Renal Pathophysiology: Acute Kidney Injury and Chronic Kidney Disease

Nursing Management for preventing kidney injury

"Prevention is the best cure." The role of the critical care nurse is to evaluate all patients for level of kidney function! Key treatment goals: -Assessment and monitoring of kidney function -Risk of infection -Fluid imbalance -Electrolyte disturbances -Anemia -Readiness to learn, and need for education Nursing management of the patient with AKI involves a variety of nursing diagnoses. "Prevention is the best cure." The critical care nurse evaluates all patients for level of kidney function, risk of infection, fluid imbalance, electrolyte disturbances, anemia, readiness to learn, and need for education. Some individuals are at increased risk for AKI as a complication during hospitalization. Patients at risk include older persons, dehydrated patients with kidney hypoperfusion, patients with increased creatinine levels before their hospitalization, and patients undergoing a radiologic procedure involving contrast dye. The critical care patient with infectious complications is at risk for AKI. Signs of infection include increased white blood cell (WBC) count, redness at a wound or intravenous line site, or increased temperature. Any indwelling catheter is a potential source for infection. When the patient no longer makes large quantities of urine and is hemodynamically stable, the catheter must be removed promptly. If the patient cannot void urine spontaneously, a scheduled intermittent urinary catheterization is preferred over an indwelling catheter. Treatment Goals Treatment goals for patients with AKI focus on prevention, compensation for the deterioration of kidney function, and regeneration of kidney functional capacity. Key treatment areas include prevention strategies, fluid balance, anemia, medications, and electrolyte imbalance. Prevention The only truly effective remedy for AKI is prevention. Effective prevention requires assessment of the patient's risk for AKI. Knowledge of the most frequent causes of AKI in critically ill patients is essential if prevention strategies are to be enacted. The critical care team collaborates closely with the clinical pharmacist to avoid medications with nephrotoxic side effects in patients with AKI or CKD. Nonsteroidal antiinflammatory medications for pain relief are avoided in patients with elevated creatinine levels. The use of intravascular contrast dye is preferably delayed until the patient is fully rehydrated.

Preventing the Progression of Chronic Kidney Disease

*** Kidney preservation is KEY!! Secondary insults accelerate loss of nephrons! -Hypovolemia -Nephrotoxic agents -Urinary obstruction and infections -NSAIDs -Hyperglycemia (Hgb A1C <7%) -Hypertension ( goal BP <140/90) -Hyperlipidemia An important characteristic of CKD is continuous progression. Regardless of the primary cause of CKD, specific identifiable secondary insults to the kidney can rapidly accelerate the loss of nephrons. Such secondary insults include an alteration in renal perfusion, as observed in congestive heart failure or intravascular volume depletion; the administration of nephrotoxic agents; urinary obstruction; and urinary infections. Common over-the-counter and prescription analgesics, such as NSAIDs, can cause rapid deterioration in renal function and should be avoided in patients with CKD. Strict control of blood glucose levels is critical to preventing and retarding the progression of renal failure in people with diabetes. The targets for key parameters of glucose are glycosylated hemoglobin of less than 7.0%, a preprandial plasma glucose of 70 to 130 mg/dL, and a peak postprandial plasma glucose of less than 180 mg/dL BP control is also essential for preventing the progression of renal failure from almost any primary etiology, not just hypertension or diabetes. BP target: less than 140/90 mm Hg. KDIGO, however, recommends a lower target of less than 130/80 mm Hg in CKD patients with an ACR ≥ 30 mg. ACE inhibitors and ARBs have been shown to offer a selective advantage in slowing the progression of diabetic and other proteinuric syndromes. Both drugs have been proved to lower BP, reduce proteinuria, and slow the progression of kidney disease. (Test) A protein-restricted diet as a means to slow the progression of renal failure is controversial. ???

Pharmacologic Management: Thiazide Diuretics

-Chlorothiazide (Diuril) or metolazone (Zaroxolyn) may be administered and followed by a loop diuretic to take advantage of the fact that these medications work on different parts of the nephron. -Inhibits Na and Cl reabsorption

Pharmacologic Management: Loop Diuretics

-Furosemide (Lasix), bumetanide (Bumex), and torsemide (Torsemide) -Block the Na-K-2Cl transporter in the nephron on the ascending limb of the loop of Henle, where most sodium is reabsorbed. -Aggressive use can lead to metabolic alkalosis

•Proteinuria

-Result of glomerular hypertension and abnormal glomerular permeability -Abnormally filtered protein is reabsorbed and stored intracellularly through endocytosis •Causes production of proinflammatory cytokines •Results in scarring and fibrosis -Very strong predictor of chronic kidney disease progression -Included in the staging of CKD Proteinuria, the result of glomerular hypertension and abnormal glomerular permeability, also contributes to CKD progression. Abnormally filtered protein is reabsorbed by proximal tubular cells through endocytosis and accumulates in the cells, causing the production of cytokines. These proinflammatory factors ultimately cause fibrosis and scarring of the tubulointerstitium. Proteinuria is a very strong predictor of CKD progression, consistent with its role in the pathophysiology of CKD and as evidenced by its inclusion in the new KDIGO CKD staging.

4 Phases of Acute Kidney Injury

1. Onset phase: Kidney injury occurs. 2. Oliguric (anuric) phase: Urine output decreases from renal tubule damage. 3. Diuretic phase: The kidneys try to heal and urine output increases, but tubule scarring and damage occur. 4. Recovery phase: Tubular edema resolves and renal function improves.

Diagnosis of Acute Kidney Injury

1st Determine if the AKI is prerenal, intrarenal, or postrenal •History and Physical Examination •Laboratory Studies -Urinary Values •Urine sodium, osmolality, specific gravity •Sedimentation •FENa -BUN and Creatinine •Diagnostic Studies Diagnosis of AKI begins with a determination of whether the AKI is prerenal, intrarenal, or postrenal. The assessment tools used to make this determination include the history and physical examination, laboratory tests, and diagnostic studies.

Laboratory Studies for severe kidney insult

Acidosis (pH < 7.35) and thus trademark of severe kidney insult •Result of accumulation of unexcreted waste products •Acid waste products are: -Strong anions (Na, K, NH4 {ammonia}) -Elevated serum phosphorus levels -Other normally unmeasured ions (sulfate, urate, lactate) that decrease the serum pH. Acidosis (pH less than 7.35) is one of the trademarks of severe acute kidney insult. Metabolic acidosis occurs as a result of the accumulation of un-excreted waste products. The acid waste products consist of strong negative ions (anions), elevated serum phosphorus levels (hyperphosphatemia), and other normally unmeasured ions (eg, sulfate, urate, lactate) that decrease the serum pH. A low serum albumin concentration, which often occurs in AKI, has a slight alkalinizing effect, but it is not enough to offset the metabolic acidosis. Respiratory compensation and mechanical ventilatory support are rarely sufficient to reverse the metabolic acidosis. Acidosis in AKI is complex, as evidenced by the fact that many patients with AKI maintain a normal anion gap; the reasons for this are unknown.

Acute Kidney Injury Network (AKIN)

Acute Kidney Injury Network (AKIN) Criteria for The Diagnosis of Acute Kidney Injury

Albuminuria - KDIGO A Stages

Albumin - to - Creatinine Ratio •A1 is defined as an ACR < 30 mg/g. "Normal" •A2 is defined as an ACR 30 to 299 mg/g. •A3 is defined as an ACR ≥ 300 mg/g. Assessed using an untimed spot urine. Albuminuria is assessed using the albumin-to-creatinine ratio (ACR) in an untimed spot urine. The threshold for an abnormally elevated ACR is 30 mg/g or greater. This addition was made in response to mounting evidence that there is an increase in mortality and progression of CKD to ESRD with higher levels of albuminuria, independent of GFR.

