RH FINAL

Hypotonic Solutions Cause…

water moves into cells → cells swell → may burst = hemolysis

Hypertonic solutions cause

water to move out of cells → cells shrink = crenation

Severe hyperkalemia treatment

Step 1: Cardiac stabilization
• Calcium gluconate stabilizes myocardial membranes
• Prevents life-threatening arrhythmias
• Does not lower potassium

Step 2: Intracellular potassium shift
• Insulin activates Na⁺/K⁺-ATPase
• Albuterol provides additional intracellular shift
• Dextrose prevents hypoglycemia

Step 3: Potassium removal
• Stool/Feces

● Sodium polystyrene sulfonate- Kayexalate

● Patiromer - Veltassa

● Sodium zirconium cyclosilicate- Lokelma

Renal/Urine

● Loop diuretic

Other

● Dialysis

A-E-I-O-U for Renal Replacement Therapy

Letter	Meaning	Example
A	Acid-base abnormalities	Severe metabolic acidosis
E	Electrolyte abnormalities	Refractory hyperkalemia
I	Intoxications	Salicylates, methanol
O	Overload	Pulmonary edema not responding to diuretics
U	Uremia	Encephalopathy, pericarditis, severe symptoms

Prerenal AKI Treatment

Volume REPLACEMENT

IV crystalloids

• 0.9% Saline

• Lactated Ringers

🦴 CKD-MBD treatment

Step 1: Control phosphorus
• Dietary restriction
• Phosphate binders

Step 2: Address elevated PTH
• Low or normal calcium
– Add active vitamin D or analogs
• High calcium
– Add calcimimetic

Step 3: Escalation
• If PTH remains elevated on two agents
• Add the remaining third class (vitamin D/ Calcimemetic)

Corrected Calcium Formula CKD-MBD

Measured Ca + 0.8 × (4 – serum albumin)

Calcium status	Preferred next step
Low or normal corrected calcium	Vitamin D or vitamin D analog
High corrected calcium	Calcimimetic

(8.5-10.2)

CKD-MBD Therapy First Step

the first step in therapy is to control the phosphorus using a phosphate binder. In advanced stages of CKD, a non-calcium based phosphate binder is strongly preferred.

• Calcium-based: calcium acetate (phos Lo), calcium carbonate

• Non-calcium-based: sevelamer (renvela), lanthanum (fosrenal), ferric citrate (auryxia), Sucroferric Oxyhydroxide (velphoro)

CKD and Cardiovascular Risk

CKD confers an increased risk of cardiovascular disease and death. Appropriate treatment of contributing comorbidities, such as hypertension, dyslipidemia and diabetes, can decrease the incidence and progression of CKD.

Cockcroft-Gault:

CrCl = [(140-age) x (Wt in kg)] / (72 x Cr). x (0.85 if female)

Patient weight	Weight used
ABW < IBW	ABW
ABW > IBW	IBW
ABW > 120% IBW	AdjBW

Major drugs causing hyperkalemia

ACEIs/ARBs

K-sparing diuretics

TMP-SMX

NSAIDs

Heparin

Loop Diuretics can cause

Metabolic alkalosis

they cause loss of chloride, potassium, and volume, which promotes metabolic alkalosis. This is a classic medication-induced acid-base disturbance.

Potassium Repletion ratio

10 mEq/L should typically increase the serum potassium by 0.1 mEq/L.

Bicarbonate deficit

0.5 L/kg × weight (kg) × (24 − HCO3-)

Three nephron processes:

Process	Effect on elimination
Filtration	Moves unbound drug into filtrate
Secretion	Actively moves drug into tubule
Reabsorption	Pulls substance back into blood

Milliosmoles vs Millimoles

A millimole (mmol) measures amount of substance.
A milliosmole (mOsm) measures the number of dissolved particles contributing to osmotic activity. water moves toward higher milliosmoles

Hepatic Encephalopathy Treatment

Therapy	Role
Lactulose	First-line; traps ammonia in gut and increases stooling
Rifaximin	Add-on for recurrent HE or inadequate control
Treat precipitating cause	Infection, GI bleed, constipation, dehydration, meds

Secondary Prevention of Variceal Bleeding

Non selective beta blockers

Propanalol

Nadalol

Carvedilol

Acute Variceal Hemorrhage Treatment

Fluid - Crystallloids

Vasoactive therapy- Octreotide 2-5 days (splanchnic vasoconstriction)

