S4 Exam 1

DKA, HHS, Diabetes Insipidus, SIADH, Hypovolemic Shock, Blood Products + Administration, AKI, CKD, IV Push Medications, Pharmacology

Metformin

• Drug of choice for T2DM

• Increases insulin sensitivity

  • Makes skeletal muscle mass more sensitive to insulin

• Decreases blood glucose levels

  • Decreases glucose absorption in the small intestine

  • Decreases gluconeogenesis by the liver

• Adverse Effects: Anorexia, nausea, diarrhea, nephrotoxicity

• Contraindications: Severe infection, decreased perfusion, decreased oxygenation (increases lactic acid production)

• Patient Education:

  • Take extended-release tablet with dinner

  • Take immediate-release with breakfast and dinner

  • Stop metformin 48 hours BEFORE and AFTER contrast media (increases risk for nephrotoxicity)

Gliptins (DPP-4 Inhibitors)

• Increase insulin release

• Decrease blood glucose levels

  • Decrease glucagon

  • Slows gastric emptying

• Precaution: Impaired renal function (give smaller dose)

• Ex) sitagliptin (Januvia)

  • Take once daily

Meglitinides (Glinides)

• Increases insulin release (stimulates pancreas)

  • Increases fat stores because insulin makes you store fat

• Patient Education: Short-acting, take 30 min before each meal

• Ex) repaglinide, nateglinide

Sulfonylureas

• Increases insulin release (stimulates pancreas)

• Precautions: Renal, hepatic, and adrenal disorders

• Interactions: Alcohol (anti-abuse reaction), NSAIDs

• Patient Education:

  • Long-acting, take 30 min before breakfast

  • Greatly increases risk for hypoglycemia

• Ex) glipizide, glyburide

Alpha-glucosidase Inhibitors

• Decrease blood glucose levels

• Slows absorption/digestion of carbs

• Adverse Effects: Diarrhea, increased gas, hepatotoxicity

• Precaution: GI disease

• Patient Education: Take with first bite of food

• Ex) acarbose, miglitol

Thiazolidinediones

• Decreases blood glucose levels

• Decreases cellular insulin resistance, which increases glucose entering the cells

• Adverse Effects: Fluid retention, hepatotoxicity

• Precautions: Exacerbation of heart failure

• Patient Education: Taken once daily

• Ex) pioglitazone, rosiglitazone

Sodium-Glucose Co-Transporter-2 Inhibitors (SGLT-2 Inhibitors)

• Decreases blood glucose levels

  • Increases excretion of glucose in the urine

• Adverse Effects: cystitis, candidiasis, polyuria, hypotension

• Contraindications: Renal disease

• Patient Education: Take before breakfast

• Ex) canagliflozin, dapagliflozin

Amylin Mimetics

• Decreases blood glucose levels

• Slows gastric emptying

• Inhibits secretion of glucagon

• Can be used for T1DM or T2DM

• Can be used with insulin

• Adverse Effects: Nausea, delayed absorption of oral meds (take 1 hour before or 2 hours after injection)

• Contraindications: Renal failure, dialysis

• Patient Education:

  • Subcut prior to meals

  • Admin 2 inches from insulin injection

  • Do not mix with insulin

  • Keep vial away from sunlight

  • Refrigerate unopened vials

  • Vials in use can be kept at room temperature but must be used within 28 days

  • Severe increased risk for hypoglycemia

• Ex) pramlintide

Incretin Mimetics (GLP-1 Analogues)

• Increases insulin release

• Decreases blood glucose levels

• Decreases glucagon secretion

• Slows gastric emptying

• Only for T2DM

• Adverse Effects: Nausea, vomiting, diarrhea, weight loss, delayed absorption of oral meds

• Contraindications: Kidney failure, irritable bowel diseases (Crohn’s disease, Ulcerative Colitis, etc.), Hx of pancreatitis

• Patient Education: Must remain in refrigerator

• Ex) exenatide, dulaglutide, semaglutide (Rybelsus, Ozempic)