(Alternate) 3 Phases of Acute Kidney Injury

Initiation phase - reduced perfusion or toxicity, renal injury is evolving, usually lasting 24-36 hours. Prevention of injury is possible! Maintenance or oliguric phase - established renal injury and dysfunction after the initiating event has been resolved. May last weeks to months. Decreased UO = ↑ (Cr, BUN, K), metabolic acidosis, ↑Na and H20 overload Recovery phase - renal injury is repaired and normal renal function is reestablished. -GFR is normal but tubules cannot concentrate urine -Diuresis is common with a ↓ Cr, urea, and ↑ in creatinine clearance

Chronic Kidney Disease Classification

KDIGO recommendations: •Classification of CKD based on Cause, Category, and Albuminuria - Collectively referred to as "CGA Staging" •Identify cause of CKD (C) •Assign GFR category (G) •Assign albuminuria category (A) In 2013 KDIGO recommended a classification based on cause of CKD, GFR category, and albumin category (referred to as CGA). Etiology of CKD was added because it provides important prognostic information and influences treatment decisions. Cause of CKD is based on the presence or absence of systemic disease, such as diabetes or lupus, and the anatomic location of the pathologic abnormality within the kidney. For GFR, KDIGO maintained the prior KDOQI stages, except that stage 3 was divided into 3a and 3b. This subdivision of stage 3 was in response to the great disparity in complications seen in patients in this stage. KDIGO added the level of albuminuria in the staging. Albuminuria is assessed using the albumin-to-creatinine ratio (ACR) in an untimed spot urine. Consequently, patients now have a "G-stage" based on GFR and an albuminuria or "A-stage," both identifying a patient's risk for CKD progression and complications. This classification system provides a common language for practitioners and patients to improve communication, enhance education, and promote research. Most importantly, it also provides a framework for evaluation and development of a treatment plan for patients with various stages of CKD.

Managing Alterations in Dietary Intake

Managing alterations in dietary intake: •Restrict fluid, sodium, potassium, and phosphate •High calorie, moderate protein restrictions •Oral nutrition is preferred •Monitor blood glucose levels The recommended energy intake is between 20 and 30 kilocalories/kg per day, with 1.2 to 1.5 grams/kg of protein per day to control azotemia The goals of nutritional therapy in renal failure are to minimize uremic symptoms; reduce the incidence of fluid, electrolyte, and acid-base imbalances; minimize symptoms of anemia; decrease the patient's vulnerability to infections; and limit catabolism. Dietary restrictions related to managing comorbid conditions and reducing cardiovascular risk also need to be considered. Because of the complexity of achieving a nutritional therapy plan that meets these goals, a collaborative health care team approach, including the ongoing participation of a dietitian, is essential. This is particularly the case in critical care, where patients are usually in a catabolic state and are at risk for substantial malnutrition. Renal diet prescriptions include restrictions in fluid, sodium, potassium, and phosphate intake, and may include supplementations of iron, vitamins, and calcium. Calorically, critically ill patients with renal disease need a high-calorie diet with a total of 20 to 30 kcal/kg/d, most of which should come from a combination of carbohydrates and lipids. In addition, adequate protein intake must be administered to prevent catabolism, and at least 50% of protein intake should be of high biologic value to ensure that the minimal intake requirements of essential amino acids are met. Protein restriction to decrease symptoms of uremia and slow the progression of renal failure is controversial but may be beneficial. In critically ill patients, parenteral nutrition may need to be instituted because of impaired bowel function or severe malnutrition, but the enteral route is preferred if feasible. In oliguric patients, the high hourly volume requirements needed for parenteral or enteral nutrition often must be offset by dialysis or isolated ultrafiltration. To determine the effectiveness of nutritional therapy, continual laboratory monitoring of serum protein, cholesterol, albumin and prealbumin, electrolytes, hemoglobin, hematocrit, and urea and creatinine levels is essential. Patient weight, volume status, and energy levels are additional monitoring parameters. Nutritional education, including information on dietary restrictions, the use and timing of phosphate binders, vitamin and mineral supplements, and measures of nutritional status should be provided.

Etiologies of Intrarenal Acute Kidney Injury

Many etiologies exist •Acute Tubular Necrosis (ATN) is most common hospital acquired form of intrarenal AKI -Ischemia and nephrotoxicity are major underlying causes of ATN Intrarenal AKI. Any condition that produces an ischemic or toxic insult directly at parenchymal nephron tissue places the patient at risk for development of intrarenal AKI. Ischemic damage may be caused by prolonged hypotension or low cardiac output. Toxic injury reaction may occur in response to substances that damage the kidney tubular endothelium, such as some antimicrobial medications and the contrast dye used in radiologic diagnostic studies. The insult may involve the glomeruli and the tubular epithelium. When the internal filtering structures are pathologically affected, the condition was previously known as acute tubular necrosis , although the newer term of AKI is now used more often. Kidney ischemia (advanced stage of prerenal acute kidney injury) Endogenous toxins (rhabdomyolysis, tumor lysis syndrome) Exogenous toxins (radiocontrast dye, nephrotoxic medications) Infection (acute glomerulonephritis, interstitial nephritis)

AT-RISK Disease States for Kidney injury

Older Age •DM and HTN •Age > 60 (prevalence 25%) Heart Failure •CAD, DM and HTN - 54% of AKI patients have HF Cardiorenal Syndrome •New classification system is to identify relevant biomarkers, treatments Older Age and Acute Kidney Injury Among adults older than 60 years, the prevalence of CKD in the United States is close to 25%. The number of older adults with CKD is increasing in tandem with the increase in diabetes and hypertension in the US population. Heart Failure and Acute Kidney Injury There is a strong association between kidney failure and heart failure. Heart-kidney interactions have been categorized into five subtypes under the term cardiorenal syndromes. The purpose of the new classification system is to identify relevant biomarkers, treatments, and future avenues for research. One feature that is often encountered is a resistance to use of high-potency loop diuretics such as furosemide. Several risk factors for atherosclerotic cardiovascular disease, notably hypertension and diabetes, are also detrimental to the kidney over the long-term. Maintenance of blood pressure below 130/80 mm Hg and blood glucose within the normal range decreases the risk of developing both CKD and the atherosclerotic cardiac diseases such as coronary artery disease and peripheral artery disease.

Pharmacologic Management OVERALL VIEW

Osmotic Diuretics - Action: increase urine output because higher plasma osmolality , increases flow of water from tissues, causing increased GFR, Increased serum sodium, potassium levels. Special Consideration: Often used in head injury to decrease cerebral edema, Can be used to promote urinary secretions of toxic substances, At low temperature mannitol may crystallize, use in-line 5-micron IV filter with >15% (.15g/1000ml) solutions. Loop Diuretics - Action: Acts on loop of Henle to inhibit sodium and chloride resorption (natriuresis). Special Considerations : Ototoxicity if administered too rapidly or with other ototoxic medications. Monitor intake and output, hydration. Monitor for hypotension. Thiazide Diuretics - Action: Inhibits sodium, chlorideresorption in distal tubule. Special Consideration: Enhanced with low-sodium diet. Synergistic effect with loop diuretics. Effective to a creatinine clearance of 10ml/min. Potassium-Sparing Diuretics - Action: Exert effects on collecting duct; retains potassium, increases sodium diuresis. Special Consideration: Weak diuretic effect; Potassium supplements not required; monitor for hyperkalemia. Used as an aldosterone blocker to treat heart failure. Vaptans - Action: Blocks V2 aquaporin channels in collecting tubules. Special Consideration: Used only in hyponatremia with hypovolemia. Monitor volume status and serum sodium frequently.

Etiology of Acute Kidney Injury

Prerenal - Hypovolemia, Hemorrhagic blood loss (trauma, gastrointestinal bleeding), Loss of plasma volume (burns, peritonitis), Water and electrolyte losses (severe vomiting or diarrhea, intestinal obstruction, uncontrolled diabetes mellitus, inappropriate use of diuretics), Systemic hypotension or hypoperfusion, Septic shock systemic inflammation, Cardiac failure or shock, Massive pulmonay embolism, Stenosis or clamping of renal artery, Increased intra-abdominal pressure (abdominal compartment syndrome). Intrarenal - Acute tubular necrosis (postischemic or nephrotoxic), Glomerulopathies, Acute interstitial necrosis (tumors or toxins), Vascular damage, Malignant hypertension, vasculitis; Coagulation defects, Renal artery/ vein occlusion, Bilateral acute pyelonephritis. (Usually easier to recover from) Intrarenal- direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply ( You will see more phases with this one) Postrenal - Obstructive uropathies (usually bilateral - fibrosis); Ureteral destruction (edema, tumors, stones, clots); Bladder neck obstruction (enlarged prostate), Neurogenic bladder.

AT-RISK Disease States: Respiratory

Respiratory Failure •Positive-pressure ventilation reduces blood flow to the kidney, lowers the GFR, and decreases urine output. •ARDS - Activation of inflammatory response = leaky vasculature leads to hypovolemia which leads to lowers the GFR, and decreases urine output Respiratory Failure and Acute Kidney Injury There is a significant association between kidney failure and respiratory failure. Mechanical ventilation can alter kidney function. Positive-pressure ventilation reduces blood flow to the kidney, lowers the GFR, and decreases urine output. These effects are intensified with the addition of positive end-expiratory pressure. AKI increases inflammation, causes the lung vasculature to become more permeable, and contributes to the development of acute respiratory distress syndrome. Patients with AKI are more likely to require prolonged mechanical ventilatory support. Patients with chronic lung conditions such as chronic obstructive pulmonary disease have a 41% increased risk of death if they also have AKI.