Adverse effects:ischemic events, hypertension, hyperglycemia, bradycardia

SBP prophylaxis

• Ceftriaxone x 5 days

Blood Transfusion PRBC’s - target hemoglobin 7g/dL

EGD with EVL

TIPS- Stent

Liver Labs (Enzymes) in cirrhosis

Aminotransferases

• AST - aspartate transaminase Present in liver, cardiac tissue, skeletal muscle, kidney, and brain

• ALT- alanine transaminase Primarily found in liver

• (AST: ALT / 2:1 in alcohol liver disease)

Alkaline phosphatase

Alk phos/ ALP Found in liver (bile duct) and bone, Important for breaking down proteins

Gamma glutamyl transpeptidase

• GGT- Found in liver and pancrease

ALL INCREASED in Acute Liver Injury

Liver labs (function) in cirrhosis

Albumin decreased

Bilirubin- Increased conc in liver falure

• total direct (conjugated)

• Indirect (unconjugated)

Protein - decreased in liver failure

Clotting factors - decreased in liver failure

PT and INR increased (time to clot)

Goals of Therapy in Liver Disease Complications

Hepatic encephalopathy	Lower ammonia / improve mental status
Varices	Reduce portal pressure / prevent bleeding
Ascites	Mobilize fluid / prevent recurrence
SBP prevention	Prevent infection
HRS-related therapy	Improve renal perfusion and outcomes

 Pathophysiology of Ascites

Portal hypertension and splanchnic vasodilation lead to effective arterial hypovolemia, RAAS activation, sodium retention, and fluid accumulation in the peritoneal cavity because of leak

SAAG > 1.1 and Ascitic protein <2.5 g/dL

Ascites Treatment

Spironolactone - good for forst episode

Loop Diuretic (furosemide 80/40 torsemide 20 bumetanide 1)- Monotherapy less efficacious than spironolactone

Spironolactone:furosemide ratio 100:40 mg- preferred for long-standing ascites

Aminoglycosides cause

Both intrinsic

Tubular and Acute necrosis

Calcium Gluconate MOA

calcium gluconate does not lower potassium levels but antagonizes its effects on the heart

. It acts by raising the action potential threshold, reducing cardiomyocyte excitability, and stabilizing the resting membrane potential.

MOA ACEi how it slows CKD progression

by inhibiting the conversion of Angiotensin I to the vasoconstrictor Angiotensin II, causing dilation of the kidney's efferent arterioles. This reduces intraglomerular pressure and hyperfiltration, which decreases proteinuria and protects nephrons from damage. ACEi are first-line for CKD with albuminuria.

Calcium chloride

Only central line

hypophosphatemia (< 1mg/dL) IV treatment

IV phos supplementation required!!

Use Potassium phosphate if serum potassium < 4 mg/dL (3 mmol phos = 4.4 mEq K+)

Use Sodium Phosphate If serum potassium >4 mg/dL (3 mmol phos = 4 mEq sodium)

Order in units that are multiples of 3 (e.g. 15 mmol, 30 mmol, 45 mmol)

When do you use 3% saline

Acute Euvolemic hyponatremia

Na < 120

mainly for severe symptomatic hypotonic hyponatremia, especially euvolemic cases, and should never be used for isotonic hyponatremia.

3% saline = 513 meq

Acute Hypocalcemia treatment

Severe, Symptomatic (iCa <1 mmol/L)

• 0.5g-1g Iv Calcium or 3g Calcium gluconate over 10 min q1h

Mild to Moderate Asymptomatic (iCa 1-1.2 mmol/L)

• 1 to 2g IV calcium gluconate over 10 minutes q1h

• Oral calcium

Severe, Asymptomatic (iCa <1 mmol/L)

• 3g IV calcium gluconate over 10 minutes q1h

chronic Hypocalcemia treatment

2 to 8g of oral calcium and Vitamin D (if low)

IV calcium should NOT be given in the same line as bicarbonate or phosphate products because of precipitation