Functions of Insulin

• Transport of glucose inside cells

• Increase uptake of glucose by liver and skeletal muscle

  • Increases glycogen

  • Decreases glycogenolysis

• Promotes K+ and Mg+ to go/stay inside the cells

  • Temporarily decreases serum K+ and Mg+ levels

• Makes fat from excess glucose

• Inhibits breakdown of fat

• Stimulates synthesis of protein

Cells that DO NOT REQUIRE INSULIN for glucose to get inside

BRICKLE

• Brain

• RBCs

• Intestines

• Cornea

• Kidneys

• Liver

• Exercising Skeletal Muscle

Insulin Drip

• High risk medication

• Required 2 RN Check

• If given too quickly, it can cause cerebral edema

• If too much is given, it causes hypoglycemia

• Monitor K+, Na+, and glucose levels

Rapid-acting insulins – Lispro (Humalog)

• ONSET: 15 to 30 minutes

• PEAK: 30 minutes to 3 hours

• DURATION: 3 to 5 hours

Short-acting insulins – Regular (Humulin R)

• ONSET: 30 minutes to 1 hour

• PEAK: 2 to 4 hours

• DURATION: 4 to 12 hours

Only insulin that is administered IV and during pregnancy

Intermediate-acting insulins – NPH insulin (Humulin N)

• ONSET: 1 to 2 hours

• PEAK: 4 to 12 hours

• DURATION: 14 to 24 hours.

Cloudy appearance

Long-acting insulins – Insulin glargine (Lantus)

• ONSET: 2 to 4 hours

• PEAK: None

• DURATION: Up to 24 hours

Ultra-long-acting basal insulin – Insulin Degludec (Tresiba)

• ONSET: 1 hour

• PEAK: None

• DURATION: 24 to 42 hours

Signs/Symptoms of Hypoglycemia

• Shakiness or tremors

• Sweating

• Tachycardia (rapid heart rate)

• Anxiety or irritability

• Hunger

• Headache

• Dizziness

• Confusion

• Blurred vision

• Difficulty concentrating

• Seizures or loss of consciousness (severe)

Signs/Symptoms of Hyperglycemia

• Polyuria (frequent urination)

• Polydipsia (increased thirst)

• Polyphagia (increased hunger)

• Fatigue

• Blurred vision

• Dry mouth

• Warm, dry skin

• Weight loss (especially in Type 1 DM)

• Slow wound healing

• Recurrent infections

Acute Kidney Injury (AKI)

A rapid reduction in kidney function resulting in a failure to maintain waste elimination, fluid and electrolyte balance, and acid-base balance. Occurs over a few hours or days.

• The causes of AKI are reduced perfusion to the kidneys, damage to kidney tissue, and obstruction of urine outflow

• The creatinine level is most commonly used in the recognition of AKI, however this value is not ideal because the creatinine level takes time to increase which can create delays in treatment

• Tissue injury metalloproteinase 2 (TIMP-2) and insulin growth factor binding protein (IGFBP-7) are biomarkers that can identify patients at risk for developing AKI during the next 12 - 24 hours

Definition of AKI

Definition of AKI is one of the following:

• Increase in serum creatinine by 0.3 mg/dL or more within 48 hours

• Increase in serum creatinine to 1.5 times or more from baseline, which is known or presumed to have occurred in the previous 7 days

• Urine volume less than 0.5 mL/kg/hr for 6 hours

KDIGO Classification System for Severity of Acute Kidney Injury

Stage 1

• Serum Creatinine: 1.5-1.9 times baseline OR ≥0.3 mg/dL (≥26.5 umol/L) increase over 48 hr

• Urine Output: <0.5 mL/kg/hr for 6 - 12 hours

Stage 2

• Serum Creatinine: 2.0-2.9 times baseline

• Urine Output: <0.5 mL/kg/hr for >12 hours

Stage 3

• Serum Creatinine: 3.0 times baseline OR Increase in serum creatinine to ≥4.0 mg/dL (≥353.6 umol/L) OR Initiation of renal replacement therapy OR In patients <18 yr, decrease in eGFR to <35 mL/min/1.73 m2