AT-RISK Disease States: Rhabdo

Rhabdomyolysis •Destruction of large muscle mass and hypovolemia •Release of creatine kinase and myoglobin from damaged muscle cells -Dramatic rise in creatine kinase (CK) -Myoglobin causing acute tubular necrosis •Metabolic acidosis & Hyperkalemia leading to cardiac arrest Management: crystalloid volume resuscitation Trauma patients with major crush injuries have an elevated risk of kidney failure because of the release of creatine and myoglobin from damaged muscle cells, a condition called rhabdomyolysis. Myoglobin in large quantities is toxic to the kidney. A major goal of treatment is to prevent rhabdomyolysis-induced AKI. The mortality rate is low, provided that adequate crystalloid volume is administered early in the course of treatment. It is important to trend the serum potassium levels. Life-threatening hyperkalemia can occur as cell lysis permits intracellular potassium to be released into the bloodstream. The level of creatine kinase (CK), a marker of systemic muscle damage, increases in patients with rhabdomyolysis. One trauma service reported that of 2083 critical care trauma admissions, 85% had elevated CK levels, and 10% developed AKI resulting from rhabdomyolysis. A CK level of 5000 units/L was the lowest abnormal value in patients who developed AKI associated with rhabdomyolysis. Crystalloid volume resuscitation is the primary treatment for preservation of adequate kidney function and prevention of AKI. In many hospitals, intravenous (IV) fluids are alkalinized by the addition of sodium bicarbonate, and urine output is increased by IV administration of the diuretic mannitol. A bicarbonate and mannitol regimen is instituted to prevent acidosis and hyperkalemia because both are frequent complications of rhabdomyolysis. Close attention is paid to hourly urine output that can be dark brown or tea-colored, CK levels, serum creatinine levels, serum potassium levels, and any signs of compartment syndrome in all patients admitted with this diagnosis.

AT-RISK Disease States: Sepsis

Sepsis •Overwhelming inflammatory response -Leaky vasculature à hypovolemic shock -Causes low glomerular perfusion pressure -Resulting in decrease urine output •Management -Vasopressor increase BP and raise SV -But raises vascular resistance within kidney Sepsis and Acute Kidney Injury Sepsis causes almost half of the cases of AKI in the critically ill. Sepsis and septic shock create hemodynamic instability and reduce perfusion to the kidney. Immunologic, toxic, and inflammatory factors may alter the function of the kidney microvasculature and tubular cells. Clinical guidelines for hemodynamic support in sepsis emphasize the need for adequate fluid resuscitation, because reversal of hypotension and restoration of hemodynamic stability can often be achieved with fluids alone, although this is not the case in severely septic patients, who may be managed with vasopressors or other therapies.

Acute Kidney Injury: What is it?

Sudden onset of reduced renal function that can result in derangement of fluid and electrolytes, acid-base homeostasis, calcium and phosphate metabolism, blood pressure regulation, and erythropoiesis •Serum creatinine vs BUN is a better marker because it is relatively unaffected by metabolic factors •Hallmark which decreases GFR and accumulation of BUN and serum creatinine ---Termed azotemia Acute kidney injury (AKI) describes the spectrum of acute-onset kidney disorders that can range from mild impairment of kidney function through acute kidney failure that requires renal replacement therapy (dialysis). Severe AKI is characterized by a sudden decline in glomerular filtration rate (GFR), with subsequent retention of products in the blood that are normally excreted by the kidneys; this disrupts electrolyte balance, acid-base homeostasis, and fluid volume equilibrium.

CKD Defined

The KDOQI defines CKD as either kidney damage with or without decreased GFR for 3 or more months or a GFR of less than 60 mL/min/1.73 m2 for greater than 3 months. Markers of damage include abnormal findings in the blood or urine tests or imaging studies. Examples are proteinuria, abnormalities in the urine sediment, increased serum creatinine, and multiple renal cysts detected on ultrasound in a patient with a family history of polycystic kidney disease. A GFR (considered to be the best overall measure of kidney function) of less than 60 mL/min/1.73 m2 was chosen for two reasons: (1) it represents a loss of half or more of the adult level of normal kidney function, and (2) below this level, the prevalence of complications from CKD increases.

Risk Factors for AKI

Today the most frequent causes of AKI in the critically ill are associated with sepsis and cardiac surgery especially with CBP (coronary bypass), this it because the MAP that you need to perfuse the kidneys is more than what we run the machine on due to the needs for surgery. Typically a patient is not admitted to the critical care unit with a diagnosis of AKI alone; there is always co-existing hemodynamic, cardiac, pulmonary, or neurologic compromise. One of the biggest things we can do is good line care to avoid sepsis.

What makes Sepsis and Cardiac Surgery so prone to AKI?

Today the most frequent causes of AKI in the critically ill are associated with sepsis and cardiac surgery. Typically a patient is not admitted to the critical care unit with a diagnosis of AKI alone; there is always co-existing hemodynamic, cardiac, pulmonary, or neurologic compromise. Many patients have underlying changes in kidney function, such as an elevated serum creatinine level, although they have no symptoms. The lack of kidney reserve places these patients at increased risk for AKI if complications occur in any other organ systems. As a result, the picture of AKI in the modern critical care unit has changed to encompass patients with kidney injury who also have multisystem dysfunction that complicates their clinical course. Kayexalate = used to treat high potassium in your blood. you need to be able to know the difference between AKI and Renal Necrosis (Which is technically an AKI, but will be considered different things)

Toxic Acute Tubular Necrosis

Toxic Acute Tubular Necrosis = Pure Intrarenal AKI •Nephrotoxin becomes concentrated in the renal tubular cells and causes necrosis. •Necrotic cells slough off and obstruct the tubular lumen. •The basement membrane of the renal cells usually remains intact, and the necrotic areas are more localized. •BUN : Cr that is 10:1 Potential nephrotoxins in toxic ATN are many - aminoglycosides antibiotics, and radiocontrast dye which are common causes in hospitalized patients. Toxic ATN occurs when a nephrotoxin becomes concentrated in the renal tubular cells and causes necrosis. The necrotic cells slough off and obstruct the tubular lumen, similar to ischemic ATN. In toxic ATN, the basement membrane of the renal cells usually remains intact, and the necrotic areas are more localized.

AT-RISK Disease States: Trauma

Trauma •Incidence of AKI doubles in first 24 hour after admission •In patients with pre-existing comorbidities risk goes up from 18% to 35% Trauma Admissions Trauma patients have different demographics than other critical care populations. Patients are always emergency admissions, are younger, are more often male, and have fewer coexisting illnesses. A 5-year retrospective study of 9449 trauma admissions to critical care units in Australia and New Zealand used the RIFLE criteria to determine incidence of AKI in the first 24 hours after admission; 18% of trauma patients developed AKI. However, if patients were older or had preexisting comorbid illnesses, their risk of AKI increased to 35%. Although these AKI numbers are high, they likely underestimate the true incidence because the study did not include patients who developed AKI later than 24 hours after admission to the critical care unit.

Comparison of Laboratory Findings

Urine Specific Gravity: 1.003 -1.030, Urine Osmo.: 300-1200, Urine protein: normal 30-150mm/24 hr The urine specimen should be obtained before a diagnostic challenge dose of diuretics is administered because these agents may alter the urine's chemical composition. The urine sodium concentration, osmolality, and specific gravity distinguish between prerenal AKI and ATN because these values reflect the concentrating ability of the kidney. In prerenal failure, the hypoperfused kidney actively reabsorbs sodium and water in an attempt to increase circulatory volume. Consequently, the urine sodium level and the fractional excretion of sodium (FENa) are low (less than 20 mEq/L and less than 1%, respectively), whereas the urine osmolality and concentration of nonreabsorbable solutes are high. In ATN in which parenchymal damage affects the kidney, the tubular cells can no longer effectively reabsorb sodium or concentrate the urine. As a result, the urine sodium concentration is often greater than 40 mEq/L, the FENa is greater than 2%, and the urine osmolality is close to that of plasma (isosthenuria). Values at the extremes are thus the most useful. The sediment in a urinalysis is also very helpful in diagnosing and distinguishing the types of AKI. In prerenal AKI, the urinary sediment is normal with only a few hyaline casts In ATN, coarse, muddy-brown granular casts and tubular epithelial cells are typically found. In postrenal AKI, the sediment is often normal but can be helpful in diagnosing kidney stones.

