Complex-Renal part 2

What happens with an Acute Kidney Injury (AKI)?

• Decrease in kidney function over a few days

• Retention of urea & nitrogenous wastes (Amonia, Uric acid)

• Dysregulation of Extracellular volume & electrolytes

What are some factors known to contribute to AKI?

• ↓ blood flow to the kidney​

• Hypovolemia​

• Hypotension​

• ↓ cardiac output & heart failure​

• Obstruction of the kidney or lower urinary tract​

• Bilateral obstruction of renal arteries or veins

What is the cause of Prerenal AKI? (before)

Interrupted blood flow, poor blood flow, or absent blood flow to the kidneys (acute/chronic)

• Severe volume depletion (dehydration)​

• Hypotension​

• Sepsis​

• Shock​

• Massive loss of blood​

• Over diuresis (volume depletion) ​

• Heart failure​

• Cirrhosis​

• Bilateral renal artery stenosis​

• Nephrosclerosis/Renal artery stenosis (RAS)​

What is the cause of Intrinsic (Intra) Renal AKI?

Injury to the tubules and/or glomeruli

• Prerenal disease w/out TX causes cells to die-leaving debris that clogs the tubules​

• CKD-when pre/postrenal go untreated-can CX INTRArenal​

• Urinary tract obstruction-(BNP) ​

• Embolisms​

• Nephrotoxins damage the glomeruli &/or tubules INSIDE the kidneys​

• Acute Tubular Necrosis (ATN)​

• Glomerular disorders, Nephritic & Nephrotic syndrome ​

What causes Postrenal AKI?

Severe-sudden obstruction of urine somewhere in the urinary tract below the kidneys (ureters, bladder, or urethra)

• 1st [most common] cause: *BPH- enlarged prostate ​

• Nephrolithiasis (Kidney stones)​

• Urethral strictures​

• Prostate or cervical cancer ​

• Pelvic mass or invasive pelvic malignancy​

• Bladder masses​

• Neurogenic bladder (can’t empty  obstruction  statis  infection)​

What is the pathophysiology behind post Renal Urinary Tract Obstruction?

• Obstruction to urine flow

• Urinary Stasis

• Elevation of urinary tract pressure

• Distention and Dilation of Renal Pelvis & Calyces (hydronephrosis)

• Impaired Renal Function

• Susceptibility for Hypertension, Infection and stone

• Permanent loss of Renal mass (Renal atrophy)

• Loss of Excretory Capacity

What is Acute Tubular Necrosis (ATN)?

A type of intrarenal issue-injury to the tubules from ischemia or toxic event

How does Acute Tubular Necrosis (ATN) happen?

• lack of blood flow and oxygen to the kidney tissues (ischemia of the kidneys).​

• ATN is a common CX of kidney failure in hospital patients

What is the cause of Acute Tubular Necrosis?

• Blood transfusion reaction​

• Injury or trauma that damages the muscles (e.g., Rhabdomyolysis- release and nephrotoxic effects of myoglobin)​

  • In large amounts, Myoglobin overwhelms the proximal tubule’s reabsorptive capacity, entering the distal nephron segments.​

• Hypotension longer than 30 minutes​

• Recent major surgery​

• Septic shock​

• Underlying illnesses (diabetes, liver disease) ↑ risks for ATN

What are the symptoms of Acute Tubular Necrosis (ATN)?

• Oliguria or anuria ​

• Can show sluggish/brown urine​

• General swelling, fluid retention​

• N/V​

• Change in LOC, coma, delirium, confusion, drowsiness, lethargy

  • due to the accumulation of toxins and disturbances in fluid and electrolyte balance

What diagnostics are needed for Acute Tubular Necrosis (ATN)?

• Serum BUN/creatinine​

• Functional excretion of Na+​

• Kidney biopsy​

• UA​

• Urine Na+​

• Urine specific gravity/osmolarity

How do you treat Acute Tubular Necrosis (ATN)?