• Urine Output: Anuria lasting for >12 hr OR <0.3 mL/kg/hr for >24 hr

Risk Factors for AKI

• Shock

• Cardiac surgery

• Hypotension

• Prolonged mechanical ventilation

• Sepsis

• Older adults/Adults with diabetes, hypertension, PVD, liver disease, or CKD are at higher risk of AKI if hospitalized

Categories of AKI

• Prerenal: caused by a source outside (or “before”) the kidney (i.e. shock, dehydration, burns, and sepsis); 60-70% of cases

• Intrinsic renal/intrarenal: occurs inside the kidney by disorders that directly affect the kidney (i.e. glomerulonephritis, pyelonephritis, allergic disorders, embolism/thrombosis of renal vessels, nephrotoxic agents)

• Postrenal: caused by urine flow obstruction (i.e. tumors, kidney stones, strictures, BPH)

Prerenal AKI

• 60 - 70% of cases

• Hypoperfusion

• Increased BUN/creatinine

• Decreased urine output

• Increased urine specific gravity

Intrarenal AKI

• Damage within the kidneys

• Acute tubular necrosis

• Increased BUN/creatinine

• Decreased urine specific gravity

• Increased or decreased urine output

Postrenal AKI

• Obstruction

• Increased BUN/creatinine

• Decreased urine output

• Increased or decreased urine specific gravity

AKI: Perfusion Reduction (Prerenal Causes)

Perfusion Reduction (Prerenal Causes)

• Blood or fluid loss

• Blood pressure medications

• Heart attack

• Heart disease

• Infection (e.g., sepsis, septic shock)

• Liver failure

• Use of aspirin, ibuprofen, naproxen, or other related drugs

• Severe allergic reaction (anaphylaxis)

• Severe burns

• Severe dehydration

• Renal artery stenosis

• Bleeding or clotting in the kidney blood vessels (coagulopathy)

• Atherosclerosis or cholesterol deposits that block blood flow in the kidneys

AKI: Kidney Damage (Intrinsic or Intrarenal Causes)

Kidney Damage (Intrinsic or Intrarenal Causes)

• Blood clots in nearby veins and arteries

• Cholesterol deposits that block blood flow in the kidneys

• Glomerulonephritis

• Hemolytic uremic syndrome

• Local infection (pyelonephritis)

• Lupus, an immune system disorder causing glomerulonephritis

• Pharmaceuticals, such as certain chemotherapy agents, antibiotics, iodinated or hyperosmolar contrast media used during imaging tests

• Scleroderma, a group of rare diseases affecting the skin and connective tissues

• Thrombotic thrombocytopenic purpura (TT), a rare platelet disorder that increases clotting

AKI: Urine Flow Obstruction (Postrenal Causes)

Urine Flow Obstruction (Postrenal Causes)

• Bladder cancer

• Cervical cancer

• Colon cancer

• Prostate cancer

• Enlarged prostate

• Kidney stones

• Nerve damage involving the nerves that control the bladder

• Blood clots in the urinary tract

AKI: Compensatory Mechanisms

With pre renal or post renal pathology, the kidneys compensates with three responses of

1. Constricting kidney blood vessels

2. Activating the renin-angiotensin-aldosterone pathway

3. Releasing ADH

These responses increase blood volume and improve kidney perfusion. However, these same responses reduce urine elimination, resulting in oliguria and azotemia (retention and buildup of nitrogenous waste in the blood)

Phases of AKI

Oliguric Phase (1 - 7 Days)

• Urine output <400 mL/day

• Fluid volume overload

• Electrolyte imbalance (hyperkalemia and hyponatremia)

• Metabolic acidosis

• Elevated BUN and creatinine

• Fatigue and malaise

Diuretic Phase (Lasts for 1 - 3 Weeks)

• An increase in urine output (can reach as high as 5 L/day)

