CKD Flashcards

1
Q

chronic kidney disease (CKD) - defined

A

*defined by 3 or more months of:
-kidney damage
OR
-decreased kidney function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

chronic kidney disease (CKD) - etiologies

A
  1. glomerular diseases:
    -DIABETES, autoimmune diseases, systemic infections, drugs, neoplasias
  2. vascular diseases:
    -atherosclerosis, HTN, ischemia, vasculitis, thrombotic microangiopathy
  3. tubulointerstitial diseases:
    -chronic UTIs, stones, obstruction, drug toxicity
  4. cystic diseases:
    -polycystic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

decreased kidney function

A

*GFR is best overall index of kidney function for healthy individuals & those with CKD
*GFR = sum of the filtration rates in all of the functioning nephrons
*healthy glomeruli collectively filter 180 liters per day
*normal GFR in healthy young adults ~125 mL/min
*GFR < 15 mL/min is defined as kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

measured GFR

A

*measurement of ideal urinary clearance filtration markers
*gold standard is inulin or lothalmate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

estimated GFR

A

*serum biomarkers input to complex equations to approximate the true GFR
*this is routinely done in clinical practice
*note that all of the equations for eGFR have limitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

chronic kidney disease (CKD) due to kidney damage - defined

A

*preserved GFR
*histopathological abnormalities
*abnormalities in serum/urine tests or abnormalities on imaging that may lead to a drop in GFR (e.g. albuminuria, polycystic kidney disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

chronic kidney disease (CKD) due to decreased kidney function - defined

A

*drop in GFR (GFR < 60 mL/min per 1.73 m^2)
*with or without kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stage I chronic kidney disease (CKD)

A

*kidney damage with normal or increased GFR
*GFR > 90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stage II chronic kidney disease (CKD)

A

*kidney damage with mild decreased GFR
*GFR 60-89

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

stage III chronic kidney disease (CKD)

A

*moderately decreased GFR
*GFR 30-59

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

stage IV chronic kidney disease (CKD)

A

*severely decreased GFR
*GFR 15-29

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

stage V chronic kidney disease (CKD)

A

*kidney failure
*GFR < 15 (or dialysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

who should be screened for CKD?

A

*all patients who have increased susceptibility or have potential inciting factors should be screened for CKD
*most screening is done with serum creatinine based estimating equations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CKD progression

A

*chronic kidney disease is often PROGRESSIVE and leads to IRREVERSIBLE loss of renal function
*once GFR falls below about 50% of normal, kidney function tends to continually decline, even if the initial insult has been eliminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

adaptive hyperfiltration

A

*a compensatory process in which the kidneys adapt to the initial damage by increasing the filtration rate in the normal (undamaged) nephrons
*results in long-term damage to the remaining nephrons
*manifested by more proteinuria and progressive CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

effects of proteinuria in chronic kidney disease (CKD)

A

*proteinuria itself contributes to progressive nephron damage
*excessive tubular reabsorption → protein overload; the reabsorbed tubular proteins signal pro-inflammatory mediators and macrophage recruitment
*complement activation → alterations of cytoskeleton, production of ROS, & synthesis of more pro-inflammatory mediators
*inflammation → accumulation of ECM collagen, fibronectin, and other components → interstitial fibrosis

17
Q

SGLT2 inhibitors in CKD

A

*SGLT2 inhibitors block reabsorption of glucose in the proximal tubule
*lowers the renal glucose threshold → substantial glycosuria (increased release of glucose in the urine)
*also have effects independent of glycemic control

18
Q

risk factors for progression of CKD

A

*PROTEINURIA!!!
*hypertension
*type of underlying disease (diabetes, PKD)
*African American ancestry
*male gender
*obesity
*smoking
*high protein diet
*phosphate retention
*metabolic acidosis

