Week 7 Renal Med Surg 2

Kidney Function General

regulate extracellular fluid
excrete waste products
control BP
produce erythropoietin
Active Vitamin D
regulate acid-base balance

Glomerulonephritis general

Inflammation of the glomeruli!

• 3rd cause of ESRD

• associated: kidney infection, nephrotoxic drugs, immune disorders, systemic diseases (SLE)

ACUTE

• symptoms come and go, temporary or reversible!

Chronic

• slowly progressive, leading to irreversible renal failure

Acute Poststreptococcal Glomerulonephritis (APG) General

Acute!, most common type of Acute GN

common in children, young adults, and adults x>60yrs old

• develops 1-2 weeks after an infection of the tonsils, pharynx, or skin by nephrotoxic strains of group A B-hemolytic streptococci; form antibodies to streptococcal antigen

Strep throat (red throat, white lesions, etc)

Acute Poststreptococcal Glomerulonephritis (APG) Clinical Manifestations

Manifestations:

• generalized edema, HTN, oliguria, hematuria, proteinuria, fluid retention!

  • not expected, indication of kidney damage

• periorbital edema —> total body = ascites and peripheral edema

  • edema around the eyes

• smoky urine (bleeding in upper urinary tract)

• HTN (increased ECF volume)

• abdominal or flank pain

• can be asymptomatic; found on routine urinalysis

Acute Poststreptococcal Glomerulonephritis (APG) Diagnosis

Diagnosis:

• H&P

• Renal biopsy = confirmation!

• Dipstick urinalysis and urine sediment microscopy

  • erythrocytes/casts

  • protein

• BUN and serum creatinine renal impairments

  • HIGHER these labs = worse the kidneys

  • If GFR is lower = worse the kidneys

BUN normal range

10-20

Creatine Normal Range

0.6 - 1.2

GFR normal range

x > 90

Acute Poststreptococcal Glomerulonephritis (APG) Treatment

treatment

• dependent on cause!

• diet restriction

• restrict diuretics!

  • kidneys are not working so diuretics won’t work

• Rest!

Cause

• streptococcal —> give antibiotics!

APG Diet Restrictions

Diet

• limit protein and meat foods

• limit fluids and sodium

Nephrolithiasis: Risk Factors

Kidney Stones

Risk factors

• Metabolic

  • abnormalities —> increased pH, calcium, oxalate, uric acid

  • decreased citrate

• Climate

  • warm —> fluid loss —> more concentrated urine

• Diet!

  • increase tea&fruit juice oxalate

  • excessive protein increase uric acid

  • low fluid intake = urine more concentrated

• Genetic

  • family hx

• Lifestyle

  • immobile, obesity, sedentary

concentration of supersaturated crystals precipitate and form stones

• reduce risk by keeping urine dilute and free flowing!

high in oxalate

nuts, leafy greens

Nephrolithiasis: Types

5 categories:

• calcium oxalate

• calcium phosphate

• cystine

• struvite (UTI)

• Uric Acid

Calcium most common

Treatment based on what type of stones!

• adjust diet or give antibiotics

Nephrolithiasis: Clinical Manifestations

First Symptom

• Sudden, severe pain! renal colic

  • flank area, back, lower abdomen

  • ureter stretches, dilates, and spasms

  • can also see nausea and vomiting, dysuria, fever, chills, moist, cool skin

Common Sites of Obstruction

• Ureteropelvic Junction (UPJ)

  • dull costovertebral flank pain or renal colic

• Ureterovesical junction (UVJ)

  • lower abdominal pain; testicular or labial pain

Nephrolithiasis: Diagnostic Studies

Diagnostic Studies

• noncontract helical (spiral) CT scan

• Ultrasound

• Urinalysis

• 24 hour urine

24 hour urine

For recurrent stones to measure calcium, phosphorus, magnesium, sodium oxalate, citrate, cysteine, sulfate, potassium, uric acid, and total urine volume

for nephrolithiasis

retrieval and analysis of stones

Nephrolithiasis: Interprofessional Care

2 Interprofessional Care

Pain Management

• acute attack

• opioids, NSAIDs, alpha adrenergic blockers

Antibiotics

• if indicated

Evaluate cause and prevent further development!