• Hypovolemia/Dehydration

• Hypotension

• BUN and creatinine levels begin to normalize

Recovery Phase (Several Months - 1 Year)

• Decreased edema

• Normalization of fluid and electrolyte balance

• Begins when GFR increases

• BUN and creatinine levels plates, then decrease

Signs/Symptoms of AKI

• Oliguria (less than 400 mL/day) or anuria with possible hematuria

• Fluid overload

  • Hypertension, edema, crackles in lungs, shortness of breath

• Dry skin and mucous membranes

• Oxygen saturation below 88%

• Mean arterial pressure (MAP) below 65 mm Hg

• Lethargy, seizures

• Muscle twitching

• Dysrhythmias (due to hyperkalemia)

Labs with AKI

• Serum creatinine (elevated)

• BUN (elevated)

• Glomerular filtration rate (decreased)

• Urine specific gravity (elevated w/ prerenal, low w/ intrarenal)

• Serum electrolytes

  • Hyperkalemia

  • Hyperphosphatemia

  • Hypocalcemia

  • Hyponatremia (prerenal) or hypernatremia (intrarenal)

• Hematocrit (decreased)

• ABGs: metabolic acidosis

Diagnostics with AKI

• KUB x-ray

• Ultrasound (postrenal)

• CT or MRI w/o contrast (prerenal, postrenal)

• Cystography, pyelography

Drug Therapy for AKI

• IV fluids: with caution, measure I&O to prevent fluid overload

• Loop diuretics (i.e. furosemide)

• Calcium channel blockers, if medication toxicity is cause

• Kayexalate (sodium polystyrene sulfonate) or sorbitol to treat hyperkalemia

• Calcium gluconate to treat hyperkalemia

• Sodium bicarb for severe metabolic acidosis

• Phosphate-binding agents for hyperphosphatemia

Therapeutic Procedures with AKI

Kidney (Renal) Replacement Therapy

• Used for patients with loss of kidney function and inadequate waste elimination

• Indications: symptomatic uremia (e.g., pericarditis, neuropathy, decline in cognition), persistent or rapidly rising high potassium levels (I.e. greater than 6.5 mEq/L), severe metabolic acidosis (pH less than 7.1), or fluid overload that inhibits tissue perfusion

• Various types of intermittent and continuous hemodialysis (HD) and peritoneal dialysis (PD)

• Life expectancy ranges from 3 to 5 years, with mortality highest in the first several months following dialysis

Intermittent KRT (Hemodialysis)

• Delivered over 3 to 6 hours, 3 to 4 times per week typically at the bedside of a critically ill patient or in a inpatient dialysis unit

• Uses a dialysis machine to mix and monitor the dialysate (the fluid that helps remove the unwanted particles and waste products from the blood), which is prescribed to restore electrolytes and minerals to normal levels in the blood

• Requires anticoagulation in the dialysis circuit

Continuous KRT

• Used in hospitalized adults (ICU only) who are too unstable to tolerate the changes in BP that occur with intermittent conventional hemodialysis

• Prescribed for over 24 hours

• Uses hemofiltration, diffusion, or a combination to remove toxins and other particles from the blood

Slow Continuous Ultrafiltration (SCUF)

• Dialysis for 12 to 24 hours

• Lower blood flow and dialysate flow rates remove both particles and water, and may be better tolerated by the unstable or critically ill patient with fewer episodes of hypotension

Nutrition Therapy for AKI

• Protein

  • Patient requires dialysis: 1 - 1.5 g/kg

  • Patient does not require dialysis: 0.6 g/kg or 40 g per day

• Sodium: 60 - 90 mEq/kg

• Potassium: restricted to 60 - 70 mEq/kg with hyperkalemia

• Fluid: calculated to equal to the urine volume plus 500 mL

• Oral supplements, enteral nutrition, or parenteral nutrition is used in patients that cannot meet caloric goals

  • Nepro, Suplena, Novasource Renal, etc.

