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CPR II Exam 3 > Clinical Approach to Proteinuria, Oliguria, and Polyuria (Selby) > Flashcards

Clinical Approach to Proteinuria, Oliguria, and Polyuria (Selby) Flashcards

1
Q

What is the difference between these terms:

  1. Anuria
  2. Oliguria
  3. Polyuria
  4. Azotemia
  5. Uremia
A
  1. urine output < 50-100 mL/day
  2. urine output < 400-500 mL/day
  3. urine output > 3000 mL/day
  4. elevated blood urea nitrogen (BUN) WITHOUT symptoms
  5. elevated BUN WITH symptoms (N/V, confusion, pruritis, metallic taste in mouth, etc)
    • symptoms are NON-SPECIFIC
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2
Q

What is the definition of Chronic Kidney Disease and what GFR categories cannot fulfill the criteria for CKD in the ABSENCE of kidney injury?

A

CKD = either markers of kidney damage and/or decreased GFR < 60 ml/min for GREATER than 3 months
- AKI = above conditions for LESS than 3 months

GFR categories 1 (>90) and 2 (60-89) CANNOT fulfill CKD criteria in the ABSENCE of evidence of kidney damage

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3
Q

What is the difference between these CKD stages:

Stage 1
Stage 2
Stage 3a
Stage 3b
Stage 4
Stage 5
A
  1. GFR > 90 –> LEAST severe
  2. GFR 60-89

3a. GFR 45-59
3b, GFR 30-44

  1. GFR 15-29
  2. GFR < 15 –> MOST SEVERE (kidney failure, ESRD)
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4
Q

What are 4 risk factors for the development of CKD?

What are 4 nephrotoxic agents that are also implicated in the development of CKD?

What are the two most likely causes of CKD in patients?

A

RF: DM, HTN, cardiovascular disease, AKI
MOST COMMONLY: Diabetes (38%) or HTN (26%)

Drugs: NSAIDs, PPIs, antibiotics, heavy metals

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5
Q

What are common signs and symptoms of Chronic Kidney Disease?

AKI has similar signs and symptoms

A
  • most pts. are asymptomatic

Sx: edema, HTN, Dec. UOP, FOAMY URINE, UREMIA
- Pericardial friction rub

  • also see ASTERIXIS (hand flapping) and Uremic Frost (urea crystal deposits get sweated out)
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6
Q

What are the 3 most common tests used to diagnose a patient with Chronic Kidney Disease?

What is a common limitation of the use of GFR as a diagnostic tool?

A

Tests:

  1. eGFR
  2. urine albumin/creatinine ratio or urine protein/creatinine ratio (random spot urine sample)
  3. urinalysis (look for RBCs/WBCs)
  • GFR is NOT reliable when pt GFR > 60 mL/min and is NOT reliable for Acute Kidney Injury due to rapidly changing creatinine lvls
    • also not good for low muscle mass, pts < 18 yo
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7
Q

What are 4 common Renal Ultrasound findings seen in pts with Chronic Kidney Disease?

A
  1. atrophic or SMALL kidneys (normal around 9-12 cm)
    • proportional to pt. height
    • should be < 1-1.5 cm difference
  2. cortical THINNING (normal around 1.0 cm)
  3. increased echogenicity (inc. WHITENESS)
    • can compare to liver and spleen
  4. elevated resistive indices (RI > 0.7-0.8)
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8
Q

What is the treatment for Chronic Kidney Disease?

What are the A, E, I, O, U indications to start dialysis on a CKD pt?

A

Tx: RENAL REPLACEMENT THERAPY (RRT)
- hemodialysis, peritoneal dialysis, transplant

A - severe ACIDOSIS
E - ELECTROLYTE disturbance (hyperkalemia)
I - INGESTION (ethylene glycols, methanol)
O - volume OVERLOAD
U - UREMIA

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9
Q

What is the definition of Acute Kidney Injury and what is staging of AKI based upon?

A

AKI = elevated serum creatinine levels and/or decreased urine output

staging of AKI is based on whichever of these two issues is WORSE in the patient

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10
Q

What are the 3 major etiologies of Acute Kidney Injury?

What are the two most common causes of Acute Tubular Necrosis?

