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Renal Disease > Patho-Renal > Flashcards

Patho-Renal Flashcards

1
Q

What is renal disease?

A

Any condition that reduces the ability of the kidneys to perform its primary function.

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2
Q

What are the 4 common markers of renal disease?

A

BUN (Blood Urea Nitrogen)
Serum Creatinine
Glomerular filtration
Creatinine Clearance

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3
Q

What is the functional unit of the kidney?

A

Nephron

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4
Q

What are some of the keep parts of the nephron?

A

Afferent arteriole-Brings blood to glomerulus

Efferent arteriole- Takes blood away from the glomerulus

Glomerulus- Serves as the entrance to renal tubular system and filters blood and acts as a filtration membrane

Juxtaglomerular apparatus: Detects low blood pressure, secretes renin.

Bowman’s capsule:

Proximal convoluted tubule:Site of reabsorption of filtered Na+, H2O, K+, HCO3-, and PO4-.
Site of secretion of H+, drugs, and other toxins.

Loop of Henle: Site of reabsorption of filtered Na+, and H2O.
Distal convoluted tubule: Site of reabsorption of filtered Na+, H2O, K+, HCO3-, and PO4-.
Site of secretion of H+, K+, and maintains acid/base balance tion of filtered H2O and primary determinant of concentration of urine.

Collecting duct: Site of action for ADH and reabsorption of filtered H2O and primary determinant of concentration of urine.

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5
Q

The movement of substances from the blood is called___
The movement of substances that have been filtered back into the blood stream is called______
The movement of substances from blood the blood stream into the renal tubules is called____ ___

A

Filtration
Reabsorption
Secretion

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6
Q

What is GFR?

A

The amount of blood that gets filtered every minute.

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7
Q

What is normal value for GFR?

A

120 ml/min. Values less than 120 min/ml indicate that the kidneys are not working well.

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8
Q

GFR is estimated by measuring serum creatinine (SCr) levels. T or F

A

True . When SCr levels go up, GFR goes down.

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9
Q

What is the equation (Cockcroft Gault) equation for figuring Creatinine clearance.

A

CrCl (mL/min) = (140-age) x Ideal Body Weight (IBW) x 0.85(female)/72 x SCr

  • Age in years
  • IBW in kilograms (use actual body weight if < IBW)
  • SCr in mg/dL
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10
Q

What are the 4 primary functions of the kidneys?

A
  1. Fluid and electrolyte balance
    a. Maintains normal blood pressure(BP) through regulation of fluid status and Na conc
    -If BP increases, kidneys responds with increased fluid and Na excretion
    -If BP decreases, kidneys responds with increased fluid and Na reabsorption.
    b. Regulated through the actions of antidiuretic hormone (ADH) and the renin angiotensin-aldosterone system (RAAS).
    Decrease in renal perfusion, low BP is detected by the Macula densa in the juxaglomerular apparatus in the kidney and responds by secreting renin. Renin converts angiotensinogen produced by the liver to angiostensin I which in turn is converted to angiostensin II by the action of angiotensin converting enzyme (ACE). The effects of Ang II are numerous:
    -Causes the adrenal cortex to secrete aldosterone. Aldosterone secretion leads to the tubular reabsorption of NaCl, K+ excretion, and water retention.
    - Causes sympathetic activity to increase.
    -Causes the efferent arteriole of the glomerulus to vasoconstrict thus increasing BP.
    -Causes the posterior pituitary gland to secrete ADH which activates the collecting duct to absorb water.
    The net result is water and salt retention. Effective circulating volume increases. Perfusion of the juxaglomerular apparatus increases.
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11
Q

What are the 4 primary functions of the kidneys?

A
  1. Endocrine Function
    o Secretes many hormones including erythropoietin and renin
    o Responsible for production of active vitamin D
  2. Acid Base Regulation
    o Controls H+ ion (acid) concentrations in the bloodstream through regulation of H+ excretion and HCO3- (base) reabsorption
  3. Elimination of waste products
    o Filters waste byproducts including urea, uric acid, drugs, and other toxins from the bloodstream into the urine for excretion
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12
Q

Define Acute Kidney Injury (AKI)

A

An abrupt decrease in renal function that results in increased BUN and SCR (over baseline)
Time frame is essential in classifying AKI as acute.
o Occurs over hours-to-days even weeks
o Does not occur gradually over the course of years
o By definition, acute is renal dysfunction occurring for < 3 months.

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13
Q

Name the 3 components of AKI

A

Pre-Renal Acute Kidney Injury
Intrinsic Acute Kidney Injury
Post Renal Acute Kidney Injury

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14
Q

What are the stages for status/severity of AKI as determined by the National Kidney Foundation (NKF)?

