Chronic renal failure 12/16 Flashcards
CRF from what insults?
glomerular, tubular, inflammatory, or vascular
CRF 3 most common causes?
DM, hypertension, glomerular disease
Uremia?
increased nitrogenous waste products in blood (azotemia) - result in nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy with asterixis, and deposition of urea crystals in skin
Why hypertenstion?
Salt and water retention
What metabolic disturbances?
hyperkalemia and metabolic acidosis
why anemia?
due to decreased EPO production by renal interstitial cells
why hypocalcemia?
due to decreased 1-alpha-hydroxylation of vitamin D by proximal renal tubule cells and hyperphosphatemia
what bone damage?
renal osteodystrophy due to secondary hyperparathyroidism, osteomalacia and osteoporosis
Treatment?
dialysis and transplant
Why CRF increases risk for RCC?
Cysts often develop within shrunken end-stage kidneys during dialysis, increasing risk for RCC.
Decr. GFR -> ↓ Production of urine → ↑ extracellular fluid volume → total-body volume overload
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Decr. GFR -> ↓ Excretion of waste products (e.g., urea, drugs)
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Decr. GFR -> ↓ Excretion of phosphate → hyperphosphatemia
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Why during early stages plasma phosphate will be typically normal?
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).
Decr. GFR -> decr. Maintenance of acid-base balance → metabolic acidosis
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Decr. GFR -> ↓Maintenance of electrolyte concentrations → electrolyte imbalances (e.g., Na+ retention)
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Reduced endocrine activity
↓ Hydroxylation of calcifediol → ↓ production of calcitriol → (in combination with ↓ excretion of phosphate) → ↓ serum Ca2+ → ↑ PTH -> SECONDARY HYPERPARATHYROIDISM
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Reduced endocrine activity
↓ Erythropoietin → ↓ stimulation of erythropoiesis
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Reduced gluconeogenesis: ↑ risk of hypoglycemia
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Clinical features. Manifestations of Na+/H2O retention –> ?
Hypertension and heart failure; Pulmonary and peripheral edema.
Clinical features. Uremia. What metabolites accumulate?
metabolites of proteins such as urea, creatinine, β2 microglobulin, and parathyroid hormone
Clinical features. Constitutional symptoms?
fatigue, weakness, headaches
Clinical features. GI symptoms?
nausea and vomiting; loss of appetite; UREMIC FETOR – ammonia or urine-like breath odor
Clinical features. Dermatologic?
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.
Clinical features. Serositis (2)?
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
Clinical features. Neurogical symptoms:3
Asterixis.
Signs of encephalopathy – seizures, somnolence, coma.
Peripheral neuropathy paresthesias
Clinical features. hematologic 3
Anemia - lab. ↓ Hemoglobin (Hb), MCV is usually normal.
Leukocyte dysfunction -> Incr. risk of infections
Incr. bleeding tendency caused by abnormal platelet adhesion and aggregation.
Diagnostic criteria.
!!!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
How is defined 2 progression?
!!!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
End-stage disease (ESRD)?
- 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
What lab if DM?
Fasting plasma glucose, HbA1c
What lab if GN?
GN: Complement levels; Serology eg ANA, ANCA, anti-GBM antibody, viral serology (HIV, HBV, HCV).
What evaluation if renal stenosis?
Renal artery stenosis: Duplex ultrasonography of the renal arteries
What is amyloidosis?
Amyloidosis and Multiple myeloma: Serum protein electrophoresis, urine Bence Jones protein, serum and urine free light chains.
!!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.
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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).
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The risk of contrast-induced nephropathy is highest in patients with eGFR < 30 mL/min/1.73 m2.
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↓ Renal excretion of phosphate →?
↓ Renal excretion of phosphate → hyperphosphatemia → calcium phosphate precipitation in tissues → ↓ Ca2+
↓ Renal hydroxylation of vitamin D →?
↓ Renal hydroxylation of vitamin D → ↓ 1,25-dihydroxyvitamin D → ↓ intestinal Ca2+ absorption → ↓ Ca2+
Chronically decreased calcium levels can cause secondary hyperparathyroidism, which can progress to tertiary hyperparathyroidism.
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Histologic classification of bone damage. Secondary hyperparathyroidism?
high turnover bone disease or osteitis fibrosa cystica (metabolic bone disease)
Histologic classification of bone damage. Osteomalacia?
defective bone mineralization
Histologic classification of bone damage. Mixed uremic bone disease
secondary hyperparathyroidism with osteomalacia
Histologic classification of bone damage. Adynamic bone disease
Adynamic bone disease: decreased bone formation without osteomalacia
!!!Hyperphosphatemia, hypocalcemia, and insufficient production of vitamin D in patients with CKD may lead to secondary hyperparathyroidism and consequent renal osteodystrophy.
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