  • IV fat emulsion (Intralipid) infusions can provide nonprotein source of calories. Used in uremic patients to avoid problems with excess sugars

Systemic Complications from AKI

Metabolic

• Metabolic acidosis

• Hyperlipidemia

• Hyperkalemia, Hyponatremia, Hypocalcemia

• Hypophosphatemia

Gastrointestinal

• Nausea/Vomiting

• Decreased peristalsis

• Enteral nutrition intolerance

• Malnutrition

• Ulcer formation

• Bleeding

Cardiopulmonary

• Peripheral and pulmonary edema

• Heart failure

• Pulmonary embolism

• Pericarditis

• Pericardial effusion

• Hypertension

• Myocardial infarction

Neurologic

• Neuromuscular irritability or weakness

• Asterixis

• Seizures

• Mental status changes

Immune/Infectious

• Pneumonia

• Sepsis

Hematologic

• Bleeding

• Thrombosis

• Anemia

Renal

• Chronic kidney disease (CKD)

• End-stage kidney disease (ESKD)

Other

• Hiccups

• Elevated parathyroid hormone

• Low thyroid hormone level

Examples of Potentially Nephrotoxic Drugs

Antibiotics/Antimicrobials

• Amphotericin B

• Colistimethate

• Polymyxin B

• Rifampin

• Sulfonamides

• Tetracycline hydrochloride

• Vancomycin

Aminoglycoside Antibiotics

• Gentamicin

• Neomycin

• Tobramycin

Chemotherapy Agents

• Cisplatin

• Cyclophosphamide

• Methotrexate

NSAIDs

• Celecoxib

• Flurbiprofen

• Ibuprofen

• Indomethacin

• Ketorolac

• Meloxicam

• Nabumetone

• Naproxen

• Oxaprozin

• Tolmetin

Other Drugs

• Acetaminophen

• Captopril

• Cyclosporine

• Fluorinated anesthetics

• Metformin

• Quinine

Examples of Potentially Nephrotoxic Substances

Organic Solvents

• Carbon tetrachloride

• Ethylene glycol

Nondrug Chemical Agents

• Radiographic contrast media (e.g., iodinated media, hyperosmolar media, and gadolinium)

• Pesticides

• Fungicides

• Myoglobin (from breakdown of skeletal muscle)

Heavy Metals and lons

• Arsenic

• Bismuth

• Copper sulfate

• Gold salts

• Lead

• Mercuric chloride

Chronic Kidney Disease (CKD)

• Progressive, irreversible disorder lasting longer than 3 months

  • GFR <60 mL/min for 3+ months

• When kidney function and taste elimination are too poor to sustain life, CKD becomes end-stage kidney disease (ESKD)

  • GFR <15 mL/min

Stages of Chronic Kidney Disease

Stage 1

• At risk; normal kidney function, but urine findings indicate kidney disease

• Albuminuria not present

• Estimated GFR: >90 mL/min/1.73m2

• Intervention: Screen for risk factors and manage care to reduce risk:

  • Uncontrolled hypertension

  • Diabetes with poor glycemic control

  • Congenital or acquired anatomic or urinary tract abnormalities

  • Family history of genetic kidney diseases

  • Exposure to nephrotoxic substances

Stage 2

• Slightly reduced kidney function

• Albuminuria may be present

• Estimated GFR: 60 - 89 mL/min/1.73m2

• Intervention: Focus on education of risk factors

Stage 3

• Moderately reduced kidney function

• Albuminuria is usually present

• Estimated GFR: 30 - 59 mL/min/1.73m2

• Intervention: Implement strategies to slow disease progression

Stage 4

• Severely reduced kidney function; noticeable jaundice can occur, particularly around the eyes

• Albuminuria is present

• Estimated GFR: 15 - 29 mL/min/1.73m2

• Intervention:

  • Manage complications

  • Discuss patient preferences and values

  • Educate about options and prepare for renal replacement therapy

Stage 5

• End-stage kidney disease (ESKD)

