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Renal > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What are the pathological stages of glomerulosclerosis?

A

injury

response

repair

maladaptation

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2
Q

What are the clinical phases of glomerulosclerosis

A

initiation - infection, hypertention, and environmental stimulus

consolidation - inflammation, excessive mediator response, and glomerular hyperfiltration

low progression - low nephron number, “progression” genes, and nephron loss

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3
Q

What are the two stages of progression in chronic kidney disease?

A

injury and chronic scarring

structural damage that leads to progressive nephron loss and eventually end-stage disease

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4
Q

What functions of the nephron are altered when the kidney is diseased?

A

sodium and phosphate excretion

potassium secretion

titratable acid excretion

bicarbonate reabsorption

protein metabolism

gluconeogenesis

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5
Q

At what point is dialysis usually required?

A

at 10% kidney function (10% GFR)

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6
Q

What is unique about oxygen utilization of the kidneys?

A

the normal O2 content of the medulla is lower than in most tissues and renal extraction of oxygen is relatively high

increased workload drives oxygenation

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7
Q

What happens if oxygen capacity is exceeded?

A

glycolysis leads to acidosis, generation of reactive oxygen species, and cellular production of hypoxic mediators

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8
Q

What are the endocrinological effects on extra-renal systems in uremia?

A

parathyroid, PTH, bone resorption

inflammation

puritis

atherosclerosis

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9
Q

What are the endocrinological effects on remaining nephrons in uremia?

A

hyperfiltration

hypertrophy

intraglomerular hypertension

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10
Q

What are the steps in progressive nephron loss?

A

nephron loss

remnant hypertrophy

increased filtered load

further scarring and increased tubular transport work

increased oxygen utilization

tissue hypoxia - leads to endothelial dysfunction

acidosis ROS HIF -> nephron loss

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11
Q

characteristics of nephron hypertrophy

A

rapdi response (24 hrs) to tissue loss

increased SNGFR

critical for maintaining adequate renal function

tubular response to maintain glomerulotubular balance

immediate benefit, long-term problem

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12
Q

What is the major mediator of nephron hypertrophy?

A

renin-angiotensin-aldosterone system

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13
Q

What are the consequences of nephron loss?

A

increased SNGFR

increased tubular reabsorption

more energy, more oxygen consumption are required

renal oxygen extraction increases from 7.3% to 13.9% in CKD

loss of peritubular vessels worsens oxygen delivery

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14
Q

What are the causes of disturbed NO-mediated vasodilation?

A

mediated by increased asymmetric dimethylarginine (ADMA)

dimethylaminoarginine dimethylaminohydrolase (DDAH) is a natural inhibitor of ADMA, which delays the progression of kidney disease in rats

uremia could therefore cause vasoconstriction, decreasing blood flow

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15
Q

How does acidosis affect kidney function?

A

common in CKD and worsened by ischemia

ammonia generation may activate alternative complement pathway

terminal components (C5-9) play a role in progression

bicarbonate feeding decreases renal tubular peroxide production an damage in CKD mice

bicarbonate supplementation slows CKD progression in humans

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16
Q

How does the generation of ROS in CKD affect renal function?

A

carbamylated low-density lipoproteins promate oxidative stress in endothelial cells in uremia

hypertension is associated with ROS activity

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17
Q

What are the hypoxic mechanisms of ROS generation in CKD?

A

superoxide is generated at the mitochondrial inner membrane by complex III enzymes

hypoxia stabilizes these enzymes

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18
Q

What are the non-hypoxic mechanisms of ROS generation in CKD?

A

TGF-beta activates NAD(P)H oxidase

ferrous iron delivered to the tubulointerstitium may generate free radicals

macrophages may produce H2O2

angiotensin II stimulates ROS production

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19
Q

How do ROS cause disease?

A

signaling molecule at low concentrations

at moderate concentrations (50-100 microM), off-target effects of oxidizing such as thiol bonds, receptors, and protein structure

in high concentrations, react with lipids and proteins to alter cell membranes and generate more free radicals

20
Q

What is the role of hypoxia-inducible factor (HIF)?

A

present in fibrotic kidneys

kockout of HIF decreases kidney fibrosis in mouse models

HIF may play an important role in kidney fibrosis, even in normoxia

21
Q

What are the factors that can affect per-nephron load?

A

low birth weight (low nephron number)

prematurity (low nephron number)

obesity (increased metabolism, increased filtration)

hypertension (hyperfiltration, activation of RAAS)

history of acute kidney injury

anemia (poor oxygen delivery)

22
Q

What are the factors that affect the GFR calculation?

