NCM 112: RENAL DISORDERS • Headache

• Flank pain
URINARY TRACT INFECTION (UTI) • Hypertension
- An infection in any part of the urinary system • Edema
• Kidneys • Decreased UOP
✓ Pyelonephritis ❑ Increased urine specific gravity
• Ureters ❑ Sediment in urine
• Bladder ❑ Blood in the urine
• Urethra • Increased BUN and CR
- Most common = LOWER (bladder, urethra)
- More common in women SIDE:
BUN: <20
CREATININE: 0.9-1.2

TREATMENT
• Antibiotics for strep infection
✓ Ensure client takes the entire course of antibiotics
• Strict intake and output measurement
• Rest
• Monitor BP
• Diet
✓ Decreased protein
✓ Decreased sodium
✓ Increased carbs
TREATMENT
• Hydration – drink LOTS of water! NEPHROTIC SYNDROME
• Cranberry juice - A kidney disorder that causes your body to pass
- No conclusive evidence this really helps! too much protein in your urine.
• Antibiotics
CAUSES
GLOMERULONEPHRITIS • Infection: bacterial or viral
- An acute inflammation of the kidney at the level of • NSAIDs
the nephron • Cancer
• Lupus
• Diabetes
• Strep
• INFLAMMATION

PATHOPHYSIOLOGY
• an inflammatory response in the glomerulus
• large holes in the glomerulus form, allowing protein to
leak into the urine
• Protein leaves the blood
✓ Proteinuria
PATHOPHYSIOLOGY ✓ Hypoproteinemia
• There is an inflammatory reaction in the glomerulus of • No protein in the blood? Client cannot hold onto fluid →
the kidney third spacing
• Antibodies lodge in the glomerulus • Fluid is collecting in the tissues, but the circulating blood
• This decreases the filtering capability of the kidney volume is low.
• Usually caused by an infection • RAAS kicks in to replace low blood volume → causes
✓ #1 = strep retention of sodium and water
• With no protein in the blood to hold it, furthers third
ASSESSMENT spacing.
• Sore throat
• Malaise

MRPP © 2022 l NOTES BY: BRYLE JUSTIN L. MAMON 23

1st SEMESTER l MIDTERM
 ASSESSMENT
• Anasarca
• Blood clots
• High cholesterol
• Proteinuria
• Hypoalbuminemia
• INTRA-RENAL – there is damage inside of the kidney
• Edema
❑ Glomerulonephritis
• Hyperlipidemia
❑ Nephrotic syndromes
❑ Nephrotoxic drugs
✓ Contrast
✓ Aminoglycosides

• POST-RENAL – something is blocking urine from leaving

the kidneys
❑ Kidney stone
❑ Tumor
❑ Urethral obstruction
❑ Enlarged prostate

TREATMENT
• Fix the cause!!
• Prednisone
• Diuretics
• ACE inhibitors
• Statins
• Anticoagulation
• Dialysis
• Diet
ACUTE
✓ High protein
• Acute Kidney Injury (AKI) or Acute Renal Failure
✓ Low sodium
– Sudden
– Happens over a few hours or a few days
RENAL FAILURE/KIDNEY FAILURE
– Causes a build-up of waste products in the blood

ACUTE
✓ Acute Kidney Injury (AKI) PRE-RENAL INTRA-RENAL POST-RENAL
✓ Acute Renal Failure (ARF) - septic shock - nephrotoxic drug - kidney stone
- glomerulonephritis - obstruction

CHRONIC
PHASES OF ACUTE KIDNEY INJURY
✓ Chronic Kidney Disease (CKD)
✓ End Stage Renal Disease (ESRD)
1. ONSET PHASE
CAUSES a) injury occurs and urine output decreases
b) hours to days
• PRE-RENAL – blood cannot get to the kidneys
❑ Hypotension
❑ Hypovolemia
❑ Shock