A

Stage SCr Criteria

Stage 1 SCr increase >0.3 mg/dL OR
1.5-1.9 times baseline

Stage 2 SCr increase 2-2.9 times baseline

Stage 3 SCr increase > 3 times baseline OR
SCr >4 mg/dL

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15
Q

Define Pre-Renal Acute Kidney Injury

A
  • An acute decline in renal function secondary to decreased renal blood flow or loss of autoregulation
  • Regardless of etiology, decline in renal function can be attributed to a decreased intraglomerular pressure.
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16
Q

What is the physiologic basis of Pre-Renal Acute Kidney Injury?

A

• A minimum filtration pressure must be maintained in the glomerulus for adequate filtration to occur
•Two primary determinants of glomerular filtration pressure:
1. Renal Blood Flow (RBF)
2. Circulating Blood Volume (CBV)

• Autoregulation: The process by which RBF is maintained through constriction/dilation of the afferent and efferent arterioles
o Prostaglandins are responsible for dilation of the afferent arteriole
o Angiostensin II is responsible for constriction of the efferent arteriole

• When autoregulation capacity is exceeded, glomerular perfusion pressure drops
o GFR drops proportionate to the drop in perfusion pressure
o Water, electrolytes, and waste products are not filtered from the bloodstream into the renal tubule

Autoregulation capacity exceeded = Decreased glomerular perfusion = Decreased glomerular filtration = Decreased CrCl/GFR = Retention of waste products in the blood stream = Increased BUN and SCr = Pre Renal Acute Kidney Injury.

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17
Q

What is the Etiology of Pre Renal Kidney Injury?

A 
Etiology two-fold: 
Decreased Circulating Blood Volume (DCBV) caused by:
-Hypovolemia
-Vomiting/Diarrhea (Severe) 
-Overdiuresis
-Polyuria (Uncontrolled DM)
-Blood loss
-Diuretics

Decreased Renal Blood Flow caused by:

  • Heart failure
  • Sepsis
  • Cirrhosis
  • Hypotension
  • Renal Artery Stenosis
  • ACE/ARB/NSAIDS (b/c PGs are being inhibited)
18
Q

What are the risk factors for Pre Renal Kidney Injury?

A
  1. Age > 65
  2. Dehydration
  3. Pre-existing KD
  4. Male gender
  5. Acute infection/Illness
  6. CV
  7. Having 1 kidney
  8. Surgery/Hospitalization
19
Q

What are the clinical manifestations or signs and symptoms of Pre-Renal Acute Kidney Injury?

A 
o  Hypotension/Orthostatic hypotension
o  Decreased skin turgor
o  Dry mucous membranes
o  Tachycardia
o  Weight loss

Laboratory signs indicative of pre-renal vs. other AKI types
o BUN:SCr ratio > 20:1
o Fractional Excretion of Sodium (FeNa) < 1% normal is 1-2 %
FeNa = (Urine Na)/(Serum Na) divided by (Urine Cr)/(Serum Cr) x 100

o Urine sodium < _20 mE/L_______________
o Urine osmolality > __500____________
o Urinalysis normal

20
Q

What are complications of Pre Renal Acute Kidney Injury?

A

Assuming pre-renal AKI is recognized early, complications usually do not arise and failure is reversible
- If patient has pre-existing kidney disease, current complications can be worsened
o Hyperkalemia
o Hyperphosphatemia
- Acute Tubular Necrosis (ATN) is a potential complication of unrecognized prolonged pre-renal injury

21
Q

What is Intrinsic Acute Kidney Injury?

A

Acute kidney damage that usually occurs as a result of direct damage or inflammation to renal structures

22
Q

What are the 3 types of Intrinsic Acute Kidney Injury?

A
  1. Acute Tubular Necrosis (ATN)
  2. Glomerulonephritis
  3. Acute Interstitial Nephritis (AIN)
23
Q

What is the Pathophysiology of Intrinsic Acute Kidney Injury?

A

• Acute Tubular Necrosis (ATN) and Acute Interstitial Nephritis (AIN) are the two most common subtypes of intrinsic renal injury
o Usually diagnosed based on clinical history and common lab tests
o ATN → Direct injury to renal tubular cells
o AIN → Kidney damage due to inflammation rather than direct toxicity
• Glomerulonephritis is also intrarenal disease; typically requires a renal biopsy for diagnosis
o Nephrologist usually required for management of glomerulonephritis

ATN Pathophysiology

Direct tubular toxicity or tubular ischemia occurs which leads to cell injury. Tubular cell death or necrosis then results. The dead cells detach from the walls of the tubule and collapse into the tubule. 2 things then occur; tubule backleak into blood and tubular obstruction. Tubular backleak results in waste product retention hence increase in BUN and SCr.
Tubular lumen obstruction leads to increased intratubular pressure which counter intraglomerular pressure and decreases it hence decreased filtration, decreased GFR. Both lead to Intrinsic Acute Kidney Injury.

