Acute Kidney Injury and Chronic Kidney Disease Study Guide, Exams of Nursing

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NURS 231 Acute Kidney Injury and Chronic Kidney Disease Study

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Acute Kidney Injury and Chronic Kidney Disease Study Guide

Before you get started : As you remember from normal physiology, the kidneys remove metabolic wastes from the blood and regulate F&E and acid-base balance. When there is acute kidney injury or chronic kidney disease, the kidneys fail. Let’s look at causes, pathogenesis, and geez … all kinds of manifestations!

Acute kidney injury is rapid in onset and often is reversible or irreversible?

Chronic kidney disease is the end result of irreversible damage to the kidneys. It develops slowly, over the course of years and often requires dialysis or transplantation. Let’s look at acute first.

Acute Kidney Injury. Rapid decline in kidney function > buildup of nitrogenous wasted products, impaired F&E balance. Most common indicator: azotemia, which means what? an accumulation of nitrogenous wastes (urea nitrogen, uric acid, and creatinine) in the blood and a decrease in the glomerular filtration rate (GFR). As a result, excretion of nitrogenous wastes is reduced, and fluid and electrolyte balance cannot be maintained.

Caused by several conditions; categorized by where the injury/condition occurs. Critical thinking time … Look at chart 34-1. See any patterns with cause and category? Pre … conditions affecting blood flow BEFORE the kidneys, intra … problem is INSIDE the kidneys, andpost … obstruction BELOW the kidneys.

1. Describe the causes/pathogenesis and discriminating manifestations of prerenal, intrarenal, and postrenal acute kidney injury (p. 892-893).

Prerenal AKI. Most common cause of acute kidney injury (AKI). Marked decrease in what?renal blood flow

List key causes from chart 34-1: Hypovolemia

Hemorrhag e Dehydratio n Excessive loss of gastrointestinal tract fluids Excessive loss of fluid because of burn injury Decreased vascular filling Anaphylactic shockSeptic shock Heart failure and cardiogenic shock Decreased renal perfusion because of sepsis, vasoactive mediators, drugs, and diagnostic agents

Normally kidneys receive 20-25% of cardiac output. Can tolerate decreased blood but if prolonged, ischemic changes can occur. NEED TO RESTORE BLOOD FLOW TO PREVENT IRREVERSIBLE DAMAGE. *Discriminating manifestation: early sign is sharp decrease in urine output.

Intrarenal AKI. Due to conditions that cause damage to kidney structures. Major cause: ischemia due to prerenal AKI, toxic insult to tubules, and intratubular obstruction.

What are intrarenal causes from chart 34-1?Acute tubular necrosis/acute renal injury Prolonged renal ischemia Exposure to nephrotoxic drugs, heavy metals, and organic solvents Intratubular obstruction resulting from hemoglobinuria, myoglobinuria, myeloma light chains, or uric acid casts Acute renal disease (acute glomerulonephritis, pyelonephritis)

Specific type: acute tubular injury or necrosis Characterized by destruction of tubular epithelial cells > renal function suppressed. Caused by extensive surgery, severe hypovolemia, sepsis, trauma, burns. Does NOT improve with restored renal blood flow like prerenal AKI. *Discriminating manifestations specific to this type:

• Hemoglobinuria, myoglobinuria discolor urine to tea to red, brown, or black
• Dirty brown granular casts and epithelial cells in urine related to acute tubular injury
• RBC casts and protein in urine related to glomerulonephritis
• WBC casts and pyuria related to acute tubulointerstitial nephritis

Postrenal AKI. Due to obstruction of urine outflow from kidneys, such as Bilateral ureteral obstruction Bladder outlet obstruction The obstruction can occur in the ureter (i.e., calculi and strictures), bladder (i.e., tumors or neurogenic bladder), or urethra (i.e., prostatic hyperplasia)

2. Describe the clinical course and manifestations of acute kidney injury (p. 893-894).

Four phases

1. Onset: from onset of precipitating event/cause to tubular injury occurs; lasts how long? Hours or days
2. Oliguric (anuric): last 8 to 14 days or longer depending on the nature of AKI; characterized by marked decrease in the GFR and sudden retention of what? endogenous metabolites, such as urea, potassium, sulfate, and creatinine, which are normally cleared by the kidneys. Is urine output highest or lowest at this point? Fluid retention > edema, water intoxication, pulmonary congestion. Maybe hypertension and uremia. What are neuro manifestations of uremia? neuromuscular irritability to seizures, somnolence, coma, and death.