MRPP © 2022 l NOTES BY: BRYLE JUSTIN L. MAMON 24

1st SEMESTER l MIDTERM
2. OLIGURIC OHASE HYPERTENSION AND CKD
a) decreased urine output 1. High blood pressure puts pressure on the renal artery
b) client often becomes fluid volume overloaded 2. Causes thickening of the openings from the blood vessels
c) 10-14 days to the kidneys
3. This results in less blood flow to the kidneys
3. DIURETIC PHASE 4. Kidneys sense low blood flow and want more! So they
a) kidneys regain ability to excrete waste, but are produce RENIN.
unable to concentrate the urine 5. Activation of the renin-angiotensin-aldosterone system
b) make large amounts of dilute urine 6. Which causes.. more hypotension
c) hypovolemia and hypotension can occur due to 7. Eventually causes glomerulosclerosis and loss of
fluid loss nephrons
d) 1-3 weeks a) pre-renal cause
b) leads to intra-renal damage
4. RECOVERY PHASE
a) full recovery – or progress to chronic kidney DIABETIC NEPHROPATHY
disease 1. Chronic high blood glucose is stressful for the body
2. Production of pro inflammatory cytokines causes
ASSESSMENT – OLIGURIC PHASE changes to kidneys:
• oliguria a) thickening of the tubular basement membrane
• edema b) thickening of the renal arterial wall
• shortness of breath c) sclerosis of the nephrons
• labs MAJOR INTRA-RENAL CAUSE OF CHRONIC KIDNEY DISEASE
✓ increased BUN and CR
✓ metabolic acidosis STAGES OF CHRONIC KIDNEY DISEASE
✓ anemia
✓ hyperkalemia STAGE GFR ACTION
✓ hyperphosphatemia 1 >90 Identify cause
✓ hypocalcemia 2 60-89 - Protect the
3 30-59 kidneys
• fatigue
- dietary
• confusion modifications,
• nausea treat
hypertension, get
ASSESSMENT – DIURETIC PHASE DM under
control. etc.
• diuresis
✓ 3-5 liters of dilute urine/day
4 15-29 Dialysis
• Hypovolemia 5 <15
• Hypotension
• Labs EARLY
✓ Hypokalemia • blood flow shifts to the remaining “good”
✓ Hyponatremia nephrons
✓ BUN and CR start to normalize • GFR goes up
• There is DIURESIS
CHRONIC
• Chronic Kidney Disease (CKD) LATE
– happens slowly over a long period of time • Increased blood flow to the “good” nephrons
– damage to the kidneys accumulates over time causes sclerosis. Turning then into “bad”
– can no longer filter waste properly nephrons. When no more “good” nephrons are
– waste products build up left.
✓ GFR goes down
PRE-RENAL INTRA-RENAL POST-RENAL ✓ Urine output decreases
- heart failure - inflammatory - BPD ✓ Uremia ensues
diseases
- diabetic
nephropathy
• hypertension

MRPP © 2022 l NOTES BY: BRYLE JUSTIN L. MAMON 25

1st SEMESTER l MIDTERM
ASSESSMENT – LATE STAGE TYPES
1. Hemodialysis
• Sodium + Water Retention 2. Peritoneal Dialysis
✓ hypertension
✓ edema HEMODIALYSIS
• Done 3-4 times per week.
• Potassium Retention → HYPERKALEMIA • Client must be anticoagulated
• Will cause rapid fluid shift (300-800 ml/min)
✓ muscle weakness/cramps
✓ Monitor BP
✓ ECG changes
✓ Monitor electrolytes
✓ fibrillations ✓ Not all can tolerate
• Client must have a fistula
• Metabolic Acidosis ✓ No BPs/sticks in the arm of the fistula
✓ kidneys can’t make bicarb anymore ✓ Palpate a thrill
✓ Auscultate a bruit
• Osteodystrophy
✓ kidneys cannot make calcitriol → can’t absorb
calcium in GI tract → HYPOCALCEMIA
✓ HYPOCALCEMIA stimulates parathyroid glands →
secondary hyperparathyroidism.
✓ Secondary hyperparathyroidism causes
osteoporosis

• Uremia
✓ build up of urea in the blood
❑ neurological changes
❑ GI changes (anorexia, vomiting)
❑ Skin changes (uremic frost)

LAB RESULT IN CKD

BUN and Creatinine Increased PERITONEAL DIALYSIS
ABG Metabolic Acidosis • uses the peritoneal membrane as the filter instead of a
POTASSIUM High machine
PHOSPHORUS High • PROCESS:
CALCIUM Low ✓ Dialysate is infused into peritoneal cavity (2000-
2500 mLs)
✓ Dwells for about 6 hours
RENAL DIET
✓ Fluid is drained, taking the toxins along with it
• Low sodium
• Low phosphorus • Drainage should be clear
• Low protein - cloudy drainage indicates an infection
• Ensure all of the dialysate comes off
✓ turn side-to-side if decreased fluid returns
TREATMENT
• This is better for clients who cannot tolerate the fluid
• Restrict fluid intake
shifts in hemodialysis
• NO K+ sparing diuretics or ACE inhibitors
- this can further aggravate K retention
• Close follow up with PCP
• Regular lab work
• Dialysis

DIALYSIS
- a treatment that gets rid of the bodies unwanted
toxins, waste products and excess fluids by
filtering the blood.

MRPP © 2022 l NOTES BY: BRYLE JUSTIN L. MAMON 26

1st SEMESTER l MIDTERM