Hypomagnesemia Treatment

Mild- 1.3-1.6 mEq/L → 0.05 g/kg

Moderate- 0.8-1.2 mEq/L → 0.1g/kg

Severe- <0.8mEq/L → 0.15g/kg

Oral agents fine if Mag > 1.0mg/DL

hypovolemia signs

Urine Output → Decreased

BUN:SCr ratio > 10:1

Blood pressure Decreased

Heart rate Increased >100

Orthostasis

Poor skin turgor, dry mucous membranes

Slow capillary refill, cool extremities

Decreased weight

Hypervolemia signs

Excess isotonic fluid in extracellular spaces

►Caused by excessive sodium/fluid intake or retention, renal failure with low urine output

• Breathing Increased rate and difficulty Tachypnea, dyspnea, crackles

• Blood pressure Increased

• HR increased

• Distended veins, edema'

• Increased weight

Pseudohyperkalemia

Hemolyzed sample - blood cells are broken from a blood sample and so

there is an increased amount of potassium

• Blood sample is near where potassium is being given

Hyperkalemia drug induced causes

• K+ sparing diuretics (spironolactone)

• NSAIDs

• ACEi

• ARBs

• Heparin

Prerenal (AKI)

urinalysis Indication - low serum sodium

Dehydration is the leading cause

Bun SCR - >20:1

Urine NAa <20

acute interstitial nephritis (AKI) INTRINSIC AKI

urinalysis indication- eosinophils

intrisic aki caused by Acute tubular necrosis (ATN)

Drugs

• Aminoglycosides

• ꞵ - lactams

• Vancomycin

Postrenal AKI

urinalysis indication- crystals

 kidney stones and enlarged prostate glands (obstruction) = cause

Pseudorenal AKI

An increase in lab markers like Scr and BUN,

however, GFR remains unchanged

Causative medications

● Fenofibrate

● Trimethoprim

Hemodialysis

Patients more commonly experience

• hypotension

• clinical instability

• due to the faster flow rate versus peritoneal dialysis.

1.2g/kg/day protein requirement

Peritoneal dialysis.

Peritonitis risk
• Malnutrition
• Technique failure

Patient doing themselves

 1.2-1.3g/kg/day

Factors that increase Dialyzability of drugs in dialysis

• Small volume of distribution
• Low molecular weight
• High-flux dialyzer
• Longer dialysis duration

Medication Changes When Dialysis Starts

Continue: such as phosphate binders and bicarbonate

Iron supplements should be switched to IV

Treatment options for CKD-MBD increase since calcium levels can be better controlled with dialysis

Stop loop diuretics

Add:
• Water-soluble vitamin supplementation

Renal Dysfunction and Half-Life

Explanation:
The more a drug depends on the kidney for clearance, the more renal dysfunction prolongs its half-life.

Concept

Total clearance = renal clearance + nonrenal clearance

Peripheral access

 peripheral lines and midline catheters,

 Central access

including IJ, PICC and femoral lines, allow for faster administration of medications that might not be tolerated well peripherally.

Respiratory Alkalosis: Treatment

■ Usually asymptomatic, especially in chronic patients

■ Treatment of the underlying causes is warranted

– Relief of pain, correction of hypovolemia, treatment of fever,

rebreathing device in anxiety, etc.

■ Oxygen should be initiated in severe hypoxemia

Mild/Moderate Metabolic Acidosis: Treatment

Asymptomatic patients with mild to moderate acidosis generally do not require emergent therapy

– Treat the underlying cause!

■ May require therapy with oral alkali agents

– E.g. sodium bicarbonate, sodium citrate/citric acid,

potassium citrate

■ May be associated with other losses of electrolytes that also need to be replenished (such as Mg2+ and K+)

Severe Metabolic Acidosis: Treatment

Management is dependent on underlying cause and patient’s status

■ Emergent dialysis may be required!

■ IV alkali therapy may be warranted, but its use is a clinical controversy

– Sodium bicarbonate is most widely used

COPD Acid base disorders

COPD causes respiratory acidosis with renal compensation over time.

patients have difficulty ventilating or “blowing off” PaCO2.

Therefore, you should see an increase in PaCO2 which will result in a decrease in pH.

In chronic process, patients with COPD hold onto bicarbonate to compensate for the increase in PaCO2, which therefore normalizes the pH.

IN acute process, the increase in PaCO2 that occurs will result in an acute respiratory acidosis.