• Life-threatening (REVERSIBLE) condition -treat the cause!​

• Preventing the buildup of fluids and wastes (IVFs and diuretics)? Depending on the cause ​

• Prevent fluid volume overload- Lasix? Depending on the cause​

• Avoid/treat hyperkalemia

What nursing considerations are needed w/ Acute Tubular Necrosis (ATN)?

• Fluid restriction and STRICT I’s & O’s!​

• Daily labs to evaluate treatments ​

What is Tubulointerstitial Nephritis (TIN)?

Inflammation that affects the tubules of the kidneys and the tissues that surround them/direct damage to the tubular structures.

What are the causes of Tubulointerstitial Nephritis?

• Most common-Nephrotoxic substances (NSAIDS, Vancomycin, IV contrast)​

• Chronic diseases (autoimmune-Lupus), genetic, metabolic disorders (DM)​

• Hypersensitivity reactions​

What are the clinical manifestations of AKI?

• Making less urine than usual or none at all​

• Edema in legs, ankles, and/or feet​

• Fatigue​

• Shortness of breath​

• Confusion or changes in mood​

• Hypertension​

• Decreased appetite​

• Nausea​

• Flank pain​

• Chest pain or pressure​

• Seizures or coma

How does AKI lead to Encephalopathy?

uremic toxins and inflammatory mediators

How does AKI lead to Heart Failure?

• Fluid overload

• Arrhythmia owing to hyperkalemia

• Hypertension

How does AKI lead to Intestinal and microbiota disruptions?

• Fluid congestion

• ischemia

• acidosis

• changes in microbiota secretome

• barrier translocations

How does AKI lead to bone marrow and immune system effects?

• Cytopenia

• systemic inflammation

• acquired immunodeficiency

How does AKI lead to Liver dysfunction?

• Fluid overload

• systemic inflammation

How does AKI lead to Lung injury?

• Fluid overload

• Kidney cell debris-related

• microvascular injury

What respiratory findings would you have with AKI?

• Crackles

• Decreased O2

• SOB

What renal findings would you see w/ AKI?

Scant to normal or excessive urine output

Possible hematuria

What neurological findings would you see w/ AKI?

• lethargy

• muscle twitching

• seizures

What causes a Urinary Tract Infection (UTI)?

• Infection within the urinary system (kidneys, ureters, bladder or urethra)​

• most often affect the bladder

What causes an Uncomplicated UTI?

An infection-lower urinary tract only (bladder & urethra)

What is the cause of a complicated UTI?

• Infection extends beyond the bladder​

• Seen in pregnancy, after menopause, kidney stones​

• Pyelonephritis (kidney infection)

What is Catheter-Associated Urinary Tract Infection (CAUTI)?

• Bacteria from a urinary catheter​

  • Biofilm develops​

  • Worse bacteria in hospital setting​

  • They bypass protective mechanisms​

What are the risk factors associated with CAUTIs?

• Co-morbidities: age-lack of sensation of pain, incontinence​

• Indwelling catheters (long-term care)​

• Immunocompromised​

How do you treat CAUTIs?

• Antibiotics ​

• Reserve or treat the problem

What are some warning signs of AKI?

• Extreme fatigue

• N/V

• Confusion/trouble concentrating

• Swelling, particularly around the hands & ankles

• Poor appetite or food may taste metalic

• Cramps (muscle spasms)

• Peeing more often

• Dry or itchy skin

What intervention is the easiest and most sensitive diagnostic for fluid volume overload due to AKI?

Daily weights (1 kg wt gain=1 L fluid)

What symptoms may result due to Fluid overload?

• SOB

• Crackles on auscultation

• changes in diagnostic film

• Edema in:

  • legs/ankles/feet

  • scrotum

What Renal Specific Health History is needed when assessing for AKI?