• get H&P, attack the cause

Nephrolithiasis: Treatment and Patient Teaching

Treatment & Patient Teaching

• Adequate hydration

• NA restriction

• Diet Changes

• Drugs

  • can change the pH of urine, prevent excess urinary secretion of a substance or correct primary disease

• Struvite stones: antibiotics

Nephrolithiasis: Treatment for Stones

Stone

• 4mm and less —> pass naturally @ HOME

  • can take weeks

• stone has passed = decrease in pain, and urine must be strained to confirm it has passed

Surgery

• if stones are too large

• causes injury or infection

• Symptoms

  • extracorporeal shock-wave lithotripsy (ESWL)

Nephrolithiasis: Nutrition Therapy

Nutrition Therapy

Obstructing Stone

• adequate fluids to avoid dehydration

  • forcing fluids not recommended! can increase pain

After Stone Removal!

• high intake of fluids (3L/day) = 2.5L urine/day

• prevents supersaturation of minerals

• reduce risk of dehydration

• limit colas, coffee, and tea

Low Sodium Diet

Diet restrictions according to type of stone!

• purine, calcium, oxalate

Acute Kidney Injury: Etiology and Pathophysiology Prerenal

Etio and Patho

Prerenal

• causes are factors that reduce systemic circulation, causing a reduction in renal blood flow

  • severe dehydration, heart failure, decreased CO

• Decreases glomerular filtration rate

  • causes oliguria

• Autoregulatory mechanisms attempt to preserve blood flow

  • RAAS

Associated diseases

• addisons

• CHF

• hypovolemic shock —> GI bleed

Acute Kidney Injury: Etiology and Pathophysiology Intrarenal

Etio and Patho

Intrarenal

• causes include conditions that cause direct damage to kidney tissue

  • prolonged ischemia

  • nephrotoxins drugs

    • vancomycin

    • metformin

    • glycoside

    • oral contrast

    • chemo drugs

• Hemoglobin released from hemolyzed RBC

• Myoglobin released from necrotic muscle cells

Nephrotoxic Drugs

• vancomycin

• metformin

• glycoside

• oral contrast

• chemo drugs

Acute Kidney Injury: Etiology and Pathophysiology Intrarenal ATN

Acute Tubular Necrosis

• results from ischemia, nephrotoxins, or sepsis

• severe ischemia causes disruption in the basement membrane

• nephrotoxic agents cause necrosis of tubular epithelial cells

• potentially reversible

If you know the cause —> stop the cause (TREATMENT)

Acute Kidney Injury: Etiology and Pathophysiology Postrenal

Postrenal

• causes include mechanical obstruction of outflow

  • lacerations

  • benign prostatic hyperplasia

  • prostate cancer

  • calculi

  • trauma!

  • extrarenal tumors

  • bilateral obstruction

Benign Prostatic Hyperplasia: General

Enlarged Prostate, non-cancerous

70% of men over 60 will have symptoms

hormonal changes associated with aging can contribute

digital rectal exam should be done regularly with older males and can diagnose BPH

Benign Prostatic Hyperplasia: Manifestations

Manifestations

• dribbling

• sensation to go

• oliguria

• nocturia

• distention

Benign Prostatic Hyperplasia: Diagnostics

Diagnostic

• PSA marker —> high case/risk

• only way to diagnose = digital rectal exam

Benign Prostatic Hyperplasia: Surgical Treatment

TURP with CBI

• transurethral resection of the prostate

Post OP of TURP = can have issues with infection, incontinence, and bleeding

• triple lumen catheter is useful for continuous bladder irrigation

• can prevent infection and decrease risk of bleeding and clots

Need to take strict I&O’s

Expected

• Hematuria!

Unexpected

• A lot of serosanguinous blood

• low VS —> hypovolemic shock —> call doctor

Acute Kidney Injury Phases

Oliguric —> Diuretic —> Recovery

Can turn into Chronic Kidney Disease if not handled

AKI: Clinical Manifestations Oliguric

Oliguric Phase

• Urinary changes — oliguria

  • less than 400 mL/day

  • w/in 1-7 days after injury

  • lasts 10 to 14 days (longer + poor prognosis)

  • Urinalysis may show casts, RBCs, WBCs

AKI: Clinical Manifestations Oliguric Phase: Metabolic Acidosis

Metabolic Acidosis

• impaired kidney cannot excrete H- ions

• Serum bicarbonate is decreased!

• Severe acidosis develops!!