What is azotemia?

increase in nitrogenous waste products in blood

Acute Kidney Injury (AKI)

rapid loss of renal function due to damage to the kidneys; formerly called acute renal failure •Incidence of 2% to 20% of non-ICU hospitalized patients and up to 67% of ICU patients. - Results in an increase in length of stay, complications, & mortality. •Mortality rate 40% to 70% among patients treated with renal replacement therapy (RRT) •Acute kidney injury after combat trauma occurs in up to 34.3% of the most critically injured patients, usually within the first 2 days after injury •Patients who survive AKI and approach normal kidney function by hospital discharge are at increased risk for later development of chronic kidney disease (CKD). Critical care patients with AKI have a longer length of hospital stay, more complications, and higher mortality. AKI-associated mortality ranges from 15% to 60%. One of the reasons for poor survival is that critical care patients often have co-existing non-kidney conditions that increase their susceptibility to the development of AKI. **Acute kidney injury after combat trauma occurs in up to 34.3% of the most critically injured patients, usually within the first 2 days after injury.1 Today the most frequent causes of AKI in the critically ill are associated with sepsis and cardiac surgery. Typically a patient is not admitted to the critical care unit with a diagnosis of AKI alone; there is always co-existing hemodynamic, cardiac, pulmonary, or neurologic compromise. Many patients have underlying changes in kidney function, such as anelevated serum creatinine level ,although they have no symptoms. The lack of kidney reserve places these patients at increased risk for AKI if complications occur in any otherorgan systems. As a result, thepicture of AKI in the moderncritical care unit has changed to encompass patients with kidney injury who also have multisystem dysfunction that complicates their clinical course.

Etiologies of Postrenal Acute Kidney Injury

• Caused by any obstruction in flow of urine from collecting ducts in kidneys to external urethral orifice. Etiologies: o Ureteral obstruction (ie, stones) o Urethral blockage (ie, strictures or BPH) o Extrinsic source (ie, tumor or fibrosis) -Sudden development of anuria (urine output less than 100 mL/24 h) should prompt verification that the urinary catheter is not occluded. Postrenal AKI. When monitoring of the urine output reveals a sudden decrease in the patient's urine output from the urinary catheter, a blockage may be responsible. Sudden development of anuria (urine output less than 100 mL/24 h) should prompt verification that the urinary catheter is not occluded. Any obstruction that hinders the flow of urine from beyond the kidney through the remainder of the urinary tract may lead to postrenal AKI. This is an uncommon cause of kidney failure in critically ill patients.

Urine Sedimentation

• Urate crystals: Tumor lysis, especially lymphoma (urate nephropathy) • Oxalate crystals: Ethylene glycol nephrotoxicity, methoxyflurane nephrotoxicity • Eosinophils: Allergic interstitial nephritis, especially methicillin • Positive peroxidase test without red blood cells: Hemoglobinuria or myoglobinuria • Pigmented casts: Hemoglobinuria or myoglobinuria • Massive proteinuria: Acute interstitial nephritis, thiazide diuretics, hemorrhagic fevers (eg, Korean, Scandinavian) • Abnormal urine protein electrophoresis: Multiple myeloma • Anuria: Renal cortical necrosis, bilateral obstruction, renal vascular catastrophe

Managing Pulmonary Alterations

•A frequent complication in patients with oliguric AKI or stage G5 CKD -Pulmonary edema -Pleural effusions -Pneumonitis -Pulmonary infections A frequent complication in patients with oliguric AKI or stage G5 CKD is the development of pulmonary edema. This complication results from fluid overload, heart failure, or both. Clinical manifestations include dyspnea; crackles on auscultation; the production of pink, frothy sputum; tachypnea; tachycardia; decreased arterial oxygen saturation (SaO2); and evidence of fluid overload on chest radiograph. Management involves fluid and sodium restriction, treating underlying cardiac disease, and possibly diuretic medications if the patient's kidneys can respond to them. Frequently, pulmonary edema becomes life threatening, necessitating intubation, emergent dialysis, or both to improve arterial oxygenation and restore fluid balance. Other pulmonary complications in renal failure include pleural effusions, pleuritic inflammation and pain, uremic pneumonitis, and pulmonary infections. Pleuritic inflammation and uremic pneumonitis occur more frequently with stage G5 CKD and are due to the effect of uremic toxins on the lungs and inadequate dialysis. Pulmonary infections, on the other hand, are common in both AKI and CKD, especially in critically ill patients. Factors associated with renal failure that contribute to pulmonary infections include decreased pulmonary macrophage activity, a generalized immunocompromised state, tenacious sputum, and a depressed cough reflex. Collaborative management includes culturing sputum, administering broad-spectrum antibiotics until organism-specific sensitivities are available, and teaching and encouraging pulmonary hygiene measures (ie, coughing and deep breathing).

Acute Dialysis Quality Initiative (ADQI)

•ADQI = Acute Kidney Diagnostic Criteria and Staging

Pharmacologic Management: Carbonic Anhydrase Inhibitor

•Acetazolamide (Diamox) acts on the proximal tubule where it inhibits the carbonic anhydrase enzyme, allowing more bicarbonate (HCO3−) to be released into the filtrate, resulting in an alkaline diuresis. •Acetazolamide is administered to treat the metabolic alkalosis that sometimes occurs following aggressive diuresis with loop diuretics. Acetazolamide is administered to treat the metabolic alkalosis that sometimes occurs following aggressive diuresis with loop diuretics. Carbonic anhydrase inhibitors slow this and cause the patient to pee bicarbonate. The loss of bicarbonate causes metabolic acidosis, or alternatively, improvement in pre-existing metabolic alkalosis.

Diabetic Nephropathy

•Affects afferent & efferent arterioles and glomerular capillaries - Tubular and interstitial fibrosis occur •Directly related to hyperglycemia •Strict blood glucose control can delay and possibly prevent progression Diabetic nephropathy is a major complication of diabetes, with an incidence of approximately 20% to 40%. In diabetes, the microvasculature in the organ systems of the body, including the kidneys, is damaged. In the kidneys, primarily the afferent and efferent arterioles and the glomerular capillaries are affected. Glomerular changes include thickening of the basement membrane, mesangial expansion from overproduction and underdegradation of extracellular matrix proteins, and diffuse glomerulosclerosis. Late in diabetic nephropathy, tubular atrophy and interstitial fibrosis also occur. Hyperglycemia is a major contributor. At the onset of diabetic nephropathy, patients may have an increased GFR (as high as 140 mL/min) because of hyperfiltration, slightly enlarged kidneys, and microalbuminuria (30 to 300 mg/d of albumin in the urine). Over the course of approximately 10 to 15 years, hypertension and protein leakage increase. Eventually, protein leakage is massive, with consequent hypoalbuminemia and edema as well as mild azotemia. At this point kidney damage is extensive, often requiring dialysis therapy within a few years.

Management of Cardiovascular Alterations

•Alterations in the cardiovascular system can cause or accelerate AKI and CKD. •Hypertension •Hyperkalemia •Pericarditis •Cardiovascular Disease Alterations in the cardiovascular system can cause or accelerate AKI and CKD. In addition, cardiovascular complications can arise as a result of renal failure itself. Common cardiovascular complications in AKI and CKD include hypertension and hyperkalemia. Pericarditis, another cardiovascular complication of renal disease, is primarily seen with CKD. Hypertension as a complication of renal failure results from excess retention of water and sodium, overactivation of the sympathetic nervous system, and stimulation of the renin-angiotensin-aldosterone system. Management may include fluid and sodium restrictions, diuretic administration, antihypertensive therapy, and dialysis to remove excess fluid. CKD is associated with high cardiovascular morbidity and mortality. In fact, patients with CKD are much more likely to suffer from cardiac disease resulting in cardiovascular death than to eventually require RRT. The predominant cardiac disorders in CKD are left ventricular hypertrophy, coronary artery disease, dysrhythmias, cardiomyopathy, congestive heart failure, and valvular dysfunction. Because most of these cardiovascular disorders develop over a period of at least a few years, they usually present early in CKD and continue to progress as renal function declines. cardiovascular disease causes renal dysfunction (ie, heart failure); CKD causes an increased risk for cardiovascular disease; other factors (eg, hypertension, diabetes mellitus, anemia, or hyperlipidemia) cause or accelerate both renal dysfunction and cardiovascular disease. Diagnostic tests useful in assessing for cardiovascular disease in these high-risk patients include routine ECGs, echocardiography, and cardiac stress testing. Modifiable risk factors that can contribute to cardiovascular disease, and that should be addressed as part of managing patients with CKD, include hypertension, obesity, hyperlipidemia, hypervolemia, anemia, smoking, hyperglycemia, calcium and phosphate imbalances, vitamin D deficiency, and metabolic acidosis.

