Chronic renal failure 12/16

Question 1

CRF from what insults?

Answer 1

glomerular, tubular, inflammatory, or vascular

Question 2

CRF 3 most common causes?

Answer 2

DM, hypertension, glomerular disease

Question 3

Uremia?

Answer 3

increased nitrogenous waste products in blood (azotemia) - result in nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy with asterixis, and deposition of urea crystals in skin

Question 4

Why hypertenstion?

Answer 4

Salt and water retention

Question 5

What metabolic disturbances?

Answer 5

hyperkalemia and metabolic acidosis

Question 6

why anemia?

Answer 6

due to decreased EPO production by renal interstitial cells

Question 7

why hypocalcemia?

Answer 7

due to decreased 1-alpha-hydroxylation of vitamin D by proximal renal tubule cells and hyperphosphatemia

Question 8

what bone damage?

Answer 8

renal osteodystrophy due to secondary hyperparathyroidism, osteomalacia and osteoporosis

Question 9

Treatment?

Answer 9

dialysis and transplant

Question 10

Why CRF increases risk for RCC?

Answer 10

Cysts often develop within shrunken end-stage kidneys during dialysis, increasing risk for RCC.

Question 11

Decr. GFR -> ↓ Production of urine → ↑ extracellular fluid volume → total-body volume overload

Answer 11

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Question 12

Decr. GFR -> ↓ Excretion of waste products (e.g., urea, drugs)

Answer 12

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Question 13

Decr. GFR -> ↓ Excretion of phosphate → hyperphosphatemia

Answer 13

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Question 14

Why during early stages plasma phosphate will be typically normal?

Answer 14

During the early stages of CKD, plasma phosphate levels will typically be normal due to the increased secretion of fibroblast growth factor 23 (FGF23). FGF23 is produced by osteoblasts in response to initial hyperphosphatemia and increased calcitriol. Increased secretion of FGF23 leads to increased phosphate secretion and suppressed conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. In advanced CKD, the effects of FGF 23 subside (most likely due to development of resistance in target tissues).

Question 15

Decr. GFR -> decr. Maintenance of acid-base balance → metabolic acidosis

Answer 15

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Question 16

Decr. GFR -> ↓Maintenance of electrolyte concentrations → electrolyte imbalances (e.g., Na+ retention)

Answer 16

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Question 17

Reduced endocrine activity
↓ Hydroxylation of calcifediol → ↓ production of calcitriol → (in combination with ↓ excretion of phosphate) → ↓ serum Ca2+ → ↑ PTH -> SECONDARY HYPERPARATHYROIDISM

Answer 17

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Question 18

Reduced endocrine activity
↓ Erythropoietin → ↓ stimulation of erythropoiesis

Answer 18

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Question 19

Reduced gluconeogenesis: ↑ risk of hypoglycemia

Answer 19

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Question 20

Clinical features. Manifestations of Na+/H2O retention –> ?

Answer 20

Hypertension and heart failure; Pulmonary and peripheral edema.

Question 21

Clinical features. Uremia. What metabolites accumulate?

Answer 21

metabolites of proteins such as urea, creatinine, β2 microglobulin, and parathyroid hormone

Question 22

Clinical features. Constitutional symptoms?

Answer 22

fatigue, weakness, headaches

Question 23

Clinical features. GI symptoms?

Answer 23

nausea and vomiting; loss of appetite; UREMIC FETOR – ammonia or urine-like breath odor

Question 24

Clinical features. Dermatologic?

Answer 24

PRURITUS; Skin color changes (e.g., hyperpigmentation, pallor due to anemia); UREMIC FROST: uremia leads to high levels of urea secreted in the sweat, the evaporation of which may result in tiny crystallized yellow-white urea deposits on the skin.

Question 25

Clinical features. Serositis (2)?

Answer 25

1.Uremic pericarditis: a complication of chronic kidney disease that causes fibrinous pericarditis. Clinical features: chest pain worsened by inhalation. Physical examination findings – friction rub on auscultation. ECG changes normally seen in nonuremic pericarditis (e.g., diffuse ST-segment elevation) are not usually seen. 2.Pleuritis

Question 26

Clinical features. Neurogical symptoms:3

Answer 26

Asterixis. Signs of encephalopathy – seizures, somnolence, coma. Peripheral neuropathy  paresthesias

Question 27

Clinical features. hematologic 3

Answer 27

Anemia - lab. ↓ Hemoglobin (Hb), MCV is usually normal. Leukocyte dysfunction -> Incr. risk of infections Incr. bleeding tendency caused by abnormal platelet adhesion and aggregation.

Question 28

Diagnostic criteria.