AIN Pathophysiology

Renal exposure to antigen occurs which leads to interstitial Type II MHC activation of T-cells which leads to overall activation of the immune system. As a result of immune system activation, cytokines and macrophages are released which cause inflammation of renal tubules and the surrounding insterstitum. This inflammation leads to renal tubule damage which leads to decreased GFR, waste product retention, increased BUN, SCr

24
Q

What is the etiology of Acute Tubular Necrosis (ATN)?

A

Radioactive Contrast dyes
Aminoglycosides
Amphotericin B
Prolonged Ischemia/Hypotension

25
Q

What is the etiology of Acute Interstitial Nephritis (AIN)?

A

Beta-Lactam antibiotics
Sulfa Drugs
NSAIDS
Pyelonephritis

26
Q

What are the risk factors for Acute Tubular Necrosis?

A 
o	Dehydration                           		        ○   
o	Pre-renal AKI
o	Age > 65
o	Pre-existing kidney disease
o	Diabetes
o	Recent surgery/hospitalization
o	Acute illness/Infection
27
Q

What are the risk factors for Acute Interstitial Nephritis?

A

No true risk factor b/c it is a hypersensitive allergic rxn

28
Q

What are clinical manifestations (SS) of ATN and AIN?

A
  • History should be consistent with ischemia, toxin exposure, or possibly new medication
  • Non-specific physical exam except fever and rash may be present with AIN

• Laboratory signs indicative of intrinsic vs. other AKI types
o BUN:SCr ratio less than or equal to 15:1
o FeNa > 2% normal is 1 to 2 %
o Urine sodium > 40 meq/L
o Urine osmolality < 350 mOsm/L
o Eosinophilia (AIN)

•   Urinalysis abnormal
o   Muddy-brown granular casts	(ATN)
o   Tubular epithelial cells 	(ATN)
o   WBC casts 			(AIN)
o   Eosinophiluria 		(AIN)
o   Varying levels of proteinuria 	(both)

• Patients are also more likely to have signs/symptoms of volume overload rather than volume depletion
o Edema
o Hypertension

29
Q

What are the complications of ATN and AIN?

A
  • Progression to chronic kidney disease (CKD) and/or worsening of CKD complications
  • Hyperkalemia
  • Fluid overload
  • Proteinuria
  • Hyperphosphatemia
  • Metabolic acidosis
30
Q

Define Post Renal Acute Kidney Injury

A

Renal injury secondary to obstruction of urine flow through the ureters, bladder, or urethra

31
Q

What is the pathophysiology of Post Renal Acute Kidney Injury?

A

Obstruction to urine flow leads to additional pressure build up. Increased intratubular build up leads to decreased GFR, waste product retention, increased BUN, SCr. These all cause Post Renal Acute Kidney Injury.

32
Q

What is the Etiology of Post Renal Acute Kidney Injury?

A 
Prostatic
Hypertrophy
Anticholinergic drugs
Tumors (pelvic or genitourinary)
Bladder outlet obstruction
Antiviral drug
33
Q

What are risk factors of Post Renal Acute Kidney Injury?

A
  • Deformities of the urinary system
  • Having one kidney
  • Dehydration
  • Pre-existing kidney disease
  • Age > 65
  • Enlarged prostate
  • Acute illness/Infection
  • Male gender
34
Q

What are the SS of Post Renal Acute Kidney Injury?

A

• History may contain information related to passage of kidney stone, dysuria, nocturia, or slowing of urine stream

• Non-specific physical exam includes:
o Enlarged prostate
o Severe back, flank, or abdominal pain
o Full bladder (even after voiding)

• Laboratory signs indicative of post-renal vs. other AKI types
o BUN:SCr ratio _Normal___________
o FeNa and urine sodium are variable with post-renal

• Urinalysis abnormal
o Red blood cells (RBCs)
o White blood cells (WBCs)
o Crystals

• Clinical Imaging
o Kidney stones
o Hydronephrosis

• Patients are also more likely to have signs/symptoms of volume overload rather than volume depletion
o __Edema___________________
o __Hypertension_____________

35
Q

What are the complications of Post Renal Acute Kidney Injury?

