Chronic Kidney Disease + Some random stuff

Question 1

CKD Definition

Answer 1

• Irreversible, progressive damage to parenchyma
• glomerulosclerosis and tubuloinerstitial fibrosis
• decreased GFR
  And one of these:
• albuminuria
• urine sediment abnormalities
• electrolyte abnormalities,
• histology abnormalities

Question 2

ESRD

Answer 2

Complete loss of kidney function, requires dialysis or txplant

Question 3

CKD Stage 1

Answer 3

• GFR >90, evidence of damage w/ no sx +/- proteinuria

Question 4

CKD Stage 2

Answer 4

• 60-80 GFR

- If caught here, slow progression w/ treatment

Question 5

CKD Stage 3

Answer 5

30-59 GFR

Often when pt comes to medical attention; most people in this stage (because they start dying after that)

Question 6

CKD Stage 4

Answer 6

Nephro referral, discuss dialysis vs txplant if

Question 7

CKD Stage 5

Answer 7

Kidney failure, imminently needs dialysis or txplant

Question 8

Etiology of CKD

Answer 8

Diabetes > HTN > glomerulonephritis > cystic kidney + vascular dz, tubulointerstitial dz, etc

Question 9

Pathogenesis of CKD

Answer 9

Primary: diseases which directly damage the kidney
Secondary: non disease events which inflict further damage in all primary kidney diseases; a reduction in renal mass

Question 10

Dx of CKD

Answer 10

• acute or chronic?
  (look at trend of creatinine)
• BMP w/ eGFR calculation, urinalysis, microscopic exam, URINE SPOT SAMPLE for proteinuria quantification
• Renal US

Question 11

Prerenal failure

Answer 11

Almost always renal artery stenosis

Question 12

Radiology of RF

Answer 12

• fibrosis (echogenic “speckles” kidneys by ultrasound – fibrosis in the renal parenchyma!)
• volume loss in parenchyma (permanenent)
• Enlarged kidneys
• Obstruction
• Cystic dz

Question 13

Anemia in CKD

Answer 13

• decreased erethropoeitin
• inflammatory cytokines destroy immature RBCs
• hepcidin release –> block iron.

Treat w/ IV iron and give epo analog

Question 14

Mineral disease in CKD:

Answer 14

Renal mass loss –> decreased GFR–> phosphate retention and decreased vit D –> hypocalcemia and hyperparathyroidism–> renal osteodystrophy

Question 15

7 Sequelae of CKD

Answer 15

1) Anemia
2) BMD (bone mineral disease)
3) HTN (worsens as GFR decreases)
4) CV disease (leading cause of mortality at all stages of CKD)
5) Uremia –> fatigue, anorexia, nausea, PRURITIS
6) Acidosis, and esp hyperK
7) Volume overload

Question 16

Treatment of CKD:

Answer 16

• Treat primary dz
• ACEI/ARB +/- diuretic for HTN**
• Tx proteinuria** ACE/ARB
• treat DM
• treat sequelae
• Low K+ diet if hyperK, low P is hypoP, low Na if V overload
• Avoid NSAIDS and contrast (nephrotoxic)

Question 17

Chronic vs. Acute renal failure

Answer 17

Chronic: time to adapt, finite GFR
Acute: no time to adapt (electrolyte imbalance) often NO GFR.
in CRF the number of functioning nephrons is decreased. whereas in AKI nephrons are globally impaired but not reduced in number.

Question 18

Pathogenesis of CKD

Answer 18

Common response to kidney damage rather than the result of primary renal disease. (Renal function continues to deteriorate even after primary disease has been treated.)

Question 19

5 most common primary renal injuries in CKD

Answer 19

Glomerulonephritis
diabetes
HTN
polycystic
interstitial nephrites.

Question 20

5 secondary phenomena in CKD

Answer 20

Glomerular hypertrophy (increase in SNGFR)
Intraglomerular HTN
Phosphate retention and hyperparathyroid
Systemic HTN
Hyperlipidemia

Question 21

5 kidney problems that NSAIDs cause

Answer 21

1) Papillary necrosis (RBC in urine, pain, similar sx to kidney stone)
2) ATN
3) HTN (via inhibition of prostaglandins)
4) MCD + AIN
5) Pre-renal AZ (hemodynamic effect)

Question 22

Maintenance of acid/base balance during CKD?

Answer 22

Increased ammonia-genesis in the remaining working nephrons.

Question 23

Three factors which control K+ secretion

Answer 23

1. Renal Flow Rate
2. Aldosterone secretion (^ aldo causes excretion of K. Remember that hyperkalemia stimulates aldo)
3. acid/base status (acidosis favors K+ retention)

Question 24

Type I RTA

Answer 24

Distal RTA is caused by defects in distal hydrogen ion excretion

Question 25

Type II RTA

Answer 25

Proximal RTA is caused by defects that reduce the capacity to reclaim filtered bicarbonate in the proximal tubule

Question 26

Type IV RTA

Answer 26

Hyperkalemic RTAs include hypoaldosteronism (type 4) and a disorder called voltage-dependent RTA

Question 27

Renin Release stimulated by?

Answer 27

1) Macula densa senses low NaCl in tubule and signals to JGA to release renin (to increase GFR)
2) SNS stimulates renin release

In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the cortical thick ascending limb, at the transition to the distal convoluted tubule.
The cells of the macula densa are sensitive to the concentration of sodium chloride in the late thick ascending limb. A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects: (1) it decreases resistance to blood flow in the afferent arterioles via vasodilation, which increases glomerular capillary hydrostatic pressure and helps return glomerulus filtration rate (GFR) toward normal, and (2) it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin

Question 28

Treatment for hyperparathyroidism 2/2 renal disease

Answer 28

phosphate binders, then vitamin D

Question 29

Vitamin D synth

Answer 29

Step 1) Skin
Step 2) Liver
Step 3) Kidney (need this last step for functioning Vit D)

Question 30

Vitamin D actions

Answer 30

1) Acts on intestine to stimulate calcium and phosphate absorption
2) stimulates phosphate reabsorption in the kidney and increases bone turnover

Question 31

Three contributors to MBD

Answer 31

1) hyperPTH
2) vitamin D deficiency
3) chronic metabolic acidosis