A

serum creatinine

age

ethnicity

gender

body weight (ideal - amount of muscle mass)

23
Q

What is the calculation for creatinine clearance?

A

men - [(140-age)*wt(kg)/(72*SCr)]

women - 0.85*[(140-age)*wt(kg)/(72*SCr)]

24
Q

Why calculate GFR?

A

more accurate representation of renal function than serum creatinine, which can be misleading

25
Q

What is the definition of chronic kidney disease (CKD)?

A

abnormal kidney function persisting for mroe than 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR

can be due to either a decreased glomerular filtration rate or to anatomic or structural abnormalities or abnormalities in the blodo or urine

can also be defined by a GFR < 60 mL/min/1.73m2 for more than or equal to 3 months, with or without kidney damage

26
Q

Definition of acute kidney injury (AKI)

A

increased in serum Cr from baseline by at least 0.3 mg/dL within 48 hours, if the baseline GFR > 60

increase serum Cr by 50% within 7 days, from baseline (any GFR)

baseline defined as lowest creatinine within past 3 months

oliguria of less than 0.5 mL/kg/hr for more than 6 hours

27
Q

What are the normal ranges for BUN and creatinine?

A

BUN - 8-27 mg/dL

Cr - 0.57-1.00 mg/dL

28
Q

azotemia

A

high BUN level

29
Q

uremia

A

high BUN level with symptoms such as confusion/encephalopathy, bleeding, and asterixis (tremor)

30
Q

What are the common causes of increased BUN:Cr?

A

prerenal AKI due to renal tubular absorption of urea, as opposed to secretion of creatinine

GI bleed

high protein nutrition

steroids

31
Q

What are some methods of differentiating AKI from CKD?

A

best way is to compare to old creatinine values

renal ultrasound - small kidney means chronic

urinalysis - broad casts means chronic

renal bone disease - presence of means chronic

32
Q

What are the etiologies of CKD?

A

include all etiologies of AKI

diabetes and hypertension are most common

autoimmune diseases and glomerulonephritis

chronic nephrotoxic medication

anatomical structural changes to the kidneys

33
Q

stage 1 chronic kidney disease

A

GFR >= 90 mL/min, proteinuria

kidney damage would be defined by the presence of anatomic or urine finding indicating kidney damage

34
Q

stage 2 chronic kidney disease

A

GFR between 60 and 89 mL/min

MDRD equation not accurate at this GFR level

CKD is not present by GFR criteria until the GFR falls below 60

35
Q

stage 3 chronic kidney disease

A

GFR between 30 and 59 mL/min

3a = GFR between 45 and 59 mL/min

3b = GFR between 30 and 44 mL/min

the lower the GFR, the more likely for complications to occur

36
Q

stage 4 chronic kidney disease

A

GFR between 15 and 29 mL/min

complications likely in this stage

renal replacement options are also discussed

referral to transplant when GFR is less than 20

37
Q

stage 5 chronic kidney disease

A

GFR less than 15 mL/min

considered end stage renal disease

patients may have a very low GFR and not be on dialysis

a stage 5 patient on dialysis is sometimes denoted as 5D

38
Q

What are the classic symptoms of CKD?

A

dysguesia

anorexia

fluid retention

fatigue

cloudy thinking

non-specific and often not present until more severe CKD has developed

39
Q

complications of CKD

A

begin at GFR < 60 cc/min - the lower the GFR, the more likely that there will be complications

anemia - kidneys make erythropoietin

bone disease

fluid and electrolyte abnormalities - usually with lower GFRs

40
Q

indications for dialysis for acute kidney injury

A

Acidosis

Electrolytes (hyperkalemia)

Ingestions (lithium, ASA)

Overload (volume, causing hypoxia, decompensated heart failure)

Uremia

41
Q

indications for dialysis for chronic kidney injury

A

any acute indication in setting of CKD (GFR < 15 cc/min)

general malaise, failure to thrive, in patient with GFR < 10-15 cc/min

42
Q

What are some methods to delay progression of CKD?

A

control blood pressure

control blood sugar if patient has DM

reduce proteinuria

smoking cessation

give sodium bicarb (?)

43
Q

management of stage 1 and 2 CKD

A

diagnose, delay progression

reduce CV risk

reduce proteinuria

44
Q

management of stage 3 CKD

A

diagnose, delay progression

reduce proteinuria

reduce CV risk

assess for complications

45
Q

management of stage 4 CKD

A

diagnose, delay progression

reduce proteinuria

reduce CV risk

assess for complications - more frequently seen

discuss renal replacement therapy (transplant or dialysis)

46
Q

management of stage 5 CKD

A

same as stage 4

prepare for transplant or initiate dialysis

Renal (28 decks)

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