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CHAPTER 28ACUTE RENAL FAILURE AND CHRONIC KIDNEY DISEASE
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ACUTE RENAL FAILURE
Etiology and Pathophysiology• ARF: an abrupt reduction in renal function
producing an accumulation of waste materials in the blood
• May be due to aging, associated with comorbidities, or due to insults to the kidney
• Renal function monitored by serum creatinine and creatinine clearance
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ACUTE RENAL FAILURE (CONT.)
• Retention of metabolic wastes (azotemia/uremia) monitored by BUN, produces widespread systemic effects (uremic syndrome)
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ACUTE RENAL FAILURE (CONT.)
Prerenal Acute Renal Failure• Due to conditions that impair renal blood flow,
such as hypovolemia, hypotension, cardiac failure, and renal artery obstruction
• Characterized by low GFR, oliguria, high urine specific gravity and osmolality, and low urine sodium
• S/S of fluid overload are present• Prolonged prerenal ARF leads to intrarenal RF
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ACUTE RENAL FAILURE (CONT.)
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ACUTE RENAL FAILURE (CONT.)
Postrenal Acute Renal Failure• Due to obstruction within the urinary collecting
system distal to the kidney; elevated pressure in Bowman capsule; impedes glomerular filtration
• Clinical findings based on duration of the obstruction
• Prolonged postrenal ARF leads to intrarenal RF
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ACUTE RENAL FAILURE (CONT.)
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ACUTE RENAL FAILURE (CONT.)
Intrarenal Acute Renal Failure• Due to a primary dysfunction of the nephrons• Most often due to problem within the renal
tubules resulting in acute tubular necrosis; may also occur with glomerular, vascular, or interstitial etiologies
• ATN may occur with nephrotoxic or ischemic insults; clinical manifestations depend on stage of ATN
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ACUTE RENAL FAILURE (CONT.)
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ACUTE RENAL FAILURE (CONT.)
Clinical Presentation of Acute TubularNecrosis: Oliguric Stage• Characterized by oliguria and progressive uremia;
decreased GFR; hypervolemia• May last 1 to 2 weeks• Dialysis may be required
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ACUTE RENAL FAILURE (CONT.)
Clinical Presentation of Acute TubularNecrosis: Diuretic Stage• Urine volume increases, but tubular function
remains impaired and azotemia continues• May last 2 to 10 days
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ACUTE RENAL FAILURE (CONT.)
Clinical Presentation of Acute TubularNecrosis: Recovery Stage• Characterized by gradual normalization of serum
creatinine and BUN• May last up to 12 months• Often a degree of renal insufficiency
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ACUTE RENAL FAILURE (CONT.)
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CHRONIC KIDNEY DISEASE
• Outcome of the progressive and irrevocable loss of nephrons
• Progressive process: CKD – CRF – ESRD• A global health problem often linked with other
comorbidities, primarily hypertension and DM
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CHRONIC KIDNEY DISEASE (CONT.)
• Defined as decreased kidney function or kidney damage of 3 months’ duration based on blood tests, urinalysis, and imaging studies; GFR <60 ml/minute/1.73 m2 for 3 months with or without indication of damage to the kidney
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CHRONIC KIDNEY DISEASE (CONT.)
Risk Factors• Most commonly associated with DM,
hypertension, recurrent pyelonephritis, glomerulonephritis, and polycystic kidney disease
• Cause alterations in glomerular perfusion and filtration, sodium reabsorption, renal sympathetic activity, and activity of the RAAS
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CHRONIC KIDNEY DISEASE (CONT.)
Pathophysiology of Progression ofChronic Kidney Disease• Glomerulosclerosis and interstitial inflammation
and fibrosis• Monitored by two staging systems
• Percentage of nephron loss• Reduction in GFR
• GFR reduction occurs with nephron loss
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CHRONIC KIDNEY DISEASE (CONT.)
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CHRONIC KIDNEY DISEASE (CONT.)
Stages of Chronic Kidney Disease• Defined by level of function per GFR• Decreased renal reserve is not associated with
S/S of renal failure; interventions required to slow disease progression
• Renal insufficiency characterized by increase in metabolic wastes at levels proportional to nephron loss; polyuria
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CHRONIC KIDNEY DISEASE (CONT.)
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CHRONIC KIDNEY DISEASE (CONT.)
Complications of Chronic Kidney Disease• Hypertension and cardiovascular disease: due to
hypervolemia, escalated atherosclerotic process, heightened RAAS activity, and increased SNS activity
• Uremic syndrome: due to retention of metabolic wastes
• Metabolic acidosis: due to retention of acidic waste products; kidneys lose ability to secrete H+ ions and bicarbonate
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CHRONIC KIDNEY DISEASE (CONT.)
Complications of Chronic Kidney Disease• Electrolyte Imbalances: retention of potassium,
phosphorus, and magnesium in the blood• Renal osteodystrophy: elevated PTH causes
altered bone and mineral metabolism; kidneys unable to reabsorb calcium
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CHRONIC KIDNEY DISEASE (CONT.)
• Malnutrition: decreased intake due to uremic syndrome, depression, dietary limitations, and changes in taste
• Anemia: due to lack of erythropoietin
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CLINICAL MANAGEMENT
Prevention• Early identification of risk; addressing lifestyle
modifications and comorbidities• Maintenance of fluid volume status and cardiac
output• Avoid and monitor nephrotoxic chemicals• Avoid and aggressively treat infections
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CLINICAL MANAGEMENT (CONT.)
Therapeutic Interventions• Slowing the progression of CKD is focus of
intervention until stage 4 or 5• Primary foci are appropriate management of ATN,
blood glucose control in diabetes, ACE inhibitors or AII blockers to reduce proteinuria, and aggressive management of hypertension and cardiovascular disease
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CLINICAL MANAGEMENT (CONT.)
Therapeutic Interventions• Nutritional needs for patients with CKD include
increased calories, calcium, and vitamin supplementation
• Fluids, phosphorus, potassium, sodium, and protein intake are usually restricted
• Drug therapy for CKD is used to control hypertension, anemia, and some of the electrolyte imbalances