Common Nephrotoxins

•Antibiotics, Antifungals -10% to 25% of patients -Onset delayed, 5 to 10 days after onset treatment •Contrast-induced nephropathy (CIN) -Occurs within 24 to 48 hours and peaks within 3 to 7 days -Incidence up to 50% in high-risk patients (diabetes and renal impairment) -Aggressive volume hydration before and after contrast agent is recommended Aminoglycosides: amikacin, gentamicin, streptomycin, tobramycin Guidelines recommend that peak and trough levels are drawn to monitor for a therapeutic range of the medication Reduce risk of Contrast-induced Nephropathy (CIN): aggressive volume expansion with isotonic crystalloids (normal saline solution) before and after contrast agent, administration of low or iso-osmolar nonionic contrast media, alkalinize urine with sodium bicarbonate, minimal necessary dose of contrast media, stopping the intake of nephrotoxic drugs 24 hours before contrast media injection, avoiding short intervals between contrast procedures MRI contrast are mostly chelates of gadolinium and are less nephrotoxic than iodinated radio contrast when used in small doses Gadolinium should not be used for patients with a GFR less than 30ml/min

Etiologies of Prerenal Acute Kidney Injury

•Any physiologic event that results in renal hypoperfusion oProlonged hypotension (sepsis, vasodilation) oProlonged low CO (HF, cardiogenic shock) oProlonged volume depletion (dehydration, hemorrhage) oRenovascular thrombosis (thromboemboli) •Medications •ACE-I and ARBs, NSAIDS (r/t inhibition of prostaglandins) Any condition that decreases blood flow, blood pressure, or kidney perfusion before arterial blood reaches the renal artery that supplies the kidney may be anatomically described as prerenal AKI. When arterial hypoperfusion secondary to low cardiac output, hemorrhage, vasodilation, thrombosis, or other cause reduces the blood flow to the kidney, glomerular filtration decreases, and consequently urine output decreases. This is a major reason the critical care nurse monitors urine output on an hourly basis. ACE -I and ARBS - causes increased efferent arteriolar resistance NSAIDS - disrupt prostaglandin-mediated afferent arteriolar vasodilation Initially, in prerenal states, the integrity of the kidney's nephron structure and function may be preserved. If normal perfusion and cardiac output are restored quickly, the kidney recovers with no permanent injury. Prerenal azotemia is associated with a lower mortality rate than other forms of AKI. - Azotemia = elevated levels of urea and other nitrogen compounds in the blood.

Patho of Prerenal Acute Kidney Injury

•Autoregulatory capacity is overwhelmed thus causing a GFR declines •Increased Na and H20 reabsorption •Urinary volume <400 mL/d or < 0.5 mL/kg/hr = Oliguria, specific gravity is increased, Urine Na is low •BUN and creatinine rise; BUN:Cr ≥20:1 ( You are going to get more BUN, because of the metabolism increase) In prerenal AKI, autoregulatory capacity is overwhelmed and the GFR decreases, changes in urinary composition and volume occur. When the GFR decreases, the amount of tubular fluid is reduced, and the fluid travels through the tubule more slowly. This results in increased sodium and water reabsorption. Because of the reduced renal circulation, the solutes reabsorbed from the tubular fluid are removed more slowly than normal from the interstitium of the renal medulla. This results in increased medullary tonicity, further augmenting water reabsorption from the distal tubular fluid. Oliguria, defined as urine output less than 400 mL/day, or urine output less than 0.5 mL/kg per hour, with an elevated serum creatinine, is a classic finding in AKI. However, if the prerenal insult is not corrected, GFR declines, blood urea nitrogen (BUN) concentration rises (prerenal azotemia), and the patient develops oliguria and is at risk for significant kidney damage. An increase in systemic BP does not necessarily imply improvement in renal perfusion. Medications that vasoconstrict may be associated with further reduction in renal blood flow as a consequence of constriction of the renal arteries. This is manifested by a further fall in urinary volume and rise in specific gravity. In turn, if the hypoperfusion state is more appropriately and specifically treated by replacement of volume, improvement of cardiac output, correction of dysrhythmias, or a combination of these approaches, the improved renal perfusion is manifested as an increased urinary volume and urine sodium concentration and as a decreased specific gravity of the urine. This ability to reverse prerenal AKI is the key to its diagnosis. AKI can also occur in the CKD patient if the CKD patient is suddenly stressed and what normal person's kidney function can take, that can take them in to an AKI symptom.

Blood Urea Nitrogen and Creatinine Levels

•Blood Urea Nitrogen (BUN) •Result of protein degradation (cell catabolism) •Prerenal ≥ 20:1 •Intrarenal: normal 10:1 •BUN to Creatinine ratio •Serum Creatinine (Cr) •Sensitive indicator of renal function •Trending is critical for critically ill patients •Small increase may signal a significant decrease in GFR •Creatinine Clearance •Normal 120 ml/min; ↓ with kidney failure Serum tests for BUN and creatinine are essential not only for diagnosing AKI but also for helping to distinguish between prerenal AKI and ATN or postrenal AKI. BUN: Not a reliable indicator of kidney injury as an individual test because it is changed by protein intake, blood in the GI tract, and cell catabolism and it is diluted by fluid administration. The BUN level is analyzed in relation to the creatinine level as a ratio. In prerenal AKI, the BUN-to-creatinine ratio is increased from the normal ratio of 10:1 to more than 20:1. This finding is caused by a state of dehydration and by the fact that, as the tubules become more permeable to sodium and water in prerenal AKI, urea is also passively reabsorbed. In ATN and postrenal AKI, when the concentrating ability of the kidneys is impaired, both the BUN and creatinine increase proportionally, maintaining the normal 10:1 ratio. Serum creatinine level is assessed daily to follow the trend of kidney function. The urinary creatinine clearance can be measured if the patient is making sufficient urine. Creatinine Clearance If the patient is making sufficient urine, urinary creatinine clearance can be measured. A normal urinary creatinine clearance rate is 120 mL/min, but this value decreases with kidney failure. Critical care patients with severe AKI manifest elevated serum creatinine and may be oliguric. Consequently, the urinary creatinine clearance rate is rarely measured during critical illness.

Management of Electrolyte Imbalances: Potassium

•Caution > 6 mEq/L •Peaked T waves •Widened QRS •Eventually VTACH/FIB Treatment: Immediate cardio-protective measures •Insulin •Kayexalate •Dialysis Typical ECG findings indicative of various degrees of hyperkalemia. A: (K+) level is about 6 to 7 mEq/L, the T waves peaked, PR int. prolonged, and ST segment is depressed. B: At about 8 to 9 mEq/L, the P wave is lost. C: At about 10 to 11 mEq/L, the QRS complex widens. Hyperkalemia is a life-threatening condition seen in patients with AKI and CKD. As the GFR decreases, the ability of the kidneys to excrete excess potassium diminishes. In critically ill patients, this renal impairment is frequently compounded by states of increased catabolism, acidosis, cellular injury, administration of potassium-based medications, and blood transfusions, all of which can raise serum potassium levels. The first ECG changes that occur, usually when serum potassium is in the range of 6 to 7 mEq/L, are the appearance of tall, tented T waves and a prolonged PR interval. Next, there is a loss of the P wave and a slight widening of the QRS complex. At this point, the serum potassium is usually in the range of 8 to 9 mEq/L. From here, the QRS complex continues to widen until a sine wave (wavy line) pattern develops. This ominous sign is closely followed by ventricular fibrillation or standstill. If hyperkalemia is identified, all potassium supplements are stopped. If the patient is producing urine, IV diuretics can be administered. Acute hyperkalemia can be treated temporarily by IV administration of insulin and glucose. An infusion of 50 mL of 50% dextrose accompanied by 10 units of regular insulin forces potassium out of the serum and into the cells. To treat smaller increases in serumpotassium, nonabsorbablepotassium-binding resins may beused. The binding resins can beadministered orally, through anasogastric (NG) tube, or rectallyto treat hyperkalemia. Cationexchange resins employ eithersodium (Kayexalate) or calcium(Sorbisterit, Ca-Resonium,Argamate) and exchange thecation for potassium across thegastrointestinal wall. Thepotassium is contained in thelower gastrointestinal tract and iseliminated with the stool.Potassium-binding resins anddialysis are the only permanentmethods of potassium removal totreat hyperkalemia.