• Chief complaint ​

• Changes in voiding (hesitancy/frequency?)​

• Any DX procedures/surgeries or catheters? ​

• OB/GYN history (female pts)​

• Kidney stones (current or PMH)​

• S/S of anemia ​

• Gastrointestinal s/s​

• Medications (including OTCs) ​

• Tobacco (↑ risk for certain kinds of cancer)​

• Illicit drugs or alcohol abuse ​

• Advanced age?​

• Any other risk factors?​

What are some assessment considerations for AKI?

• Assess for JVD​

• Auscultate for crackles from pulmonary edema​

• Assess for edema​

• Cardiac monitoring​

• Daily weights​

• Skin integrity & hydration​

• Flank pain, nausea/vomiting​

• Changes in urination​

• Psychosocial support

How do you diagnose AKI?

• Overall clinical picture (patient)​

• Vital signs (HR/BP changes ↑or ↓)​

• GU focused History & Physical (H&P)​

• Intake and output (I & O)​

• UA ​

• Renal function tests​

• U/S, KUB, CT, and/or MRI​

• Urography, pyelography, cystography, angiography​

• Endoscopic procedures (lithotripsy)​

• Biopsies​

• Urine specific gravity

What are some treatments for AKI?

• Prevention, Prevention, Prevention!​

• Eliminate underlying cause​

• Pharmacological therapy​

• Maintain F&E balance & avoid fluid excess​

• Nutrition therapy​

• Renal replacement therapy (Dialysis)​

In order to avoid using nephrotoxic meds (especially in older adults), what med should you use for AKI?

Calcium-channel blockers

Diuretics (Furosemide, Mannitol, ethacrynic acid)

If the pt developled hyperkalemia, due to AKI, how would you treat?

• Monitor for s/sx, obtain serial CMP​

• Sodium polystyrene sulfonate ​

• Kayexalate, sorbitol​

• IV dextrose + insulin & calcium gluconate

If the pt developed hyperphosphatemia due to AKI, how would you treat?

Phosphate binders

If the pt developed severe metabolic acidosis due to AKI, how would you treat?

sodium bicarbonate (NaHCO3)​

How much fluid should the pt w/ AKI excrete in 24 hrs?

No more than 500-600 mL

What should a pt on a renal diet limit?

Potassium and sodium (2-3g/day)

What is Specific Gravity in a UA?

a measure of the overall density of urine compared to water

shows the total concentration of all chemical particles in the urine.​

What is considered Low specific gravity?

Less than 1.005

• diluted more than normal, overhydration

What is considered High specific gravity?

Greater than 1.030

• concentrated urine, dehydration, kidney disease, or certain meds

What are the Most common Risk factors of Kidney Disorders?

• Diabetes is the #1 cause w/ Hypertension is #2

• Recent infection

• Certain meds

• Severe dehydration

• Exposure to heavy metals or toxic solvents

• Blood loss, shock

How do you prevent & decrease the risk of AKI?

• Remove/Reverse the source (Toxins?)​

• Restore blood flow​

• Rehydrate volume depleted patients ASAP​

• Monitor BUN, creatinine, & electrolytes​

• Monitor renal FX & serum drug levels​

• Prophylactic RX before contrast dye (MUCOMYST and IVFs?)​

• Treat UTIs/obstructions/strictures​

What is the initiation phase of AKI?

Initial insult to cause the AKI:

• significant blood loss, fluid loss, diabetes insipidus

• Tissue oxygenation 25% below normal

• Urine output below 0.5 mL/kg/hr

Duration: hours to days

What is the Oliguria phase of AKI?

↑ serum concentration of substances normally excreted by kidneys and ↓ in UOP ​

• Urine output below 400 mL/day, possibly as low as 100 mL/day

• Increases in BUN and Creatinine levels

• Electrolyte disturbances, acidosis, and fluid overload

Duration: 8-14 days or longer

What is the Diuresis phase of AKI?

