Renal Exam 1

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167 Terms

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Which diuretics are classified as Natriuretics?
* Carbonic Anhydrase Inhibitor (CAIs)
* Loop Diuretics
* Thiazide & Thiazide-like Diuretics
* Potassium Sparing Diuretics

\*Now Call Larry The K-angaroo\*
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What is the general MOA of Natriuretics?
Agents that increase renal sodium excretion

* Increase \[Na\] in urine → Increase \[H2O\] output → Decrease \[H2O\] in body
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Carbonic Anhydrase Inhibitors Target
Carbonic Anhydrase

* IV (Lumen)
* II (Intracellular)
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Carbonic Anhydrase Inhibitors Site of Action
Proximal Convoluted Tubule - PCT
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Carbonic Anhydrase Inhibitors MOA
Inhibit BOTH isoforms of CA (IV & II) + enhance renal absorption
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What are the 3 drugs in the class of CAIs?
* **Acetazolamide**
* Methazolamide
* Ethoxzolamide
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Are CAIs highly efficacious?
NOT highly efficacious
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What are the side effects of CAIs?

* **Acetazolamide**
* Methazolamide
* Ethoxzolamide
* Increase HCO3- in urine = Basic urine → Urinary alkalization
* Decrease HCO- in blood = acidic blood → Metabolic acidosis
* Renal stones from alkaline urine calcium phosphate
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Does CAIs cause metabolic acidosis or metabolic alkalosis?
Metabolic acidosis
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How does CAIs impact the potassium levels of the blood?
Hypokalemic
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What are the CI for CAIs'?
**Hepatic cirrhosis**

* Hyperammonemia
* Hepatic encephalopathy

**Hyperchloremic acidosis/ COPD**

**Caution w/ Sulfa Allergy**
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What are the drug-drug interactions of CAIs?
* **Increase in amphetamine levels**
* increase excretion of **aspirin**
* **CNS toxicity**
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What is the dosage form and administration for CAIs?
* Tablets & Capsules
* Well absorbed orally
* IV solution
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Loop Diuretic Target
NKCC2
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Loop Diuretic Site of Action
Thick Ascending Limb (TAL)
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Is the Thick ascending limb a major reabsorption location for sodium?
Yes, 25% of Na is filtered as NaCl

* But is impermeable to water
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Loop Diuretic MOA
Inhibit NKCC2 @ TAL → increase renal NaCl excretion + Ca/Mg
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What does NKCC2 stand for and where do these ions go after entering the cell?
* Na - reabsorbed via Na/K pump @basolateral membrane
* K - Secreted via channel back to the lumen
* Cl - reabsorbed via channel @basolateral membrane

\*\*\*Ca, Mg, & Na follow the electrochemical gradient caused by the K and Cl channels
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What does the K channels & Cl channels cause within the cell and what is impacted?
* Lumen-positive transepithelial potential difference
* Helps w/ Ca, Mg, and Na reabsorption
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What drugs are in the class of Loop Diuretics? (Strongest)
* Sulfonamide-Based
* Bumetanide
* Furosemide
* Toresmide
* Non-sulfamide deriv.
* Ethacrynic acid
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What is the dosage form for the sulfonamide-based Loop Diuretics?

* Bumetanide
* Furosemide
* Torsemide
Rapid ORAL absorption + onset
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Of the loop diuretics, which is the most potent?
Bumetanide (X40)
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What are the SE of Loop Diuertics?
* Abnormalities in fluid
* Electrolyte balance - ALWAYS HYPO
* **OTOTOXICITY (ethacrynic acid)**
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Due to the inhibition of NKCC via loop diuretics, what is the impact on the ions?
* K can not cross → can not create the Lumen-positive transepithelial potential difference →
* K, Ca, Mg, Na are stuck on the lumen side
* Hypokalemia
* Hypocalcemia
* Hypomagnesemia
* Hyponatremia
* Hypovolemia
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Loop diuretics cause:
* Hyperuricemia
* Hyperglycemia
* Hyperlipidemia
* Sulfa Allergy
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Loop Diuretics are contraindicated with:
* Hepatic cirrhosis
* Hyperchloremic acidosis
* COPD
* Sulfa Allergy
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Loop Diuretics have DDI with:
* OTOTOXIC AGENTS
* aminoglycosides (ABX)
* Amphotericin B (Antifungal)
* Digitalis glycosides
* **NSAIDs**
* Thiazides
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Thiazides + Thiazide-Like Diuretics Target
NCC