Staging of Kidney Injury

•Clinical Practice Guidelines -Acute Kidney Injury Staging •Kidney Disease Improving Global Outcomes (KDIGO) •Acute Disease Quality Initiative (ADQI) •Acute Kidney Injury Network (AKIN) -Chronic Kidney Disease •KDIGO

Pathophysiology of CKD

•Common morphologic features: -Fibrosis, loss of native renal cells, infiltration by monocytes and macrophages •Intact nephron theory: -Hyperfiltration response in non-diseased nephrons enable the kidneys to maintain excretory and hemostatic functions -Eventually nephrons reach maximal filtration -Prolonged hyperfiltration may accelerate loss of nephrons •Possible mediators of CKD progression are: -Hypoxia, proteinuria, and angiotensin II The outstanding common morphologic features seen in CKD include fibrosis, loss of native renal cells, and infiltration by monocytes and macrophages. The mediators of the process are many and include abnormal glomerular hemodynamics, hypoxia, proteinuria, and vasoactive substances such as angiotensin II. Intact nephron theory: because each of the more than 1 million nephrons in each kidney is an independent functioning unit, as renal disease progresses nephrons can lose function at different times. When an individual nephron becomes diseased, nephrons in close proximity increase their individual filtration rates by increasing the rate of blood flow and hydrostatic pressure in their glomerular capillaries. This hyperfiltration response in the nondiseased nephrons enables the kidneys to maintain excretory and homeostatic functions, even when up to 70% of the nephrons are damaged. Eventually, however, the intact nephrons reach a point of maximal filtration, and any additional loss of glomerular mass is accompanied by an incremental loss in GFR and subsequent accumulation of filterable toxins. Although hyperfiltration is initially an adaptive measure to nephron loss, over time it can accelerate the loss of nephrons, because the hyperfiltration causes endothelial injury, stimulation of profibrotic cytokines, infiltration by monocytes and macrophages, and detachment of glomerular epithelial cells. In addition, hypertrophy of the nondiseased nephrons caused by hyperfiltration leads to increased wall stress and even more injury. This is why many interventions to slow down the progression of renal failure involve measures that reduce glomerular hydrostatic pressure. One such example is the use of ACE inhibitors and ARBs, which prevent angiotensin II-mediated efferent arteriolar vasoconstriction and subsequent nephron hyperfiltration. Other possible mediators of CKD progression are hypoxia and angiotensin II. In CKD, the loss of peritubular capillaries by various causes results in reduced capillary perfusion of the tubules. The resultant hypoxia favors the release of proinflammatory and profibrotic cytokines, leading to fibrosis and cell injury. Angiotensin II stimulates growth factors and cytokines that contribute to fibrosis aside from its hemodynamic effects on the glomerulus. It also promotes glomerular hypertension and hyperfiltration caused by efferent arteriolar vasoconstriction and systemic hypertension.

Anemia

•Etiology -Erythropoietin deficiency •Erythropoetin stimulates bone marrow to produce erythrocytes (RBC) -Decreased RBC survival time -Blood loss -Decrease lifecycle of erythrocyte with dialysis •Management -Epoetin alfa (Epogen, Procrit) -Blood products -Iron supplements, Vitamin B12 & B6, Folate -Blood conservation measures **Anemia is an expected side effect of kidney failure that occurs because the kidney no longer produces the hormone erythropoietin. As a result, the bone marrow is not stimulated to produce erythrocytes (red blood cells). Additionally, the normal erythrocyte survival of 80 to 120 days is decreased in patients with CKD on dialysis to 70 to 80 days, increasing their risk for anemia. Care is taken to prevent blood loss in patients with AKI, and blood withdrawal is minimized as much as possible. Irritation of the gastrointestinal tract from metabolic waste accumulation is expected, and stress ulcer prophylaxis must be prescribed. Anemia associated with CKD may be treated pharmacologically by the administration of recombinant human erythropoietin. Three medications are approved by the FDA for treatment of CKD-associated anemia in the United States: epoetin alfa (Procrit, Epogen), darbepoetin alfa (Aranesp), and methoxy polyethylene glycol-epoetin beta (Mircera). These agents stimulate erythrocyte production by the bone marrow. Adjunctive treatments include administration of iron supplements, vitamin B12 , vitamin B6, and folate.

Management of Fluid Balance in CKD

•Fluid and salt restriction is a mainstay of therapy to prevent fluid overload. •Sodium is restricted to less than 2,000 mg/d •Fluid intake is limited to 500 mL plus the patient's previous day's 24-hour urine output •Diuretics if GFR > 10-15 Clinical management of fluid balance is important for patients with renal failure, and management differs between AKI and CKD In CKD, fluid and salt restriction is a mainstay of therapy to prevent fluid overload. Sodium is restricted to less than 2,000 mg/d, and fluid intake is limited to 500 mL plus the patient's previous day's 24-hour urine output. Diuretics are also used to manage volume overload. Patients are usually able to respond to diuretics until their GRF falls below 10 to 15, at which point extensive renal damage prevents an adequate response. By the time CKD progresses to stage G5, oliguria is typically manifested, and signs and symptoms of fluid overload, such as edema, hypertension, pulmonary edema, heart failure, and jugular vein distention, occur unless dialysis therapy is instituted. An ongoing assessment of fluid status, including obtaining accurate intake and output measurements with daily weights and monitoring for fluid complications, is imperative.

Managing Gastrointestinal Alterations

•GI bleeding •Gastritis, ulcerative esophagitis, duodenitis •Anorexia, nausea and vomiting, diarrhea, GERD, uremic fetor •Stomatitis •Constipation Stopped Here>>>> A potentially life-threatening gastrointestinal complication in both AKI and CKD is gastrointestinal bleeding as it relates to renal failure include platelet and blood-clotting abnormalities; anticoagulation with dialysis, access patency, or both; ingestion of irritating drugs (eg, NSAIDs, aspirin); arteriovenous malformations (with CKD), and increased ammonia production in the gastrointestinal tract from urea breakdown. High urea levels are prone to cause gastritis, ulcerative esophagitis, and duodenitis as evidenced by biopsy. Assessment parameters include examining all vomit and stool for gross and occult blood; monitoring iron, hemoglobin, hematocrit, and red blood cell indices; and paying close attention to signs of intravascular volume depletion. If gastrointestinal bleeding is suspected, radiographic and endoscopic examinations are often required to diagnose and treat specific lesions. Management depends on the specific lesion, but often includes volume restoration with crystalloids and blood products as well as administration of histamine-2 receptor (H2) blockers, proton-pump inhibitors (PPIs), or both. Other gastrointestinal complications associated with renal failure occur primarily in CKD and include anorexia, nausea, vomiting, diarrhea, constipation, gastroesophageal reflux disease (GERD), and oral cavity alterations, such as stomatitis, a metallic taste in the mouth, and uremic fetor (the smell of urine and ammonia on the breath). Oral alterations and symptoms of anorexia, nausea, and vomiting are partially attributable to high levels of uremic toxins, which affect the intestinal mucosa and stimulate vomiting centers in the brain. The reason GERD is common is unclear, but it may be due to delayed gastric emptying, increased gastrin production, and use of medications that affect lower esophageal sphincter tone (ie, calcium-channel blockers). Collaborative management involves initiating (or providing) adequate dialysis, providing prophylactic antacids and H2 blockers or PPIs, and administering antiemetics. Good oral hygiene is also essential.