• Estimated GFR: <15 mL/min/1.73m2

• Intervention: Implement renal replacement therapy or kidney transplant; without death results from ESKD

Albuminuria Stages (Albumin-to-Creatinine Ratio) in CKD

Albumin in the urine is a marker of kidney damage, whereas GFR reflects kidney function

The risk for progression of CKD, ESKD, and mortality is increased when urine albumin increases

First Stage (A1)

• None to mildly increased albumin up to 29 mg/g creatinine (<3 mg/mmol)

Second Stage (A2)

• Albumin values of 30 - 300 mg/g creatinine (3 - 30 mg/mmol)

Third Stage (A3)

• Greatest kidney damage

• Albumin values >300 mg/g creatinine (>30 mg/mmol)

Selected Causes of Chronic Kidney Disease

Glomerular Disease

• Glomerulonephritis

• Basement membrane disease

• Goodpasture syndrome

• Intercapillary glomerulosclerosis

Infection

• Pyelonephritis

• Tuberculosis

Tubular Disease

• Chronic hypercalcemia

• Chronic potassium depletion

• Fanconi syndrome

• Heavy metal (lead) poisoning

Vascular Disease of the Kidney

• Ischemic disease of the kidney

• Bilateral renal artery stenosis

• Nephrosclerosis

• Hyperparathyroidism

Inherited or Genetic Conditions

• Hypoplastic kidneys

• Medullary cystic disease

• Polycystic kidney disease

Systemic Vascular Disease

• Intrarenal renovascular hypertension

• Extrarenal renovascular hypertension

Metabolic Kidney Disease

• Diabetes

• Amyloidosis

• Gout (hyperuricemic nephropathy)

• Milk-alkali syndrome

• Sarcoidosis

Connective Tissue Disease

• Progressive systemic sclerosis

• Systemic lupus erythematosus

• Polyarteritis

Urinary Tract Disease

• Obstructive uropathy

Risk Factors for CKD

• Age

• Acute kidney injury

• Diabetes mellitus

• Hypertension

• Lupus

• Chronic glomerulonephritis, pyelonephritis, polycystic kidney disease

• Nephrotoxic meds (NSAIDs, chemo, antibiotics)

• Renal artery stenosis

• Pregnancy

CKD: Neurologic Symptoms

Uremia, drug toxicity, and fluid/sodium retention lead to changes in mentation

• Lethargy and daytime drowsiness

• Inability to concentrate or decreased attention span

• Seizures

• Coma

• Slurred speech

• Asterixis (jerky movements or "flapping" of the hands)

• Tremors, twitching, or jerky movements

• Myoclonus

• Ataxia (alteration in gait)

• Paresthesias from peripheral neuropathy (glove-and-stocking pattern)

CKD: Cardiovascular Symptoms

Hypertension due to retention of water and sodium; overactivation of RAAS; hyperlipidemia due to changes in fat metabolism; heart failure due to anemia & hypertension; pericarditis; hyperkalemia can cause dysrhythmias

• Cardiomyopathy

• Hypertension

• Peripheral edema

• Heart failure

• Uremic pericarditis

• Pericardial effusion

• Pericardial friction rub

• Cardiac tamponade

• Cardiorenal syndrome

CKD: Urinary Symptoms

Altered excretion of wastes, water, and electrolytes; progressive destruction of renal tubules

• Polyuria, nocturia (early)

• Oliguria, anuria (later)

• Proteinuria

• Hematuria

• Diluted, straw-colored urine appearance (early)

• Concentrated and cloudy urine appearance (later)

CKD: Integumentary Symptoms

Calcium-phosphorus imbalances and uremic deposits lead to itching

• Decreased skin turgor

• Yellow-gray pallor/ash gray skin

• Dry skin

• Pruritus

• Ecchymosis

• Purpura

• Soft-tissue calcifications

• Uremic frost (late, premorbid)

CKD: Musculoskeletal Symptoms

Hyperphosphatemia - phosphate binds w/ calcium, causing hypocalcemia; parathyroid hormone is stimulated to break down bone for calcium