Gradual ↑ in UOP & stabilization of lab values. Uremic symptoms may still be present along with hyperkalemia​

• Occurs when cause of AKI is corrected

• Renal tubule scarring and edema

• Daily urine output above 400 mL

• Possible electrolyte depletion from excretion of more water and osmotic effects of bun

Duration: 7-14 days

What is the Recovery phase of AKI?

Improvement of renal function over 3-12 months with lab values WNL and likely 1-3% decrease in GFR​

• Decreased Edema

• Normalization of fluid and electrolyte balance

• Return to normal

Duration: Several months to 1 year

What is the “RIFLE” classification of Kidney Disorders?

• Widely accepted criterion for AKI ​

• A ↓GFR > 50% ​

• An increase in serum creatinine above baseline​

• With/without a change in urine volume

• Risk

  • ↑ serum creatinine 1.5 x baseline OR​

    GFR decreased ≥ 25%

  • 0.5 mL/kg/hr for 6 hours or more

• Injury

  • ↑ serum creatinine 2 x baseline OR​

    GFR decreased ≥ 50%

  • 0.5 mL/kg/hr for 12 hours

• Failure

  • ↑ serum creatinine 3 x baseline OR​

    GFR decreased ≥ 75% OR​

    Serum creatinine ≥ 354 mmol/L with acute rise of at least 44 mmol/L

  • <0.3 mL/kg/hr for 24 hours OR​

    Anuria for 12 hours

• Loss

  • Persistent AKI = complete loss of kidney function > 4 weeks

• ESKD (end stage kidney disease)

  • ESKD (end-stage kidney disease) > 3 months

What are some of the most common causes of kidney disorders?

• Uncontrolled Diabetes AKA-Diabetic nephropathy (modifiable risk factor)​

  • Develops over years​

  • High glycose levels cause narrowing of the blood vessels/damages the glomeruli ​

• Uncontrolled HTN- (modifiable risk factor)​

  • Cuts off the normal blood supply to the kidneys​

  • Can cause Nephrosclerosis, hardening of the renal arteries​

• Heart Disease/Atherosclerosis (modifiable risk factor)​

  • Can decrease blood flow to the kidneys​

  • Build up plague in the renal arteries​

• Obesity (modifiable risk factor)​

  • Puts people at risk for HTN, DM, heart disease, etc.​

• Smoking (modifiable risk factor)​

  • Increases risk for developing heart disease-decreasing blood flow to the kidneys​

  • Also increases the risk of ALL cancers (Kidney cancers in this case)​

• Family History​

  • Non-modifiable risk factor….​

What is Glomerular Disease?

Umbrella term to describe damage to the glomeruli (acute/chronic)

What is Primary Glomular Disease?

Damage within the kidneys: Non-systemic​

• Causes ​

  • Idiopathic/Auto-immune mediated process​

  • Postinfection glomerulonephritis, ​

What is Secondary Glomerular Disease?

• Diabetes (most common CX)​

• Lupus or sickle cell​

• Chronic systemic disease damages glomeruli

What is Nephrotic Syndrome?

• ​Increased glomeruli permeability-excessively leaks out proteins (proteinuria)

What is Nephritic Syndrome?

• Inflammation of the glomeruli causes bleeding to the glomeruli (hematuria)​

What are the characteristics of Nephrotic Syndrome?

• Damage to the glomeruli CX marked ↑ glomeruli permeability​

• CX MASSIVE Proteinuria​

• ↓ serum albumin & ↓ serum protein ​

• H2O & Na+ retention ​

• Anticoagulants dump into urine=risk of clots​

• Immunoglobulins dump into urine=risk of infections

What are some of the causes of Nephrotic Syndrome?

• Autoimmune disorders/idiopathic​

• Kidney lesion/disease, ​

• Systemic diseases (lupus, diabetes)

How do you diagnose Nephrotic Syndrome?

• Blood work: albumin, cholesterol, sCr/BUN/GFR, creatinine clearance ​

• U/A checking for blood vs protein**​

• Kidney biopsy for confirmation

How do you manage Nephrotic Syndrome?