Clinical Manifestations/Physical Exam of AKI

•Gen: Fatigue, muscle weakness...etc. •Neuro: Confusion, apathy, lethargy, obtundation, coma, HA...etc. •GI: Anorexia, nausea, vomiting, GI bleed...etc. (The build up the waste products builds up a nauseous effect, also if your kidneys are not perfusing your GI is probably not perfusing) •Resp: Acute respiratory distress, pneumonia •CV: Dysrhythmias, HTN, AMI, Pericarditis, HF..etc. •Skin: Edema, pruritus •Hem: Anemia, T-Cell supp.,Infec..etc •Immune: T-Cell supp., Infec. IV site, wounds, lungs, UTI (metabolic acidosis could lead to a decrease in the immune function, we can cause a problem in the reproduction of the cells, usually a late sign) •Lytes: K, Phos, Mg, Na, Ca, HCO3, pH

Management of Electrolyte Imbalances: Calcium and Phosphorus

•Hypocalemia with hyperphosphatemia > 5.5 mg/dL •Treatment: Replace calcium w/ Vit. D, limit phosphate in diet in combination with Phos binders (Sevelamer hydrochloride and lanthanum carbonate) •Dialysis for acute or dramatic rise in phosphate - S/S of hyperphosphatemia is pruritis (severe itching) Serum calcium levels are reduced (hypocalcemia) in kidney failure due to multiple factors, including hyperphosphatemia. Chronically elevated serum phosphorus levels, above 5.5 mg/dL, are associated with higher mortality rates for patients with kidney failure. Most calcium in the bloodstream is bound to protein. Calcium levels can be measured in two ways: total calcium (tCa) or ionized calcium (iCa). Unfortunately, protein-calcium binding confounds the measurement of accurate calcium levels. The metabolically active, non-protein-bound portion is known as the ionized calcium and is the preferred method of measurement. Maintaining adequate calcium stores in the body is achieved by administration of calcium supplements and vitamin D. A second method used in tandem with calcium supplements to achieve normal calcium levels is to lower the level of phosphorus in the blood stream. Phosphorus occurs in many foods. After ingestion, a medication binding agent may be administered orally or by nasogastric tube. After the dietary phosphorus is bound to the binding substance, it is eliminated from the body, lowering the serum phosphorus level. There are three generations of dietary-phosphorus binders. The third-generation binders are non-aluminum-, non-calcium-based medications. They include sevelamer hydrochloride (RenaGel) and lanthanum carbonate (Fosrenol).

Management of Electrolyte Imbalances: Sodium

•Hyponatremia <135 mEq/L Clinical Findings: Disorientation, muscle twitching, nausea, vomiting, abdominal cramps, headaches, dizziness seizures, postural hypotension, cold, clammy skin, decreased skin turgor tachycardia, oliguria •Hypernatremia >145 mEq/L Clinical Findings: Extreme thirst, dry, sticky mucous membranes, altered mentation, Seizures (later stages) Sodium Alterations in sodium level are an expected finding in kidney failure (see Table 26.4 ). Both hypernatremia (elevated serum sodium) and hyponatremia (low serum sodium) are associated with increased mortality with kidney failure this is unrelated to whether or not the patient has a diagnosis of heart failure. -Q4 hours oral care, Good oral care is one of the most important things you can do to help prevent pneumonia

Pharmacologic Management: Osmotic Diuretics

•Increases urine output because higher plasma osmolality, increases flow of water from tissues, causing increased GFR, increased serum sodium, potassium levels •Osmotic diuretics, such as mannitol, are prescribed to increase urine output and decrease fluid overload. •Mannitol is filtered by the glomerulus, not absorbed by the nephron, and works in the proximal tubule and the descending section of the loop of Henle via aquaporin water channel.

Pharmacologic Management: Vaptans

•Inhibit the effect of antidiuretic hormone (vasopressin) on the V2 aquaporin channels in the collecting ducts of the kidney. •Blockage of the aquaporin channels renders the collecting ducts impermeable, resulting in solute-free water excretion or aquadiuresis. •Vaptans are used to correct symptomatic hypervolemic hyponatremic (dilutional) states. •The clinical intent is to eliminate water and retain sodium. A new class of medications collectively described as vaptans inhibits the effect of antidiuretic hormone (vasopressin) on the V2 aquaporin channels in the collecting ducts of the kidney. Blockage of the aquaporin channels renders the collecting ducts impermeable, resulting in solute-free water excretion or aquadiuresis. Vaptans are used to correct symptomatic hypervolemic hyponatremic (dilutional) states. The clinical intent is to eliminate water and retain sodium.

Ischemic Acute Tubular Necrosis

•Ischemia causes -Reduced levels of ATP - and increases Toxic oxygen-free radicals (loss antioxidant protection) •Cell swelling, injury, necrosis -Necrotic cells block the tubular lumen. •Due to prolonged hypoperfusion and microemboli - BUN: Cr thus causing a 20:1 (r/t systemic effects of prerenal hypoperfusion/ischemia) Ischemic ATN results from prolonged hypoperfusion. A sequence of pathophysiologic processes results in the sloughing off of necrotic cells that block the tubular lumen. Ischemic ATN causes profound renal vasoconstriction and reduced renal blood flow. Vasoconstriction is caused by norepi, angiotensin II, thromboxane A2, and more.

Pharmacologic Management: Dopamine

•Low-dose dopamine (2 to 3 mcg/kg/min), previously known as renal-dose dopamine, is infused to stimulate blood flow to the kidney. (THIS IS NOT USED OFTEN ANYMORE) •Dopamine is effective in increasing urine output in the short term, but tolerance may develop. •Prolonged vasopressor use may worsen pre-renal injury Low-dose dopamine (2 to 3 mcg/kg/min), previously known as renal-dose dopamine, is frequently infused to stimulate blood flow to the kidney. Dopamine is effective in increasing urine output in the short term, but tolerance may develop.

Management of Skeletal Alterations

•Management of skeletal alteration includes loss of bone density and formation of calcium phosphate crystals. -Goals of care: •Regulate phosphate •Maintain calcium levels •Treat vitamin D deficiency •Control metabolic acidosis In renal failure, disturbances in calcium and phosphate balance set the stage for secondary hyperparathyroidism and high-turnover renal osteodystrophy (renal bone disease). As the GFR declines, glomerular filtration of phosphate also decreases, and serum phosphate levels begin to rise. This results in decreased serum ionized calcium levels because calcium binds with phosphate. Calcium decrease because of the kidneys' inability to convert vitamin D to its active form, which is needed for adequate intestinal absorption of calcium. In response to decreased ionized calcium levels, elevations in serum phosphorus levels, and reduced vitamin D3 synthesis, the parathyroid glands secrete parathyroid hormone (PTH). Over time, the continuous PTH stimulation leads to hyperplasia and proliferation of the parathyroid cells, resulting in secondary hyperparathyroidism. PTH causes the reabsorption of calcium and phosphate salts from bones, thus increasing the serum calcium level at the expense of bone density and mass. PTH also causes calcium reabsorption and phosphate excretion in the kidneys; however, as renal failure progresses, this effect of PTH is not realized. Eventually, as calcium and phosphate continue to be reabsorbed from bones, both levels rise in the serum concomitantly. Calcium phosphate crystals can form and precipitate in various parts of the body (a condition known as metastatic calcifications), including the brain, eyes, gums, valves of the heart, myocardium, lungs, joints, blood vessels, and skin. Other insults to bones that can occur in renal disease include bone demineralization in response to metabolic acidosis and low-turnover renal osteodystrophy from aluminum deposits in the bone or overuse of vitamin D3 therapy. Complications from renal bone disease include bone pain, fractures, pseudogout from deposits of calcium oxalate in synovial fluid, periarthritis from calcifications of the joints, proximal muscle weakness, spontaneous tendon rupture, and pruritus. Metastatic calcifications can result in calcified blood vessels and valves, skin lesions, red-eye syndrome from crystal deposition in the conjunctiva, and, most seriously, ischemic ulcers.

Managing Integumentary Alterations

•Managing of integumentary alterations include dryness, pruritus, uremic frost, ecchymosis, and purpura. •Pigment changes include hyperpigmentation (PERMANENT SKIN COLOR CHANGE USUALLY) •Contributing factors: iron deficiency anemia, decreased sweat and sebaceous glands, deposition of calcium phosphate into the skin, hyperparathyroidism, hyperphosphatemia Alterations in the integumentary system in renal failure include xerosis (dryness), pruritus, pallor, ecchymosis and purpura, and pigmentation changes. Pigment changes include hyperpigmentation, especially at sun-exposed sites, or a yellow discoloration to the skin. CKD is also associated with hair loss and nail changes, such as the absence of the lunula, splinter hemorrhages, Beau lines (white lines across the fingernails), and onychomycosis. Possible contributing factors to these alterations are iron deficiency anemia, decreased activity of sweat and sebaceous glands, retained skin pigments, platelet dysfunction and capillary fragility, deposition of calcium phosphate crystals into the skin, hyperparathyroidism, hyperphosphatemia, increased vitamin A levels in the epidermis, and impaired cellular immunity. Uremic frost, a white powdery substance composed of urates on the skin, is due to crystallization of urea; These skin alterations, particularly pruritus and xerosis, may lead to localized infection from excoriation and secondary skin changes, such as lichen simplex and keratic papules. Collaborative management for skin alterations includes phosphate regulation, nutritional supplementation, correction of anemia, antihistamine medications, and meticulous skin care and turning to prevent skin breakdown. Dialysis therapy helps as well by removing metabolic waste products. However, because of potential allergies to the dialysis system components, dialysis therapy can also aggravate some conditions, such as pruritus. Patient education should include information on factors contributing to skin alterations, the importance of keeping the skin clean and well moisturized, and ways to avoid excoriation (such as keeping the fingernails trimmed).