* Sodium - Chloride
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Thiazides + Thiazide-Like Diuretics Site of Action
Distal Convoluted Tubule - DCT
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Is the Distal Convoluted Tubule permeable to water?
No, the DCT is impermeable to water
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What patient population works best w/ TZD?
Ideal for Pts w/ HPT
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Drugs in the Class Thiazides
* HCTZ (prototype)
* Chlorothiazide
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Drugs in the Class Thiazide-Like Diuretics
* Chlorthalidone
* Metolazone
* Indapamide
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What are the SE of Thiazide & Thiazide-Like Diuretics?
* Abnormalities in fluid
* Electrolyte balance
* **Sulfa allergy**
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Due to the inhibition of NCC via thiazide diuretics, what is the impact on the ions?
* Na & Cl can not enter →
* Na/Ca Antiporter increases to compensate →
* ENHANCES Ca2+ reabsorption →
* **Hypercalcemia**
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Which thiazide/thiazide-like diuretic can only be administered parenteral?
Chlorothiazide
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Thiazides can cause hypokalemia. What does this increase the risk of?
Cardiac arrhythmia
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Drug-Drug Interactions of Thiazides
* Quinidine
* QT Prolongation → torsade de pointes arrhythmia
* NSAIDs - reduce effectiveness
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Water permeability at the cortical collecting duct, is controlled by what hormone?
Antidiuretic hormone (ADH)
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How much sodium is filtered at the Cortical collecting duct?
2-3% - via Na channels → regulated by aldosterone THE
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The cortical collecting duct is a major site of what ion secretion?
Potassium

* Major site where all diuretic-induced changes in K+ balance
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Target of K+ Sparring Diuretics
ENac

* Aldosterone
* Mineralocorticoid receptor
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Site of Action for K+ Sparring Diuretics
Cortical Collection Duct (CCD)
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K+ Sparring MOA

1. Inhibits Na+ influx through ENac →
2. Inhibits interaction w/ aldosterone w/ mineralocorticoid → decrease ENaC expression
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K+ Sparring Diuretics: ENaC Inhibitors
* Amiloride
* Triamterene

\*\*\*EAT
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K+ Sparring Diuretic: Mineralocorticoid Receptor Antagonists
* Spironolactone
* Non-selective
* Eplerenone
* Selective

\*\*\*MS. E
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SE of K+ Sparring: Triamterene
Kidney Stones → precipitate in urine
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SE of K+ Sparring: Spironolactone
* Gynecomastia
* Impotence
* Decreased libido

\*Eplerenone - less anti-androgenic effect
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Do K+ Sparring Diuretics cause metabolic acidosis or alkalosis?
* Metabolic acidosis
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What impact does K+ Sparring have on the ion potassium?
Hyperkalemia
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K-Sparring Contraindications
* Pts w/ Hyperkalemia
* Renal failure
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Drug-Drug Interactions of K+-Sparring
* K+ sparing diuretics
* ACEI
* K+ supplements
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How do Aquaretics work?
Increase excretion of solute-free water

* ONLY WATER
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What two classes are Aquaretics?
* Osmotic
* Vasopressin
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Site of Action for Osmotic Diuretic
* Proximal Convoluted Tubule (PCT) +
* Thin Descending Limb (TDL)
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MOA of Osmotic Diuretics
* Increase osmotic pressure w/in the tubule →
* Retention of water in lumen→
* Increased urine output
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What drugs are in the class of Osmotic diurtetics?
* Mannitol
* Glycerin
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How does the osmotic diuretic, Mannitol, engage with the glomerulus?
* Filtered by glomerulus but NOT reabsorbed
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What dosage form is the osmotic diuretic, Mannitol given?
IV ONLY
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What are the SE of osmotic diuretics?

* Mannitol
* Glycerin
* Increase extracellular fluid volume →
* Hyponatremia (HA, N/V)
* Excessive use leads to DEHYDRATION & hypernatremia
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Vasopressin (ADH) Antagonist Target
Antidiuretic Hormone
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Vasopressin (ADH) Antagonist Site of Action
Renal Collecting Duct
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Vasopressin (ADH) Antagonist MOA
* Direct vasopressin receptor antagonists inhibit the translocation →
* Increase water excretion
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Vasopressin (ADH) Drugs
* Vasopressin (non-selective agonists)
* Desmopressin (V2 selective agonists)
* Canivaptan (non-selective)
* Tolyaptan (V2 selective)
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SE of Vasopressin (ADH) Antagonist