• Strict I&O (watch for oliguria)/↓ Na+, K+, ↓ fluids​

• Control BP/Diuretics/IV albumin​

• Anticoagulants dump into urine=risk of DVT/PE (Heparin?)​

• Corticosteroids or immune suppressors​

What is Nephritic Syndrome characterized by?

• Inflammation of the glomerulus and capillaries ​

• Hematuria, ↑ BP, oliguria, and edema​

• Autoimmune response triggered by an infection or other disease.

What are the clinical manifestations of Nephritic Syndrome?

• Urine: Hematuria, Azotemia (high lvls of nitrogenous waste products), & Oliguria ​

• HTN​

• Blurred vision, fever, weakness, fatigue, ↓ appetite/vomiting/abdominal pain

How do you diagnose Nephritic Syndrome?

• Labs: BMP (sCr ↑ quickly)​

• U/A: Tea-colored, or dark urine​

• Renal biopsy: May be used to confirm an underlying disease.

What treatment is needed for Nephritic Syndrome?

• Fluid and Na+ restriction​

• Diuretics​

• ACE inhibitors/ARBs to ↓ pressure in the glomeruli/control BP ​

• Antibiotics for infections​

• Immunosuppressants​

• Dialysis

What is Glomerulonephritis?

• The immune system attacks the kidneys/inflames/injures glomeruli​

• So, they bleed (and small amounts of puss too)

Can be caused by Strep

What are the s/s of Glomerulonephritis?

• Remember: “HAD STREP”​

• H ypertension ​

• A positive strep titer​

• D ecreased GFR​

• S welling in face/eyes (edema)​

• T ea-colored urine (hematuria & ↓UOP)​

• R ecent strep infection ​

• E levated BUN and creatinine ​

• P roteinuria (mild)​

What diagnostics are needed for Glomerulonephritis?

• U/A with culture ​

• CMP and inflammatory markers​

• Renal ultrasound​

• Kidney BX​

How do you manage Glomerulonephritis?

• Daily wts and renal labs​

• Dietary: ↓ protein, salt, iron​

• Watch for fluid volume overload

What do you do in Acute cases of Glomerulonephritis?

• Treat any infections, esp. Strep​

• Antihypertensives (TX: HTN)​

• Diuretics (fluid/volume overload)​

What is the cause of Chronic Glomerulonephritis?

• Repeated acute glomerulonephritis episodes ​

• Hypertension related nephrosclerosis (disease) ​

• Hyperlipidemia ​

• Secondary glomerular disease; ​

  • Lupus, DM, Goodpasture syndrome (rare/autoimmune disorder-antigens attacks kidneys [and lungs] which leads to inflammation and bleeding)

What is the pathophysiology of Chronic Glomerulonephritis?

• Glomeruli injury-shrinks the kidneys​

• Bands of scar tissue build up-kidneys become rough and irregular (fibroids)

• Starts as AKI-progression leads to CKD & CKD side effects​

  • Hyperkalemia​

  • Metabolic acidosis​

  • Anemia​

  • Hypoalbuminemia​

  • Hyperphosphatemia and hypocalcemia​

What are some diagnostics for Chronic Glomerulonephritis?

• UA/CMP/CBC​

• Chest X-ray/kidney ultrasound/ EKG​

How would you medically manage Chronic Glomerulonephritis?

• Symptoms guide treatment​

• Daily weights/protein diet with adequate calories​

• Avoid NSAIDS, nephrotoxic medications, and diagnostic studies with IV contrast ​

• Dialysis early on to prevent complications​

What is Polycystic Kidney Disease (PKD)?

Autosomal dominant genetic disorder that causes the build up of fluid filled cysts that destroy nephrons and reduced renal function.

Where are some other places that cysts can form in a pt w/ Polycystic Kidney Disease?

• Liver​

• Blood vessels​

• Brain​

• Heart

What are some common s/s of Polycystic Kidney Disease (PKD)?