A 
Progression to chronic kidney disease (CKD) and/or    worsening of CKD complications
•  Hyperkalemia
•  Fluid overload
•  Proteinuria
•   Hyperphosphatemia
•   Metabolic acidosis
    Hematuria
    Post-obstructive diuresis
36
Q

What is Chronic Kidney Disease (CKD)?

A
  • A slow, progressive decline in kidney function due to long-term injury
  • Normal kidney function is a GFR of approximately ____120_______ml/min/1.73m2
  • CKD defined as a GFR <60ml/min/1.73m2 or the presence of kidney damage for at least 3 months.
  • Kidney damage includes:

o Proteinuria
o Hematuria
o Evidence of cysts
o Damage on biopsy

37
Q

Describe the NKF Staging System for CKD in terms of Severity.

A

Stage Description GFR (ml/min/1.73m2)
1 Kidney damage w/ normal GFR > or = to 90
2 Kidney damage w/ mildly decreased GFR 60-89
3a Mildly to moderately decreased GFR 45-59
3b Moderately to severely decreased GFR 30-44
4 Severely decreased GFR 15-29

5 Kidney failure <15 or dialysis

38
Q

What is the pathophysiology of CKD?

A

Because this is a chronic condition that happens over time, there was already damage to the kidneys like scarring of the glomerulus (glomerulosclerosis). This leads to decreased number of nephrons or decreased functionality of nephrons. The decreased GFR that results from this is detected by the remaining functional nephrons which make physiologic alterations to compensate and try to maintain GFR. The compensation is carried out by afferent arteriole dilation and efferent arteriole constriction thus increasing glomerular blood flow and increased efferent arteriole resistance. As a result, glomerular filtration pressure increases thereby overworking the already damaged kidneys thus leading to glomerular hypertrophy and increased permeability to proteins. Further damage of the glomerulus occurs b/c large protein molecules which should not be filtered are leading to severe glomerulosclerosis. All these sequence of events ultimately leads to progressive decreased of GFR and CKD.

• Initially, the changes in glomerular blood flow and filtration pressure are beneficial and necessary to maintain adequate GFR
o Over long periods of time, these changes become destructive and lead to progressive renal dysfunction
• Angiotensin II is responsible for vasconstriction of the efferent arteriole, which results in increased glomerular filtration pressure
• Prostaglandins are responsible for vasodilation of the afferent arteriole, which results in increased glomerular filtration pressure
• Uncontrolled diabetes → hyperglycemia → increased cytokines → glomerular hypertrophy and damage to the glomerulus → allowing larger molecules to be filtered → diabetic nephropathy
• Uncontrolled hypertension → glomerular hypertension → glomerular hypertrophy and damage to the glomerulus → allowing larger molecules to be filtered → proteinuria
o Protein passing through the glomerular filter causes further glomerular damage

39
Q

What is the Etiology of CKD?

A

DM
HTN
Glomerulonephritis Polycystic kidney disease
Autoimmune disease (lupus) Recurrent urinary tract infections
Persistent acute kidney injury Unknown

40
Q

What are the risk factors for CKD?

A 
Development of CKD
Age>65
Low Birth Weight
African American Race
Family History
Systemic Inflammation / Autoimmune Dz
Dyslipidemia
Diabetes Mellitus
Hypertension
Glomerulonephritis
Progression of CKD
DM
HTN
Proteinuria
Smoking
Obesity (BMI > 30 kg/m2
Dyslipidemia
41
Q

What are the clinical manifestations of CKD?

A

• History may be consistent with diabetes or hypertension
• Presence and severity of signs/symptoms are dependent on the stage of CKD
o Most likely to be symptomatic at stage 3 CKD

• Non-specific review of systems and physical exam
o General symptoms
 Fatigue, confusion, altered taste, anorexia, pruritis
o Volume overload
Hypertension, edema

• Laboratory signs indicative of chronic kidney disease
o Increased BUN and SCr for >3 months (BUN:SCr ratio ~15:1)
o Increased potassium, phosphate, PTH
o Decreased bicarbonate
o Calcium imbalance
o Decreased hemoglobin/hematocrit
Anemia and osteodystrophy are indicative of long-standing renal insufficiency

• Urinalysis may be abnormal
o Proteinuria

42
Q

What are the complications of CKD?

A
  • Proteinuria
  • Fluid Overload/Hypervolemia
  • Hyperkalemia
  • Metabolic Acidosis Renal Osteodystrophy
  • Vitamin D Deficiency
  • Hyperphosphatemia
  • Calcium Imbalance
  • 2o Hyperparathyroidism Renal Osteodystrophy
  • Malnutrition
  • Anemia

Renal Disease (1 decks)

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