• Muscle weakness and cramping

• Bone pain

• Fractures

• Renal osteodystrophy (bone metabolism and structural damage from poor absorption of calcium, continuous bone calcium loss, and high phosphorus levels)

CKD: Respiratory Symptoms

Fluid overload leads to pulmonary edema; metabolic acidosis leads to compensatory Kussmaul respirations

• Uremic halitosis (breath that smells like urine)

• Tachypnea

• Deep sighing, yawning

• Kussmaul respirations

• Uremic pneumonitis

• Shortness of breath

• Pulmonary edema

• Pleural effusion

• Depressed cough reflex

• Crackles

CKD: Hematological Symptoms

Decreased production of erythropoietin, destruction of RBCs due to uremia, iron & folic acid deficiencies, reduced immunity due to destruction of WBCs by uremia; poor platelet function

• Anemia

• Abnormal bleeding and bruising

• Reduced white blood cell count

• Increased risk for infection

CKD: GI Symptoms

Uremia causes inflammation and destruction of highly vascular tissues i.e. intestinal mucosa

• Anorexia

• Nausea

• Vomiting

• Metallic taste in the mouth

• Changes in taste acuity and sensation

• Uremic colitis (diarrhea)

• Constipation

• Uremic gastritis (possible Gl bleeding)

• Uremic fetor (breath odor)

• Stomatitis

CKD: Reproductive Symptoms

• Decreased fertility

• Infrequent or absent menses

• Decreased libido

• Impotence

• Sexual dysfunction

CKD: Metabolic Symptoms

• Hyperparathyroidism

• Hyperlipidemia

• Alterations in vitamin D, calcium, and phosphorus adsorption and metabolism

• Metabolic acidosis

• Hyperkalemia

CKD: Psychosocial Symptoms

• Depression

• Fatigue

• Sleep disturbances

• Sexual dysfunction

• Cognitive impairment

• Unemployment

Uremia Symptoms

• Metallic taste in the mouth

• Anorexia

• Nausea

• Vomiting

• Muscle cramps

• Uremic frost on skin (layer of urea crystals from evaporated sweat; may appear on the face, eyebrows, axillae, and groin)

• Fatigue and lethargy

• Hiccups

• Edema

• Dyspnea

• Paresthesias

Labs For CKD

• Creatinine & BUN (elevated; creatinine >4 mg/dL)

• GFR (reduced; normal is >90 ml/min)

• Urinalysis

  • Hematuria, proteinuria, glycosuria, pyuria, low specific gravity, decreased osmolality (early) or increased osmolality (late)

• Hemoglobin & hematocrit (low, anemia)

• Serum electrolytes

  • Hyperkalemia

  • Hypocalcemia

  • Hyperphosphatemia

  • Hyponatremia (early) or hypernatremia (late)

• Serum bicarbonate (low, if acidotic)

Diagnostics for CKD

• X-Ray: visualize renal osteodystrophy

• CT/US: visualize progression of disease

  • Kidneys shrink (except when caused by polycystic kidney disease) and may be 8 to 9 cm or smaller

Drug Therapy for CKD

• Loop diuretics (furosemide, bumetanide)

  • For pulmonary edema/fluid overload and to encourage waste elimination

  • Not used after dialysis is started

• Antihypertensives

  • ACEIs are most effective; monitor potassium

• Digoxin (improves cardiac contractility and thus perfusion)

• Phosphate binders (i.e. calcium acetate, calcium carbonate, sevelamer)

  • Helps reduce loss of calcium from bones

  • Take with meals

• Cinacalcet (reduces activity of parathyroid hormone to prevent bone loss)

• Iron & vitamin D supplements (to support RBC production & preserve bones)

• Multivitamins

• Epoetin alfa (to correct anemia)

• IV morphine

  • Reduces oxygen demand of the heart in heart failure

• Albumin

  • To reduce edema/prevent fluid overload

• Kayexalate (to reduce potassium levels in hyperkalemia)