19
Q

mainstays of CKD management to slow progression

A
  1. treat the underlying cause, if possible
  2. address modifiable risk factors (correct HTN, initiate statin therapy, encourage smoking cessation, use ACEi or ARB + SGLT2 inhibitor)
  3. prepare for renal replacement therapy (RRT = dialysis) or transplant
20
Q

medical complications of CKD

A

*HTN
*cardiovascular disease
*anemia
*secondary hyperparathyroidism
*metabolic acidosis
*dyslipidemia
*uremia

21
Q

pathogenesis of CKD → HTN

A
  1. sodium retention: Na+/H2O balance disrupted as GFR declines
  2. increased activation of RAAS: prob due to regional ischemia & scarring
  3. enhanced activity of sympathetic nervous system
  4. secondary hyperparathyroidism: rise in intracellular calcium → vasoconstriction
  5. impaired nitric oxide synthesis & endothelium-mediated vasodilation
22
Q

why is HTN an important complication of CKD?

A

*HTN is an independent risk factor for cardiovascular disease (CVD)
*each increment of 20/10 mmHg above 115/75 doubles your risk of a cardiovascular event
*CVD is the leading cause of death in patients with CKD

23
Q

treatment of HTN when diabetes or CKD present

A

*goal is < 140/90
*initiate ACEi or ARB +/- SGLT2 inhibitors

*purpose: slow progression of CKD and reduce rate of cardiovascular complications

24
Q

pathogenesis of CKD → anemia

A

*CKD results in decreased EPO (erythropoietin) from peritubular cells
*as GFR decreases, anemia is more severe

*other causes include:
-absolute of functional iron delivery
-shortened RBC survival (esp dialysis pts)
-blood loss due to uremic platelet dysfunction
-nutritional deficiencies
-inflammation
-ACEi use

25
Q

treatment of anemia in pts with CKD

A

*exclude non-renal causes of anemia (GI blood loss, B12 deficiency, etc)
*correct iron deficiency (oral or IV iron supplementation)
*initiate erythrocyte stimulating agents (ESA) - recombinant human EPO

note - generally do not treat to a Hb > 12-13

26
Q

pathogenesis of CKD → secondary hyperparathyroidism

A
  1. decreased GFR → substantial increases in phosphate retention
  2. FGF-23 increases to improve renal phosphate clearance (increase excretion of phosphate)
  3. high FGF-23 levels suppress 1,25 Vitamin D activity
  4. low vitamin D activity → HYPOCALCEMIA
  5. PTH secretion increases to maintain normocalcemia
  6. clinically apparent rise in phosphorous is a very late finding
27
Q

complications of secondary hyperparathyroidism due to CKD

A
  1. mineral bone disease → renal osteodystrophy → increased risk of fractures, esp hip fractures → increase in mortality
  2. soft tissue and extra-skeletal calcifications (in coronary or peripheral arteries, skin or soft tissue [calciphylaxis])
28
Q

treatment of secondary hyperparathyroidism in CKD pts

A

*control serum phosphate levels
*control metabolic acidosis
*suppress PTH levels (active oral vitamin D supplementation - calcitriol)
*consider subtotal parathyroidectomy

29
Q

pathogenesis of CKD → metabolic acidosis

A

*increasing tendency to retain hydrogen ions in patients with CKD
*leads to progressive metabolic acidosis
*consequences: increased bone resorption, enhances protein catabolism, contributing to malnutrition

30
Q

treatment of metabolic acidosis in CKD pts

A

*oral bicarbonate supplementation

31
Q

pathogenesis of CKD → dyslipidemia

A

*abnormal lipid metabolism is common in patients with renal disease/CKD
*initiate statin therapy to treat

32
Q

pathogenesis of CKD → uremia

A

*uremia: clinical syndrome attributed to accumulation of uremic toxins (we often use UREA as a marker)
*associated with ADVANCED CKD (stage V)
*symptoms: fatigue, pruritus, dysgeusia, anorexia, nausea, vomiting, restless legs
*signs: serositis, pericarditis, asterixis, skin changes, weight loss/malnutrition, platelet dysfunction, peripheral neuropathy

33
Q

treatment for uremia in advanced CKD pts

A

*renal replacement therapies (dialysis or transplant)