CKD Flashcards Preview

Renal > CKD > Flashcards

Flashcards in CKD Deck (67):
1

How is CKD defined?

Loss of functioning nephrons leading to a decreased GFR. GFR typically estimated by creatinine clearance and changes in serum creatinine.

2

How is CKD diagnosed?

1. Hx: voiding complaints, abnormal urine appearance
2. PE: HTN, edema, flank masses
3. Lab Data: previous urinalysis, serum creatinine, BUN
4. Imaging: ultrasound- shrunken kidneys, size disparity, more dense echotexture

3

What is the #1 cause of secondary HTN?

CKD

4

What are the diagnostic considerations for CKD?

1. prerenal, intrinsic renal, or post renal
2. acute vs chronic
3. glomerular vs tubular
4. inflammatory vs non-inflammatory
5. with or w/o systemic disease

5

What are the factors that favor CKD vs AKI?

1. Most commonly asymptomatic
2. Availability of old records
3. Peripheral neuropathy
4. Bone changes (chronic hyperparathyroidism)
5. Presence of small, shrunken kidneys
6. Waxy casts: ONLY present in CKD

6

What is the best way to distinguish glomerular vs tubular process?

Heavy proteinuria with RBC and granular casts present with glomerular process. Less/absent proteinuria with tubular process.

7

What are the 3 factors favoring tubular etiology?

1. absence of heavy proteinuria
2. inability to concentrate or dilute the urine: specific gravity ~1.010=~300 mOsm/kg
3. Hyperkalemia and metabolic acidosis out of proportion to the degree of renal insufficiency

8

What are the 3 factors favoring glomerular etiology?

Note: urinalysis most important consideration here.
1. 2+ proteinuria
2. RBC casts
3. specific gravity 1.015+

9

What does tubulointerstitial nephritis imply?

Active inflammation surrounding the tubules and interstitium. Examples include pyelonephritis and allergic interstitial nephritis.

10

What does glomerulonephritis imply?

Active inflammation within the glomerulus.

11

What are the urinary features of glomerulonephritis?

Hematuria. Presence of RBC and granular casts. May also have WBCs in the urine w/o bacteria. Proteinuria present but usually 2+ or less.

12

What is the most common cause of eosinophils in the urine?

Allergic interstitial nephritis

13

What is allergic interstitial nephritis characterized by?

Sterile pyuria (pus in urine).

14

T or F. CKD is progressive unless the initial injuring stimulus is removed.

F: progressive even if the initial stimulus is removed.

15

What is uremia?

Term used to describe the constellation of signs and symptoms associated with advanced renal failure.

16

What are the typical signs and symptoms of uremia?

Early morning nausea, malaise, anorexia, hiccups.

17

Uremia is always fatal unless you do what?

Reversible factors are identified which can improve GFR or renal replacement therapy is instituted.

18

Which organ systems are affected by chronic renal insufficiency?

Trick question. ALL of them. Rookies.

19

What are the 5 most common etiologies of advanced kidney disease in the US?

1. diabetes mellitus
2. hypertensive nephrosclerosis
3. acute and chronic glomerular diseases
4. polycystic kidney disease
5. tubulointerstitial diseases

20

What are the 3 types of disease dependent mechanisms of nephron injury?

1. vascular
2. glomerular
3. tubular

21

What are the 3 disease independent mechanisms of nephron injury?

1. systemic HTN
2. glomerular HTN (afferent arteriole vasodilation)
3. glomerular hypertrophy (increased single nephron GFR)

22

What are the 5 effects of disease independent processes?

1. epithelial cell injury promoting proteinuria
2. hyaline accumulation in mesangial expansion leading to reduced capillary SA for GFR
3. vascular capillary microaneurysms
4. endothelial cell injury
5. tubulointerstitial fibrosis

23

Greater than a 50% loss of nephron mass results in increased risk for what?

HTN and proteinuria. Proteinuria can be accompanied by focal segmental glomerulosclerosis on kidney biopsy. This is especially true when condition present for more than 10 years.