What electrolyte imbalance may occur? Manifested how? Hyperkalemia is usually asymptomatic until the serum potassium level rises above 6 to 6. mEq/L, at which point characteristic electrocardiographic changes and symptoms of muscle weakness are seen.

3. Diuretic: kidneys try to heal and urine output increases or decreases? What happens to BUN, creatinine, potassium, phosphate levels? GFR increases or decreases?

may remain elevated or continue to rise, even though urine output is increased.

4. Recovery: renal fx improves, fluid and electrolyte becomes balanced. Tubular fx restored. Sometimes some kidney damage remains.

Let’s shift gears to Chronic Kidney Disease (CKD). Regretfully the prevalence and incidence of this debilitating disease are rising. CKD is classified into 5 stages, according to glomerular filtration rate (GFR), which correlates with number of functioning nephrons.

3. Discuss the causes and pathophysiology of chronic kidney disease (p. 895-896). Causes: diabetes, hypertension, obesity, glomerulonephritis, SLE, and polycystic disease. Circle 2 main causes.

Pathophysiology: a pathologic process that results in the loss of nephrons and a decline in renal function as determined by the GFR that has persisted for more than 3 months. Kidneys do compensate ... remaining nephrons hypertrophy or atrophy? And filters more particles fromblood. As those become destroyed, clinical manifestations of kidney failure appear. accumulation of nitrogenous wastes; alterations in water, electrolyte, and acid–base balance; mineral and skeletal disorders; anemia and coagulation disorders; hypertension and alterations in cardiovascular function; gastrointestinal disorders; neurologic complications; disorders of skin integrity; and disorders of immunologic function. The point at which these disorders make their appearance and the severity of the manifestations are determined largely by the extent of renal function that is present and the coexisting disease conditions. Many of them make their appearance before the GFR has reached the kidney failure stage.

4. Correlate the clinical manifestations of chronic kidney disease with pathophysiological mechanisms (p. 896-901, figure 34-4).

Clinical Manifestations Pathophysiological Mechanisms

Nitrogenous wastes accumulation: azotemia

Early or late sign? Increased BUN (blood urea nitrogen)) and serum creatinine. Creatinine: by product of what? muscle metabolism With CKD, creatinine is not excreted so increases in serum. Uremia: urine in blood; uremic state includes S&S of what: altered fluid, electrolyte, and acid–base balance; alterations in regulatory functions (e.g., blood pressure control, production of red blood cells, and impaired vitamin D synthesis); and the effects of uremia on body function (e.g., uremic encephalopathy, peripheral neuropathy, pruritus)

F&E, acid-base disorders One of earliest signs: polyuria with urine that is isotonic with plasma (can’t concentrate urine). Sodium and water retention > hypertension, peripheral edema, heart failure. NOTE: we restrict CKD patients’ sodium and water intake … if they develop diarrhea and vomiting … very dangerous. Potassium retention > hyperkalemia or hypokalemia? > muscle

Clinical Manifestations Pathophysiological Mechanisms

weakness, ECG changes. pH ion retention > metabolic acidosis > skeletal buffering (see next topic)

Disorders of calcium and phosphorus metabolism and bone disease

Serum phosphate increases or decreases? Serum calcium increases or decreases? Remember: phosphate and calcium are inversely related. Parathyroid hormone released to increase serum calcium. Vitamin D activation is impaired.

All of this leads to ….. skeletal disorder, ‘renal osteodystrophy’. High-bone turnover, or osteitis fibrosa: increase bone resorption andformation. Which one predominates? bone resorption Low-bone turnover, 2 types:

1. Osteomalacia: characterized by a slow rate of bone formation and defects in bone mineralization, which may be caused by vitamin D deficiency, excess aluminum deposition, or metabolic acidosis.
2. Adynamic osteodystrophy: characterized by low number of osteoblasts, with the osteoclast number being normal or reduced

It is now recognized as being as common as high–bone- turnover osteodystrophy and is especially common among people with diabetes. Bone disease leads to bone tenderness and muscle weakness, bone fractures.

