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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