is negative unless superimposed infection. Micro may be totally benign or show evidence of superimposed infection (e.g. RBCs & WBCs).

37

Causes of low FENa

Pre-renal azotemia, nonoliguric ATN, ATN from radiocontrast (causes vasoconstriction), rhabdomyolysis or hemolysis

38

Compare urine Na, Ucr/Pcr, urine osmolality and FENa for pre renal and ATN AKI

Pre-renal: Urine Na 20, Uosm is increased and FENa 20, Ucr/Pcr 2.

39

Complications of acute kidney injury

Loss of fluid balance and electrolyte regulation leading to volume overload (ie. Pulm edema) and electrolyte abnormalities (hyperkalemia and acidosis)

40

Treatment of acute kidney injury

Pre-renal: optimize renal perfusion by improving cardiac output or replacing intravascular volume. Post-renal: relieve obstruction. ATN: dialysis, diuretics