A

Etiologies:

  1. PRErenal: low effective circulating volume
  2. Intrinsic: ATN, interstitial nephritis, glomeruloneph.
  3. POSTrenal: bladder outlet, ureteral obstruction
    • also Renal Pelvis (papillary necrosis most common)

Acute Tubular Necrosis: Ischemic (50%) and Toxic (35%)

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11
Q

What are the 3 most common tests used to diagnose Acute Kidney Injury?

What findings for BUN/Cr, FeNa, and FeUrea are seen in prerenal azotemia vs Acute Tubular Necrosis?

A
  1. Urinalysis with microscopy
  2. urine albumin/Cr or protein/Cr ratio
  3. renal ultrasound

BUN/Cr = >20:1 (Prerenal Azotemia)
FeNa: <1% (Prerenal Azotemia) or >2% (ATN)
FeUrea: <35% (Prerenal Azotemia) or >50% (ATN)

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12
Q

What pathologies are these urinary patterns typically indicative of:

  1. Renal tubular epi, transitional epi, granular casts
  2. WBC, WBC casts, urine eosinophils
  3. dysmorphic RBCs, RBC casts
  4. proteinuria (<3.5g/day), hematuria, dysmorphic RBCs
  5. heavy proteinuria (>3.5g/day), lipiduria, low hematuria
  6. hyaline casts
  7. WBCs, RBCs, bacteria
A
  1. Acute Tubular Necrosis
  2. Acute Interstitial Nephritis or Pyelonephritis
  3. vasculitis or glomerulonephritis
  4. nephrITIC syndrome
  5. nephrOTIC syndrome
  6. non-specific, PreRenal Azotemia
  7. urinary tract infection
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13
Q

How would these causes of AKI be treated:

  1. Prerenal patients
  2. Acute Tubular Necrosis patients
  3. Glomerulonephritis patients
  4. Acute Interstitial Nephritis patients

How else are AKI patients treated?

A
  1. IV fluids
  2. supportive care
  3. immunosuppression or plasmapheresis
  4. discontinue offending agents (maybe steroids?)
  • should also correct underlying disease if possible, but main treatment will be SUPPORITIVE
    • avoid hypotension, stop nephrotoxins, renal replacement if needed (HEMODIALYSIS)

TIME IS NEPHRONS –> CORRECT QUICKLY

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14
Q

What is the definition of Nephrotic Syndrome?

What happens if serum albumin levels are NORMAL in a patient suspected of having Nephrotic Syndrome?

A
  • proteinuria (>3-3.5g/day), hypoALBUMINEMIA, peripheral edema, hyperlipidemia, and lipiduria
  • if pt. has normal serum albumin lvls if setting of nephrotic range proteinuria, they do NOT have TRUE nephrotic syndrome
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15
Q

What are 4 major complications of Nephrotic Syndrome?

A
  1. edema (inc. urinary Na retent. –> inc. TBW and Na)
  2. hyperlipidemia (hepatic lipoprotein synthesis)
  3. infection (loss of IgG)
  4. thrombosis (loss of antithrombic factor)
    • risk inc. with albumin < 2.0-2.5 g/dL

can also lead to Vitamin D deficiency and Anemia (urinary loss of transferrin and erythropoietin)

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16
Q

What is the pathogenesis of Edema in patients with nephrotic syndrome?

A
  • more probably do to Overfill Theory
  1. inc. sodium reabsorption leads to inc. water retention
  2. proteinuria with hypoalbuminema leads to dec. intravascular oncotic pressure
17
Q

What are two major classical presentations of Nephrotic Syndrome aside from Proteinuria, Lipiduria, and Hyperlipidemia?

What is the most common cause of Nephrotic Syndrome in the United States, and what are two other likely causes?

A
  1. new onset HYPERTENSION
  2. new onset EDEMA
  • most common cause of Nephrotic Syndrome in the United States is DIABETIC NEPHROPATHY
  • could also be caused by Minimal Change Disease, Focal Segmental Glomerular Sclerosis (FSGS), etc…
18
Q

What is the best way to diagnose Nephrotic Syndrome?

A

RENAL BIOPSY

medulla sample is NOT diagnostic; must obtain a sample from the CORTEX in order to make the diagnosis

19
Q

What is the Definition of Nephritic Syndrome?

How does its urinary sediment differ from the urinary sediment of Nephrotic Syndrome?