Hematologic disorders Anemia due to what? Contributes to what manifestations? several factors, including chronic blood loss, hemolysis, bone marrow suppression because of retained uremic factors, and decreased red cell production because of impaired production of erythropoietin and irondeficiency.

weakness, fatigue, headache, irritability, depression, insomnia, and decreased cognitive function. There is also an increasing concern regarding the physiologic effects of anemia on cardiovascular function.

Coagulopathies (bleeding disorders) due to impaired platelet function. Manifested by what? epistaxis, menorrhagia, gastrointestinal bleeding, and bruising of the

Clinical Manifestations Pathophysiological Mechanisms

skin and subcutaneous tissues.

Cardiovascular disorders Hypertension: early manifestation; due to inc. vascular volume, inc.vascular resistance, dec. renal vasodilation, inc. activation of RAAS.

Heart disease: left ventricular hypertrophy and ischemic heart disease.Causative factors: extracellular fluid overload, shunting of blood through an arteriovenous fistula for dialysis, and anemia.

Congestive heart failure and pulmonary edema occur

late. Pericarditis: due to what? Manifestations? because of the uremia and prolonged dialysis

viral pericarditis, with all its potential complications, including cardiactamponade. The presenting signs include mild-to-severe chest pain with respiratory accentuation and a pericardial friction rub. Fever is variable in the absence of infection and is more common in dialysis than uremic pericarditis

Gastrointestinal disorders Describe: Anorexia, nausea, and vomiting are common in people with uremia, along with a metallic taste in the mouth that further depresses the appetite.2 Early morning nausea is common. Ulceration and bleeding of the gastrointestinal mucosa may develop, and hiccups are common. A possible cause of nausea and vomiting is the decomposition of urea by intestinal flora, resulting in a high concentration of ammonia. PTH increases gastric acid secretion and contributes to gastrointestinal problems. Nausea and vomiting often improve with restriction of dietary protein and after initiation of dialysis and disappear after kidney transplantation

Neuromuscular disorders Neuropathy due to atrophy and demyelination of nerve fibers, maybe due to uremic toxins. Peripheral nervous system involvement: restless leg syndrome. Central nervous system involvement: uremic encephalopathy; reduced alertness and awareness > inattention, memory loss > delirium, coma Motor function impaired. Fine movement difficult, impaired gait, asterixis.

Clinical Manifestations Pathophysiological Mechanisms

Altered immune function Risk^ for^ infection^ due^ to^ impact^ of^ high^ levels^ of^ urea^ and metabolicwastes on immune and inflammatory response.

Disorders of skin integrity Describe: Skin manifestations are common in people with CKD.2 The skin is often pale owing to anemia and may have a sallow, yellow– brown hue. The skin and mucous membranes are often dry, and subcutaneous bruising is common. Skin dryness or xerosis is caused by a reduction in perspiration because of the decreased size of sweat glands and the diminished activity of oil glands. Pruritus is common; it results from the high serum phosphate levels and the development of phosphate crystals that occur with hyperparathyroidism. Severe scratching and repeated needlesticks, especially with hemodialysis, break the skin integrity and increase the risk for infection. In the advanced stages of untreated kidney failure, urea crystals may precipitate on the skin as aresult of the high urea concentration in body fluids. The fingernails may also become thin and brittle.

Sexual dysfunction Due^ to^ high^ levels^ of^ uremic^ toxins,^ neuropathy,^ hormonal imbalance, anemia, psychological factors, and drugs.

Elimination of drug Impaired^ absorption,^ distribution,^ and^ elimination^ of^ drugs.^ Can result in adverse effects and toxicity.

Excellent video: Khan Academy Chronic Kidney Disease (15:50) Manifestations start at 9:20.

Great work … 2 renals down, only 1 more renal Study Guide to go.

References: Norris, T. L. (2020). Porth’s Essentials of Pathophysiology, 5th^ edition. Wolters Kluwer.