* Vasopressin (non-selective agonists)
* Desmopressin (V2 selective agonists)
* Canivaptan (non-selective)
* Tolyaptan (V2 selective)
* Polyuria (dehydration)
* Liver issues for **Tolyaptan**
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Drug-Drug Interactions for Vasopressin Antagonists
* **CYP3A4 inhibitors**
* Liver Pt or liver drugs
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Functions of Kidney:
* EXCRETORY: Electrolytes / Toxins / Drugs - For both acute & chronic KF
* ENDOCRINE: Erythropoietin – Associated with CKD
* METABOLIC: Vitamin D – associated with CKD
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GFR (glomerulus filtration rate):
Estimates how much glomerulus filters
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GFR (glomerulus filtration rate): Normal Output
120ml/min/ 1.73 m^2
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GFR Relationship w/ Age
Inverse → GFR declines with age
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Populations that will have a altered GFR
* Elderly (L)
* Female (L)
* cachectic (malnutritious) (L)
* Obese
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Why do we not round GFR tests?
May lead to an underestimate of renal function → overdose
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SCR (serum creatine): Lab value
\- how much filtration occurring
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• Creatine: product of creatine metabolism from
muscle
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Low SCr for elderly with
low muscle mass
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HIGH SCr
kidneys can’t get rid of Cr, working HARD would still filter out to urine
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Small changes in SCr
big differences in CrCl
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SCr will lag behind ___
Will lag behind GFRs decline by 1-2d
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IBW Male
50kg + (2.3\* inches>5ft)
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IBW female
45\.5kg + (2.3\* inches>5ft)
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If actual BW > IBW x1.2 →
Use adjusted

* ▪ Adjusted BW= 0.4\* (actual BW-IBW)+ IBW
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If actual BW < ideal BW
Use Actual (under-wt)
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If actual BW/Ideal BW< 1.2 →
Use ideal
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Cockcroft-Gault Equation.
CrCl =\[ \[(140-Age) x IBW\]/(72 x SCr) \] x 0.85 (IF FEMALE)
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What is the purpose of Cockcroft-Gault Equation?
Estimate CrCl to determine drug dosages
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How to detect an AKI:
* ↑ in SCr by >0.3mg/dl within 48h
* ↑ in SCr to >1.5xs baseline (known/ presumed to have occurred within 7 days)
* Oliguria: urine volume
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Staging of AKI (KDIGO): Stage 1
detect!

* SCr: 1.5-1.9xs baseline or >0.3mg/dl ↑
* UOP:
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Staging of AKI (KDIGO): Stage 2
* SCr: 2.0-2.9 sx baseline •


* UOP:
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Staging of AKI (KDIGO): Stage 3
* SCr: 3 X baseline OR ↑ in SCr to >4mg/dl OR initiation of dialysis
* UOP:
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Risk Factors for an AKI
* DM,
* HTN,
* HF,
* CKD ,
* Age
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Risk Exposures of AKI
* Volume depletion (dehydration)
* **nephrotoxicity meds,**
* radiocontrast agents,
* sepsis, - body shows systemic infection
* Hypotension + Tachycardia
* urinary system obstruction - post renal
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Complications AKI
* ↑K,
* Uremia,
* metabolic acidosis,
* fluid overload,
* PO4 3- in blood
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Prerenal: Causes of Intravascular Volume Depletion
* Hypovolemia (vol. depletion)
* GI loss,
* hemorrhage,
* Diuretic therapy
* Dehydration
* Dry membranes, Low BP, High HR
* Extensive burns
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Prerenal: Causes of Effective Circulating Blood Volume
* Decreased effective circulatory volume
* distributive shock
* **Systemic vasodilation - SEPSIS**
* **CHF**
* Decreased cardiac output
* Sx: Fluid overload
* JVP
* Pitting edema
* ascites
* Fluid build up in abdomen
* Pulmonary crackles
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Prerenal Causes: Medications
\
* NSAIDs
* ACEi
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AKI - Prerenal Diagnostic Criteria
* UNa:
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Prerenal: COMPENSATORY RESPONSES:
* stimulate the **sympathetic** NS (fight or flight)
* release **antidiuretic** hormone if **hypotension** is present
* stimulate **RAAS** (renin-angiotensin-aldosterone system)

Na reabsorbs, water follows to **help** w/ **dehydration**
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Prerenal: Response of RAAS
* Renal Hypoperfusion
* Angiotensinogen
* //Renin
* Angiotensin I
* //Ace
* **Angiotensin II**
* → **Vasoconstriction**
* **Aldosterone**
* Increase **Na** **reabsorption** in collecting ducts
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Prerenal Sodium Concentration in Urine
* Kidney holds onto Na to maintain intravascular volume (UNa >20) →
* Decrease in urine sodium concentration