Answer 28

!!!Criteria for chronic kidney disease (CKD) include the persistence of eGFR < 60 mL/min/1.73 m2 (≥ G3a) and/or of any of the following markers of kidney damage for > 3 months: * Albuminuria: e.g., urine albumin-to-creatinine ratio (UACR) > 30 mg/g (≥ A2) * Urine sediment abnormalities: e.g., hematuria * Abnormalities due to tubulointerstitial dysfunction, e.g.: Electrolyte and acid-base imbalances; Retention of nitrogenous wastes; Reduced production of erythropoietin, 1,25-dihydroxyvitamin D, and/or renin * Histological abnormalities on biopsy * Imaging showing structural abnormalities: e.g., polycystic kidney disease * History of renal transplant

Question 29

How is defined 2 progression?

Answer 29

!!!CKD progression is the presence of either of the following: * A decline in renal function, leading to a change in eGFR category * A sustained decline in eGFR of > 5 mL/min/1.73 m2 per year

Question 30

End-stage disease (ESRD)?

Answer 30

* Irreversible kidney dysfunction with eGFR < 15 mL/min/1.73 m2 * AND manifestations of uremia requiring chronic renal replacement therapy with either dialysis (hemofiltration or hemodiafiltration) or renal transplantation

Question 31

What lab if DM?

Answer 31

Fasting plasma glucose, HbA1c

Question 32

What lab if GN?

Answer 32

GN: Complement levels; Serology eg ANA, ANCA, anti-GBM antibody, viral serology (HIV, HBV, HCV).

Question 33

What evaluation if renal stenosis?

Answer 33

Renal artery stenosis: Duplex ultrasonography of the renal arteries

Question 34

What is amyloidosis?

Answer 34

Amyloidosis and Multiple myeloma: Serum protein electrophoresis, urine Bence Jones protein, serum and urine free light chains.

Question 35

!!Renal biopsy is only indicated in patients in whom the underlying cause of CKD is still unclear after noninvasive testing, the results are likely to influence management, and the potential benefits are thought to outweigh the risks.

Answer 35

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Question 36

Nutritional management * Fluid intake: Ensure appropriate fluid intake and avoid dehydration. * Protein and energy consumption Mediterranean diet, ↑ fruit and vegetable intake (Can significantly improve the lipid profile and weight and blood pressure control) Protein restriction (e.g., 0.55–0.60 g/kg/day) in patients with CKD category G3–G5 (This reduces the risk of ESRD (end stage renal disease) and mortality. A higher protein intake goal of 0.6–0.8 g/kg/day may be considered in patients with diabetes). * Electrolytes Sodium restriction (< 2.3 g/day) (This reduces blood pressure and helps achieve better volume control; it may also help reduce proteinuria). Potassium intake adjustment Phosphorus intake adjustment * Micronutrients: Consider multivitamin supplementation for patients with inadequate dietary vitamin (e.g., vitamin D) intake. (Patients with CKD are at risk of vitamin B1 deficiency, vitamin B2 deficiency, vitamin B6 deficiency, vitamin C deficiency, vitamin K deficiency, and/or vitamin D deficiency).

Answer 36

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Question 37

The risk of contrast-induced nephropathy is highest in patients with eGFR < 30 mL/min/1.73 m2.

Answer 37

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Question 38

↓ Renal excretion of phosphate →?

Answer 38

↓ Renal excretion of phosphate → hyperphosphatemia → calcium phosphate precipitation in tissues → ↓ Ca2+

Question 39

↓ Renal hydroxylation of vitamin D →?

Answer 39

↓ Renal hydroxylation of vitamin D → ↓ 1,25-dihydroxyvitamin D → ↓ intestinal Ca2+ absorption → ↓ Ca2+

Question 40

Chronically decreased calcium levels can cause secondary hyperparathyroidism, which can progress to tertiary hyperparathyroidism.

Answer 40

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Question 41

Histologic classification of bone damage. Secondary hyperparathyroidism?

Answer 41

high turnover bone disease or osteitis fibrosa cystica (metabolic bone disease)

Question 42

Histologic classification of bone damage. Osteomalacia?

Answer 42

defective bone mineralization

Question 43

Histologic classification of bone damage. Mixed uremic bone disease

Answer 43

secondary hyperparathyroidism with osteomalacia

Question 44

Histologic classification of bone damage. Adynamic bone disease

Answer 44

Adynamic bone disease: decreased bone formation without osteomalacia

Question 45

!!!Hyperphosphatemia, hypocalcemia, and insufficient production of vitamin D in patients with CKD may lead to secondary hyperparathyroidism and consequent renal osteodystrophy.

Answer 45

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