24

What dietary restriction slows nephron loss?

Restriction of protein reduces workload of glomeruli. Note, normal intake of protein raises GFR. Watch out for malnutrition though. Patients (like Andrew) usually don't adhere well.

25

What accelerates progressive nephron loss?

HTN. Patients with CKD and HTN go on dialysis sooner and thus die faster.

26

What has been shown to preserve renal function in both proteinuric and non-proteinuric renal diseases?

Maintenance of normal BP with anti-hypertensives and dietary Na restriction.

27

HTN seen in CKD patients is largely driven by what?

Volume. Thus, Na control is crucial.

28

What class of anti-hypertensives are advantageous in treating CKD?

ACE inhibitors and angiotensin II receptor blockers. They reduce systemic pressure and reduce glomerular capillary pressure.

29

What are the 4 adverse effects of activation the RAAS system?

1. vasoconstriction which contributes to systemic HTN
2. Na retention
3. glomerular HTN (efferent arteriole vasoconstriction)
4. increased release of TGF-beta which promotes fibrosis

30

What is the best index of overall kidney function?

GFR

31

What is the best clinical estimate of GFR?

Creatinine clearance. Renal function monitored by serial measurements of serum creatinine concentration.

32

Creatinine production and excretion (aka serum concentration) is entirely dependent upon what?

Muscle mass

33

So, if serum creatinine is entirely dependent upon muscle mass, why does an elevated serum creatinine indicate kidney disease?

Serum creatinine will go up in order to excrete the same amount of creatinine that you are making. So, if you are the same body weight and losing nephron mass, you still will produce and excrete the same amount of creatinine every day even though you're serum creatinine concentration went up. ENTIRELY dependent upon muscle mass. (If there's an easier way to explain this or I messed it up, please correct.)

34

T or F. Increased creatinine excretion occurs with decreased GFR.

T: serum creatinine will therefore over-estimate true GFR=problematic.

35

What can mask the presence of nephron loss?

Increased filtration in the remaining, healthy nephrons.

36

What is a complication of diabetics occuring in 30-40% of type I patients?

Diabetic nephropathy

37

In regards to the kidney, what is the earliest change seen in diabetic nephropathy?

Hyperfiltration resulting in glomerular capillary HTN and glomerular hypertrophy.

38

What are the clinical effects of diabetic nephropathy?

The first abnormality seen is microalbuminuria. Over time, this leads to overt proteinuria, reduced GFR, and HTN.

39

What is seen histologically in diabetic nephropathy?

Increased mesangial matrix, glomerular collapse, and glomerulosclerosis.

40

What is advantageous about using ACE inhibitors in CKD?

ACEi's lower glomerular capillary pressure as well as lowering systemic BP. Diuretics and direct vasodilators do not do this.

41

Administration of captopril early in the course of CKD lowers what?

Proteinuria. Can avoid overt proteinuria in the later stages of disease. Captopril also slows doubling of serum creatinine.

42

Describe the progression of renal disease.

1. Microalbuminuria
2. Proteinuria
3. Doubling of serum creatinine
4. ESRD
ALL of these eventually contribute to fatal cardiovascular events.

43

What is the intact nephron hypothesis?

Damaged nephrons generally function appropriately, therefore, loss of renal homeostasis is secondary to a decreased number of nephrons. Note, chronic renal insufficiency=decreased # of normally functioning nephrons.

44

What is the trade off hypothesis?

In order to maintain homeostasis despite reduced GFR, secondary events occur which assist to maintain homeostasis at the expense of adverse side effects.

45

What are some examples of the trade off hypothesis?

1. Ca/PO4 balance maintained leads to hyperparathyroidism
2. Na balance: HTN
3. K balance: hyperaldosteronism and HTN
4. inc filtration of residual nephrons leads to disease independent nephron injury

46

What is the nomogram equation used to estimate GFR?

GFR=(140-age)/Pcr. Multiply by 0.85 if patient is female.

47

When are nomograms useful? Not useful?