Cinacalcet

(Senispar)

Calcimimetic

Approved for treatment of secondary hyperparathyroidism in patients requiring dialysis

• Starting dose 30mg PO daily

• Take with food for maximum absorption

• Adverse Effects

– Hypocalcemia (do not initiate if calcium below normal)

Etelcalcetide

Parsabiv®)

IV calcimimetic indicated to treat

secondary hyperPTH in CKD patients receiving dialysis

– More convenient delivery (IV with HD)

Lanthanum CKD-MBD

Non-calcium phosphate binder (Fosrenol)

Ergocalciferol

– Precursor Vitamin D - 25 hydroxyvitamin D (activation in kidney)

• Nutritional vitamin D2

• Requires renal activation

(Calciferol/Drisdol)

Calcitriol

Active Vitamin D (1,25-hydroxyvitamin D3)
Directly suppresses PTH

(Rocaltrol PO / Calcijex IV)

Cinacalcet

(Senispar)

Calcimimetic

Approved for treatment of secondary hyperparathyroidism in patients requiring dialysis

– Hypocalcemia (do not initiate if calcium below normal)

Etelcalcetide

Parsabiv®)

IV calcimimetic indicated to treat

secondary hyperPTH in CKD patients receiving dialysis

– More convenient delivery (IV with HD)

Fractional Excretion of Sodium (FENa) in AKI

FENa (%)	AKI Etiology
<1	Prerenal
>2	Intrinsic (sodium wasting)
Variable	Postrenal

Hyperphosphatemia treatment in CKD

Calcium carbonate

hyperkalemia treatment

sodium polystyrene sulfonate

oral iron therapy

Recommended:200mg elemental iron/day

Absorption – Increased with Vitamin C coadministration

Polysaccharide iron  Nu Iron extended release

Ferric citrate (Auryxia®) ORAL Fe PREPERATION

IV Iron therapies

Iron dextran	INFeD® DexFerrum®
		each HD session)	iron deficiency
Sodium ferric gluconate	Ferrlecit®
Iron sucrose	Venofer®

Erythropoiesis-Stimulating Agents (ESA) Epoetin Alfa

All injectable

Epogen®,

Procrit®

Erythropoiesis-Stimulating Agents (ESA) Methoxy- PEG epoetin beta

Mircera®

ESAs (Erythropoiesis-Stimulating Agents) Major adverse effects

• Major adverse effects: hypertension; thrombosis; antibody-mediated pure red cell aplasia (rare)

• High-yield “don’t use”: do not use in oncology patients receiving chemotherapy

Phosphate binders (major adverse effects)

GI effects; hypercalcemia with calcium-based products; aluminum toxicity with aluminum products

decreased absorption of iron, zinc, antibiotics → separate administration times

Vitamin D therapy (CKD-MBD) major adverse effects

hypercalcemia and hyperphosphatemia (noted with active vitamin D/calcitriol

iron advrse effects

hpersensitivity

BBW anaphylactic shock - Iron dextran (InFed) (Dexferrum)

Hypotonic (sodium disorders)

LOW serum osmolality (<280 mOsm/kg

Isotonic (sdiu disorder)

NORMAL serum osmolality (280- 295 mOsm/kg)

Causes- hyperglycemia/hyperlipidemia

Hypertonic (sodium disorders)

HIGH serum osmolality (>295 mOsm/kg)

Causes: severe hyperglycemia with dehydration, mannitol use

Hypotonic Hypovolemic Hyponatremia

Volume replacemen

0.9% Saline or LR

3% only if patient having seizures or in a coma and serum sodium < 120 mEq/L

Hypotonic Euvolemic Hyponatremia

syndrome of inappropriate antidiuretic hormone (SIADH)

► Most common cause of hypotonic euvolemic hyponatremia

FLUID RESTRICT

Hypotonic Hypervolemic Hyponatremia

Edema-forming states

►Heart failure, cirrhosis, nephrotic syndrome

►Renal failure

Treatment

• Fluid restriction

• soidum restriction

• Diuretics

Respiratory Acidosis: Treatment

Mechanical ventilation may be warranted

Aggressive treatment of underlying causes

– Bronchodilators, naloxone, etc.

Respiratory Alkalosis: Treatment

Treatment of the underlying causes is warranted

– Relief of pain, correction of hypovolemia, treatment of fever,

rebreathing device in anxiety, etc.

■ Oxygen should be initiated in severe hypoxemia

Causes of Anion-gap Metabolic

Acidosis

Methanol

• Uremia

• Diabetic ketoacidosis

• Propylene glycol

• Isoniazid

• Lactic acidosis

• Ethanol

• Salicylate