Will show Kussmaul respirations: rapid, deep respirations in an effort to compensate by increasing the exhalation of carbon dioxide (acid)

Metabolic Acidosis

Increased H- ions

Bicarbonate is low

AKI: Clinical Manifestations Oliguric Labs

Labs

• Sodium balance

  • increased excretion of sodium! —> hyponatremia

• Potassium excess

  • Impaired ability of kidneys to excrete sodium —> hyperkalemia

    • usually asymptomatic

    • may have weakness

    • ECG changes

AKI: Clinical Manifestations Oliguric Hematologic & Waste & Neurologic

Hematologic Disorders

• leukocytosis: result of infection

Waste Product Elimination

• Elevated BUN and Serum creatinine levels (indicative of kidney injury) and low GFR

Neurologic Disorders d/t nitrogenous waste products in brain and nervous tissues

• fatigue and difficulty concentrating

• seizures, stupor, coma

AKI: Diuretic Phase Clinical Manifestations

Manifestations

• Urine output —> 3L or 5L (polyuria)

  • dumping of electrolytes

• increased urea concentrations —> osmotic diuresis

• Monitor for hyponatremia, hypokalemia, and dehydration

  • give fluids and maybe electrolyte replacements

AKI: Recovery Phase

GFR increases, BUN and Creatinine decreases

First 2 weeks = major improvement!

Can take up to 12 months for kidney function to stabilize!!

Influenced by comorbidities

Older Adults affected, may not recover completely

AKI: Diagnostic Studies

Diagnostic Studies

• thorough history

• serum creatinine

• Urinalysis

  • urine sediment containing abundant cells, casts, or proteins suggests intrarenal disorders

• Kidney ultrasonography

  • kidney disease or obstruction

• Renal scan

  • assess abnormalities in kidney blood flow, tubular function, and the collecting system

• CT scan

  • identify lesions, masses, obstructions, vascular anomalies

• Renal Biopsy

  • confirming intrarenal causes of AKI

AKI: Contraindicated Diagnostic Studies!

Contraindicated

• MRI WITH CONTRAST MEDIUM

• Magnetic Resonance ANgiography (MRA) with gadolinium contrast medium

  • Contrast-induced nephropathy (CIN)

Hyperkalemia Therapies

Temporary: move K+ into cells!

• IV Insulin and Sodium bicarbonate

• D50 stabilizes the blood glucose

Low Dysrhythmias — stabilizes myocardium

• calcium gluconate

Remove K+ from body

• Sodium polystyrene sulfonate (Kayexalate) or Patiromer (Veltassa)

• Dialysis

AKI: Interprofessional Care Nutritonal Therapy

Nutritional Therapy

• Maintain adequate caloric intake

  • mostly carbs and fat: prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown

• Restrict Sodium: prevent edema, HTN, and HF

• Increase Dietary Fat: non protein calories

• Parenteral nutrition: if GI tract nonfunctional to provide adequate nutrition

AKI: Gerontologic Considerations

More susceptible to AKI

• dehydration

• hypotension

• diuretic therapy

• aminoglycoside therapy

• obstructive disorders

• surgery

  • infection

Chronic Kidney Disease General

leading cause

• diabetes 50%

• HTN 25%

goes undiagnosed until later stage

progressive, irreversible kidney damage —> pathologic abnormalities

disease staging based on decrease in GFR

• ESRD: x < 15 mL/min

Chronic Kidney Disease

stage

Chronic Kidney Disease: Clinical Manifestations

Uremia

• syndrome in which kidney function declines to the point = systemic!

• often occurs when GFR x<15mL/mi

Results of retained substances

• urea, creatinine, hormones, electrolytes, water

CKD: Clinical Manifestations Neurologic System

Expected as kidney disease progresses

• result of

  • increased nitrogenous waste products

  • electrolyte imbalances

  • metabolic acidosis

  • atrophy and demyelination of nerve fibers

CKD: Clinical Manifestations Cardiovascular System

Clinical Manifestations:

• fluid overload

• hyperlipidemia

• HTN

• dysrhythmias

• heart failure

CKD: Clinical Manifestations Respiratory System

Resp System:

• uremic halitosis

  • urine-like odor of the breath

• shortness of breath

• tachypnea

• crackles

• kussmaul respirations

CKD: Clinical Manifestations Hematologic System

Hematologic

• anemia

  • decrease production of erythropoietin

    • decrease functioning of renal tubular cells

  • decreased iron stores

  • folic acid lost in dialysis

• bleeding tendences!

  • defect in platelet function

CKD: Clinical Manifestations GI system

GI

• cause: excessive urea!!

