Chronic Kidney Disease

Question 1

CKD Stage 1

Answer 1

Normal GFR ( > 90) with evidence of kidney damage

Question 2

CKD Stage 2

Answer 2

GFR 60-89 with evidence of kidney damage

Question 3

CKD Stage 3

Answer 3

GFR 30-59 ml/min

Question 4

CKD Stage 4

Answer 4

GFR 15-29 ml/min

Question 5

CKD Stage 5

Answer 5

GFR < 15 ml/min or dialysis

Question 6

Common causes of CKD

Answer 6

Diabetic nephropathy
Hypertensive nephrosclerosis 
Acute Kidney Injury
Glomerulonephritis
Polycystic Kidney Disease
Interstitial nephritis
Obstruction

Question 7

What is the most important factor in the management of CKD?

Answer 7

Controlling hypertension!

Treat to a goal of <130/80

Question 8

Role of ACEI or ARB in CKD management

Answer 8

All patients should be on an ACEI or ARB - slows progression of CKD independent on effect of lowering BP; decreased efferent arteriolar tone reduces elevated glomerular capillary pressure, reducing glomerular injury

Question 9

Electrolyte derangements in CKD

Answer 9

Hypernatremia (failure of kidney to maximally concentrate urine)

Hyponatremia (failure of kidney to maximally dilute urine)

Hyperkalemia (failure of increased tubular secretion mechanism occurs at GFR < 20)

Question 10

Acid/base disturbances in CKD

Answer 10

Non anion gap metabolic acidosis occur with GFR reduction > 25%

Due to the failure of remaining nephrons to compensate for loss of nephrons by increasing NH3 production, allowing excretion of acid in the form of NH4+ to occur at normal levels

Question 11

Uremia - Definition

Answer 11

Clinical syndrome resulting from retention of substances that are normally excreted into the urine but instead accumulate, causing toxicity

Question 12

Clinical presentation of uremic syndrome

Answer 12

Encephalopathy (neurological toxicity)
Anemia
Pericarditis/CHF 
Pulmonary edema
Anorexia, nausea/vomiting
Bone, calcium, phosphorous disorders

Question 13

Role of PTH in CKD

Answer 13

When GFR falls, calcium decreases and phosphorous increases; PTH increases in order to restore Ca2+ and phosphorous levels, at the expense of progressively increased PTH levels; eventually the kidney cannot respond to higher levels of PTH with further decreased phosphorous reabsorption, and so hyperphosphatemia develops along with hypocalcemia and elevated PTH levels

Increased PTH leads to bone disease (demineralization, fractures, bone pain) as well as systemic toxicity

Question 14

Role of Vitamin D in CKD

Answer 14

As GFR falls the damaged kidney can no longer produce active 1,25 dihydroxy Vitamin D; this may be compensatory to decrease serum phosphorous because vitamin D stimulates the absorption of calcium and phosphorous from the gut

Question 15

FGF-23

Answer 15

A hormone produced by osteocytes in bone, causing phosphaturia and decreased renal production of 1,25 dihydroxy Vitamin D, which further decreases phosphorous (and Calcium) absorption from the intestine

Levels rise in CKD in order to prevent phosphorous overload

Question 16

Indications for starting dialysis

Answer 16

Uremic encephalopathy
Uremic pericarditis
Persistent hyperkalemia
Severe volume overload/pulmonary edema

Question 17

What is the most common pathogen responsible for dialysis catheter infections?

Answer 17

Gram positive bacteria (Staph, strep)

Question 18

What is the prognosis for dialysis?

Answer 18

Mortality is 20% in the first year and 50% by 5 years

Question 19

Survival of a liver donor graft

Answer 19

12-14 years

Question 20

Survival of a deceased donor graft

Answer 20

8-10 years

Question 21

Standard criteria donor (SCD)

Answer 21

Brain death; intact cardiopulmonary system until organ retrieval

Question 22

Donation after cardiopulmonary death (DCD)

Answer 22

Organ retrieval occurs after cardiopulmonary death; increases warm ischemia type

Question 23

Extended criteria donor (ECD)

Answer 23

Donor age > 60 OR age 50-59 with two of the following:

Death by CVA
Elevated creatinine
Medical hx of HTN

Question 24

Organ transplant HLA matching

Answer 24

6 locations - each of HLA-A, HLA-B, and HLA-DR

Impacts long-term graft survival as well as strength of immunosuppression

Question 25

Standard approach to immunosuppression

Answer 25

Triple therapy:

1. Calcineurin inhibitor (Cyclosporine, Tacrolimus)
2. MMF OR Sirolimus
3. Prednisone

Question 26

Calcineurin

Answer 26

Prevents NFAT-mediated T cell clonal expansion

Adverse effects: Nephrotoxicity, gout, HTN, hyperlipidemia

Question 27

T-cell mediated rejecjtion

Answer 27

Causes tubular and/or large vessel inflammation with lymphocytes present on renal biopsy

Treated with high dose steroids and/or T-cell depletion using anti-thymocyte globulin

Question 28

B cell-mediated rejection

Answer 28

Caused by antibodies directed against donor HLA antigens; renal biopsy shows peritubular capillary and glomerular inflammation, and complement-mediated tissue damage

Treated by antibody removal via plasmapheresis and antibody suppression with IVIG or Rituximab