Only useful in steady state conditions like chronic renal insufficiency. It cannot be used for acute renal failure.

48

Describe the 5 stages of CKD.

1. GFR=90+
2. 60-89
3. 30-59
4. 15-29
5 <15 or dialysis (complete kidney failure)

49

T or F. There is a true normal GFR value used for all patients.

F: no true normal value b/c it's dependent upon muscle mass (mainly) and age.

50

Patients with CKD are at highest risk for what?

Cardiovascular disease. CKD patients get bumped straight to the "highest risk" category for CVD.

51

Describe the effects of renal insufficiency on the nervous system.

1. early to moderate renal insuff: subtle changes in intellectual function particulary in the ability to concentrate
2. more severe: overt encephalopathy manifested by asterixis (flapping of hand when wrist is extended)
3. advanced: peripheral neuropathy

52

Why does HTN develop in CKD patients?

Decreased GFR leads to decreased filtered Na and thus Na retention. HTN develops to offset this Na retention and maintain Na balance within the body (b/c HTN increases pressure natriuresis). However, HTN accelerates nephron loss. Example of trade off hypothesis.

53

Describe the effects of chronic renal insufficiency on the heart.

1. early chronic renal failure: HTN with leads to LVH
2. Late renal failure: volume overload, marked anemia, symptoms of CHF
3. late or advanced: pericarditis (chest pain and pericardial friction rub)

54

What endocrine abnormality is associated with chronic renal failure?

Fasting hypoglycemia is more common in patients with advanced renal failure.

55

What are the 3 factors leading to fasting hypoglycemia in patients with advanced renal failure?

1. Decreased insulin degradation
2. Decreased gluconeogenesis by the kidney
3. Impaired protein/calorie intake resulting in decreased glycogenolysis by the liver

56

Why is anemia seen in patients with CKD?

Decreased EPO secretion by the kidney.

57

Describe the anemia in CKD patients.

Normocytic normochromic anemia with low reticulocyte count. Burr cells present. Responsive to exogenous EPO (but this raises BP). Note: anemia resolves some symptoms of chronic renal failure.

58

Describe the effects of renal insufficiency on the GI system.

With progressive loss of GFR, pt's have decreased appetite which leads to reduction in protein intake. Nausea can develop with gastroparesis. And on the severe end, N/V can develop. All contribute to protein calorie malnutrition.

59

What is the BUN:Creatinine ratio in CKD?

Normal (10:1). However, the concentrations of both increase just proportionately. Remember: the ratio is >20:1 in prerenal AKI.

60

Creatinine concentration increases solely as a function of what?

GFR

61

BUN concentration increases as a function of what 2 things?

GFR and urine flow rate

62

Why is hypocalcemia (resulting in increased PTH) seen in CKD patients?

Decreased GFR leads to decreased amounts of 1-alpha-hydroxylase. Thus, low levels of vitamin D and you can't absorb calcium in the gut. Hyperphosphatemia also contributes by inhibiting the enzyme.

63

What are the 4 adverse effects of hyperphosphatemia (seen in CKD patients)?

1. PO4 complexes w/ Ca thus reducing its serum concentration
2. Inhibits 1-alpha-hydroxylase
3. Directly stimulates parathyroid tissue to enhance PTH secretion
4. Metastatic calcification (vascular problems)

64

What effects are there on K balance in CKD patients?

With progressive renal insufficiency, there is a decreased ability to excrete a K load leading to hyperkalemia.

65

What is special about K balance and renal insufficiency?

K balance is the last to go. Homeostasis is remained until GFR drops below 15. Important bc hyperkalemia is life-threatening.

66

What acid-base disorder is seen in CKD and why?

Metabolic acidosis with a normal plasma anion gap. With loss of nephron mass, there is a decreased ability to excrete acid into the urine.

67

Describe the effects of CKD on phosphorus balance.

Decreased GFR leads to the decreased ability to excrete phosphate resulting in hyperphosphatemia. It is one of the first solutes in which homeostasis is lost.