A
  • proteinuria (<3.5 g/day), HEMATURIA, HTN, and potentially acute renal failure
  • Nephritic Syndrome has ACTIVE URINARY SEDIMENT (hematuria, RBC casts, dysmorphic RBCs) while Nephrotic Syndrome has BLAND urinary sediment
20
Q

What is the best way to diagnose Nephritic Syndrome?

A

RENAL BIOPSY (similar to Nephrotic Syndrome)

medulla sample is NOT diagnostic; must obtain sample from the CORTEX in order to make the diagnosis

21
Q

What is a finding that is helpful in the diagnosis of Nephritic Syndrome?

A

LOW COMPLEMENT LEVELS
- only a few diseases cause complement lvls to drop

C3 and C4 = classical pathway activation
C3 ONLY = alternative pathway activation

22
Q

What is Diabetes Insipidus and what are its two main categories?

A

DI - urine output of > 3L/day
- dec. ability to concentrate urine resulting in polyuria and polydipsia

  1. Solute Diuresis
    • glucosuria, urea, sodium, mannitol
  2. Water Diuresis
    • primary polydipsia, central or nephrogenic DI
23
Q

What are the two basic requirements for forming concentrated urine?

A
  1. Hypertonic Medullar Interstitium
    • generates osmotic gradient
    • for water reabsorption
  2. High lvls of Antidiuretic Hormone (ADH)
    • inc. water permeability in DCT and CD
24
Q

Antidiuretic Hormone (ADH or Vasopressin)

What is it and what two locations is it synthesized in?

What are the two stimuli that cause its release?

A
  • preprohormone synthesized by specialized nuclei in the HYPOTHALAMUS (MAGNOCELLULAR NUCLEI)
    1. Suproptic Nuclei (SON) = majority of production
    2. Paraventricular Nuclei (PVN)
  • transported to posterior pituitary in secretory granules
  • released in response to osmotic and non-osmotic stimuli:
    1. inc. in serum osmolality (osmoreceptors)
    2. dec. in BP/inc. in volume (baroreceptors and atrial stretch receptors)
25
Q

What is ADHs effect on the Collecting Duct?

A
  • ADH binds to the V2 receptors and inc. cAMP lvls which leads to insertion of AQP-2 and Urea transporters into the luminal and basolateral membranes
  • this explains what UREA LEVELS GO UP in pts. with dehydration (BUN/Cr > 20:1)
26
Q

What is the difference in pathophysiology of Central and Nephrogenic Diabetes Insipidus?

A

CDI: due to dec. release of ADH
- most commonly idiopathic cause

NDI: due to dec. response to ADH

  • hereditary causes seen mainly in CHILDREN (rare)
  • also LITHIUM TOXICITY and HYPERCALCEMIA
27
Q

What is the net result of Hypercalcemia-induced Polyuria similar to?

A
  • net result similar to LOOP DIURETIC USE
  • basolateral calcium sensor in Thick Ascending Loop leads to inactivation of luminal potassium channel, ultimately leading to inactivation of Na/K/2Cl cotransporter
  • CaSR on the apical side of the Collecting Duct are activated by elevated calcium lvls, causing AQP-2 degradation by Autophagosomes = nephrogenic DI (TRUE NDI mechanism()
    • Li through ENaC channels stimulates similar action
28
Q

What is the clinical manifestation of Diabetes Insipidus?

What are 3 tests used to diagnose this disorder?

What is the Water Deprivation Test?

A

C: polyuria, nocturia (typically presenting symptom), polydipsia, hypernatremia

Dx:

  1. 24 hr urine volume collection (confirms polyuria)
  2. urine osmolality < 300 mOsm/kg
  3. Water Deprivation Test

WDT: when water intake is restricted, urine Osm and ADH increases; water intake restricted until pt. loses 3-5% of body weight, then vasopressin is administered to see urine osmolarity response

29
Q

What is the treatment for Central vs Nephrogenic Diabetes Insipidus?

How should a DI pt. with Hypernatremia be treated?

A

CDI: vasopressin

NDI: dec. solute intake, thiazides (mild. vol. depletion), NSAIDs (dec. medullary prostaglandins), vasopressin

  • if pt has Hypernatremia, replace their free water deficit with water or IV D5W

CPR II Exam 3 (12 decks)

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