• Hematuria, polyuria, & proteinuria​

• Hypertension​

• Renal calculi​

• UTI​

• Palpable cysts on physical exam​

• Visible cysts on U/S​

How do you medically manage Polycystic Kidney Disease (PKD)?

• No cure (tolvaptan slows the decrease in kidney function, but leads to polyuria and liver injury)

• Supportive

• BP control

• Antibiotics for infections

• Renal replacement therapy

• Genetic testing/counseling

• Family screening for potential donors

• Kidney transplantation

What are some Risk factors for chronic kidney disease (CKD)?

• Age, gender, ethnicity, genetic component, low birth weight

• Drug intoxicity, Hypertension, Diabetes

• Autoimmune disease, UTI, Hyperuricemia

• Dyslipidemia, obesity, oxidative stress

What would you see w/ Stage 1 CKD?

Kidney damage w/ normal kidney function but other test results suggest signs of kidney damage

GFR 90 or higher

What would you see in Stage 2 CKD?

Kidney damage w/ mild loss of Kidney function w/ other tests suggesting kidney damage

60-89 GFR

What would you see w/ Stage 3 CKD? (3a)

Mild to moderate loss of Kidney function

45-59 GFR

What would you see in Stage 3b CKD?

Moderate to severe loss of Kidney function

30-44 GFR

What would you see w/ Stage 4 CKD?

Severe loss of Kidney function

15-29 GFR

What would you see w/ stage 5 CKD?

Kidney Failure

less than 15 GFR

What are some risk factors for Chronic Kidney Disease (CKD)?

• Age 60+

• Smoker

• Diabetes

• High BP

• Heart Disease

• Obesity

• Family History

What Assessing and Diagnosing is needed for Chronic Kidney Disease?

• Glomerular Filtration Rate​

• Sodium and Water Retention​

• Acidosis​

• Anemia​

• Calcium and Phosphorus Imbalance

What are the clinical manifestations of CKD?

• Decreased Glomerular Filtration Rate​

• Sodium & Water Retention​

• Hyperkalemia​

• Acidosis​

• Anemia​

• Calcium & Phosphorus Imbalances​

What are the management goals for CKD?

• Maintain kidney function and homeostasis for as long as possible​

• Identify reversible factors and treat with medications and diet therapy ​

• Utilize dialysis to remove wastes and control F&E​

What are some medical considerations when managing CKD?

• Control HTN​

• Control DM​

• Control hemoglobin A1C​

• Diurese them as needed

What nursing considerations are needed to manage CKD?

• Fluid restrictions/Avoiding overload ​

• Sodium restrictions when they have HTN and edema​

• Strict I&Os​

• Dietary carbohydrates for energy​

• A diet low in sodium, potassium, & phosphorus ​

• Daily weights​

• Educate the patient on their disease process at discharge ​

What imbalances would hyperkalemia present w/ the kidneys?

• ↓ excretion of K+ through filtration ​

• Metabolic acidosis in exchange for H+​

• Catabolism​

• Dangerous Dysrhythmias

Why would ammonia build up in a pt w/ CKD?

Renal pts lose the of ability to excrete nitrogen

Ammonia (NH3-) builds up in the blood/body

Why would the pt have acidosis w/ CKD?

• Can’t excrete acid through the urine​

• CKD patients live in a [nearly] constant state of acidosis ​

• Long term: bone and muscle loss, hyperglycemia, worsened CKD, death

Why would a pt w/ CKD experience Anemia?

• CKD -↓ erythropoietin (EPO) production​

• Shortening the life span of the RBCs (ANEMIA)

Why would a pt. w/ CKD have poor vitamin D levels/absorption?

Impaired ability for the parathyroid hormones to active vitamin D and thus they are at a loss

Why would a pt w/ CKD exhibit Hypocalcemia?

Causes calcium to leave bone and changes in bone structure and calcification in vessels