  • stomatitis with ulcerations

  • blood in stools

  • vomiting

  • constipation

CKD: Clinical Manifestations Integuementary System

Skin

• pruritus

  • intense itching

  • blood loss or infection

• uremic frost

  • urea crystalizes on skin

CKD: Clinical Manifestations Infection

Infection

• changes in WBC function

• altered immune response and function

• hyperglycemia and external trauma

CKD: Clinical Manifestations Electrolyte/Acid-Base Imbalances

Metabolic Acidosis

• results from kidneys impaired ability to excrete excess acid (primary ammonia)

• defective reabsorption and regeneration of bicabonate

CKD: Diagnostic Studies

Diagnostic Studies

• H&P

• Dipstick evaluation of protein

• urinalysis

• renal ultrasound, scan, ct scan, biopsy

• LABS

  • all mostly low

  • potassium usually high

CKD: Drug Therapies

Hypertension

• ACE-inhibitors (-pril) and ARB agents (-tan)

• not beta blockers, these meds help the kidneys

Anemia

• erythropoietin (EPO)

• iron supplements

• folic acid sipllements

• avoid blood transfusions

  • increase the development of antibodies

  • only cure is transplant, and multiple transfusions = rejection of transplant

Dyslipidemia

• statins (atorvastatin)

• fibrates (gemfibrozil)

Complications

• drug toxicity

  • digoxin, diabetic agents

  • antibiotics

  • opioid medications

CKD: Nutritional Therapy

Nutritional Therapy

• protein intake

• fluid restriction

Sodium restriction

• from 2 to 4 g/day

• salt substitutes should be avoided

POtassium Restriction

• 2 to 3g / day

• high potassium foods be avoided!

Dialysis: General

Two methods

• peritoneal

• hemodialysis

Gfr X < 15

blood is filtered and cleaned in a machine and ran back into the machine

Dialysis: Peritoneal Dialysis

Catheter through anterior abdominal wall —> peritoneal space

Aseptic technique!

BIGGEST COMPLICATION —> INFECTION!

• peritonitis —> infection

Peritoneal Dialysis: Solutions and Cycles

3 Phase

• can be done manually by gravity or by a machine

• 1- Inflow (fill): 2 to 3L over 10 minutes!

• 2- Dwell (equilibration): 20 to 30 minutes → 8 Hours

• 3- Drain: 15 to 30 minutes

• Cycle is repeated

Called an exchange

• volume depends on size of peritoneal cavity

Unexpected

• cloudy —> infection

• blood —> ripping/tearing

• fecal matter —> tear in intestines

• less drainage than what we put in

Expected

• greenish brown color

• more drainage than what we put in

Peritoneal Dialysis Complications

Complications

• exit site infection

• peritonitis

• hernias

• lower back problems

• bleeding

• pulmonary complication

  protein loss

  • only kidney complication where we increase protein!

Peritoneal Dialysis Effectiveness of Chronic PD

Short training program

Advantages

• simplicity

• home based program

• increasing patient participation

• no need for special water systems

  • equipment set-up is relatively simple

Hemodialysis General

Vascular Access sites

• types of access

  • arteriovenous fistulas and grafts

  • temporary vascular access

Fistula and Graft

combining a vein and an artery

• hear a bruit

same thing except another device combines them

• has a thrill

Hemodialysis Procedure

two needles placed in fistula or graft

1. pulls blood from circulation to HD machine

2. used to return dialyzed blood to the patient

Heparin is added to prevent clotting

BIGGEST COMPLICATION: HYPOVOLEMIA

Hemodialysis Pre Procedure

Before

• assess fluid status

  • weight, BP, peripheral edema, heart and lung sounds

  • weight from last postdialysis and current

• assess vascular access

• assess temperature

• monitor VS every 30 to 60 minutes

Hemodialysis Settings and Schedules

Majority treated at an outpatient center

• dialyzed for 3 to 4 hours

• 3 days per week

Other schedule options

• short daily HD

• Long nocturnal HD

• home HD

Kidney Transplant

live (27%) or deceased (73%) donors

monitor patient after procedure for fluid and electrolyte imbalance

hydration is key!

placed on immunosuppressive therapy for live to prevent rejection!

infection is a high risk!!

contraindications

• advanced cancer, refractory/untreated herat disease

• chronic respiratory failure, extensive vascular disease

• chronic infection

• unresolved psychosocial disorders

HIV+ or hep B or C are not contraindicated