Fractional Excretion of Na+ (FENa)

•Measured early to differentiate between prerenal AKI and intrarenal AKI (parenchymal). •A FENa value below 1% suggests prerenal compromise -The kidneys reabsorb sodium and water in an attempt to increase circulatory volume •A FENa value above 2% implies the kidneys cannot reabsorb the sodium due to kidney damage. •Invalid with diuretic use in past 24 hrs •Required values to calculate FENa are Serum Na, Urine Na, Serum Cr, Urine Cr The fractional excretion of sodium (FENa) in the urine can be measured early to differentiate between prerenal AKI and intrarenal AKI (parenchymal). An FENa value less than 1% (in the absence of diuretics) suggests prerenal compromise because resorption of almost all of the filtered sodium is an appropriate response to decreased perfusion to the kidneys. A FENa value above 2% implies the kidney cannot concentrate the sodium and that the damage is intrarenal (ATN). Urinary sodium is measured in milliequivalents per liter (mEq/L). If diuretics are administered, the test is meaningless. A urinary sodium concentration less than 10 mEq/L (low) suggests a prerenal condition. A urinary sodium level greater than 40 mEq/L (in the presence of an elevated serum creatinine and the absence of a high sodium load) suggests intrarenal damage has occurred. The use of diuretics invalidates any results. (The interpretation of results is similar to the FENa.) Urinary sodium is measured inmilliequivalents per liter. Interpretation ofresults is similar to the FENa. Aurinary sodium concentrationless than 10 mEq/L (low)suggests a prerenal condition. Aurinary sodium level greater than40 mEq/L (in the presence ofelevated serum creatinine andthe absence of a high sodiumload) suggests that intrarenaldamage has occurred

Management of Acid-Base Alterations

•Metabolic acidosis -AKI and CKD typically result in metabolic acidosis because of the nephrons' inability to secrete and excrete hydrogen ions and reabsorb bicarbonate ions as renal failure progresses -In CKD, metabolic acidosis begins to manifest as the patient reaches G stage 3a and the GFR falls below 60 mL/min/1.73 m2. •Clinical manifestations: HA, N/V, deep & rapid resp. (Kussmaul resp.), altered mental status, hyperkalemia, tyachycardia •IV sodium bicarbonate (severe acidosis) - Evidenced by a blood pH < 7.2 or a plasma bicarbonate < 12 to 14 mEq/L) AKI and CKD typically result in metabolic acidosis because of the nephrons' inability to secrete and excrete hydrogen ions and reabsorb bicarbonate ions as renal failure progresses. In critically ill patients, this acid-base disturbance may be intensified because of concurrent conditions, such as lactic acidosis or diabetic ketoacidosis, and because such patients are in a high-catabolic state, which increases the release of intracellular acids into the circulation. Clinical manifestations of metabolic acidosis include headaches, nausea and vomiting, deep and rapid respirations (Kussmaul respirations), altered mental status, hyperkalemia, and tachycardia. In severe metabolic acidosis, bradycardia and hypotension may manifest because of myocardial depression and vasodilation. There is also a dramatic depression of the patient's level of consciousness, often resulting in stupor or coma. In CKD, metabolic acidosis begins to manifest as the patient reaches G stage 3A and the GFR falls below 60 mL/min. Although the metabolic acidosis associated with CKD is usually mild (CO2, 16 to 22 mEq/L), it is associated with many adverse consequences, including fatigue, protein catabolism, and bone demineralization. The bones become demineralized because bone phosphate and carbonate are used as buffers against excess hydrogen ions. Laboratory assessments of acid-base status using arterial blood gas (ABG) values and venous carbon dioxide content guide therapy. Patients with a plasma bicarbonate level less than 22 mEq/L warrant treatment. Therapy involves the administration of alkaline medications (eg, Bicitra, sodium bicarbonate tablets), dialysis, or both. The use of IV sodium bicarbonate is reserved for severe acidosis (evidenced by a blood pH < 7.2 or a plasma bicarbonate level less than 12 to 14 mEq/L) because of potential complications of extracellular volume excess, metabolic alkalosis, and hypokalemia. Intractable acidosis is an indication for dialysis, which removes excess hydrogen ions and adds a buffer to the body. Throughout any kind of acid-base therapy, it is necessary to monitor serum bicarbonate, pH, and calcium and potassium levels closely.

Pharmacologic Management: Acetylcysteine

•N-Acetylcysteine (Mucomyst, Mucosil) is an N-acetyl derivative of the amino acid l-cysteine. •It has been used for many years as a mucolytic agent to assist with expectoration of thick pulmonary secretions. It is also prescribed for patients with mildly elevated serum creatinine levels before a radiologic study using contrast dye.

Urine Output Patterns

•Nonoliguria -(greater than 500 mL/d) •Oliguria - (less than 500 mL/d) •Anuria -(less than 50 mL/d)

Managing Alterations in Psychosocial Functioning

•Patients often experience feelings of fear, anxiety, and powerlessness. Patients frequently have an alteration in self-concept as well as body image disturbances because of both physical and functional changes that occur in renal failure Patients and their families may have difficulty coping owing to stress, limited resources or support, inadequate or ineffective coping mechanisms, interruptions in usual family roles, or a combination of these factors. It is important that the health care team attend to these and other psychosocial complications of renal failure to treat the patient and family holistically. Specific interventions include thorough patient and family teaching, active involvement of the patient and family members in managing the condition, ensuring adequate rest and sleep for the patient, exploring the patient's and family's feelings and concerns, providing support, and obtaining the active involvement of social services and clergy as appropriate.

Diagnostic Studies Kidneys

•Renal Ultrasonography oR/O obstruction •CT and MRI oEvaluate for masses, vascular disorders and filling defects •Renal angiography oEvaluate for renal artery stenosis •Renal biopsy oDiagnosis, prognosis, and therapy evaluation Renal ultrasonography, an important diagnostic test in the evaluation of AKI, is especially useful in ruling out an obstruction, and has the advantage of being noninvasive. With a high-grade obstruction, dilation of the urinary collecting system is detectable on ultrasonography within 1 to 2 days of the onset of the obstruction. Ultrasonography may also reveal proximal renal calculi as a cause of postrenal obstruction. In addition, it can be used to estimate renal size, which is helpful in distinguishing between AKI and advanced CKD. Often in advanced CKD, the kidneys are small (less than 9 cm) and echogenic. CT and MRI to evaluate for masses, vascular disorders, and filling defects in the collecting system, and renal angiography to evaluate for renal artery stenosis. It is notable that the iodinated contrast media used in some studies are allergenic and nephrotoxic, and that GBCAs can cause NSF in patients with severe kidney disease (GFR < 30 mL/min). Renal biopsy may be helpful in patients thought to have intrarenal AKI that is not ATN, especially if significant proteinuria or unexplained hematuria is revealed on urinalysis. In addition to having diagnostic value, the results of a biopsy may help determine prognosis and therapy. For any diagnostic test, the benefits of the study must be weighed against potential risks.

Renal Auto-Regulation

•Renin - angiotensin - aldosterone System (RAAS) • In response to ↓ renal perfusion à Renin released from the JGA (afferent arterioles) •Renin à Angiotensin II and the release of aldosterone from the adrenal cortex •Resulting systemic vasoconstriction and sodium water retention -Prostaglandin Synthesis •Locally acting vasodilators and inhibit the aggregation of blood platelets. •PGE1 & PGI2 produced locally within the kidney in response to decreased RBF. -When we give NSAIDS we prevent prostogladin formation and thus the kidneys ability to protect themselves Decrease in renal perfusion results in the release of renin from juxtaglomerular cells in the walls of the afferent arterioles. This activates the renin-angiotensin-aldosterone cascade, the end result being the production of angiotensin II and the release of aldosterone from the adrenal cortex. Angiotensin II causes profound systemic vasoconstriction, and aldosterone induces sodium and water retention. Angiotensin II also helps maintain the GFR by increasing efferent arteriolar resistance and by stimulating intrarenal vasodilator prostaglandins, increasing hydrostatic pressure in the glomeruli. In this way, the kidneys can preserve the GFR over a wide range of mean arterial pressures. However, when renal perfusion is severely compromised, the capacity for autoregulation is overwhelmed, and the GFR decreases. Even with moderate hypovolemia or congestive heart failure, certain drugs, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and nonsteroidal anti-inflammatory drugs (NSAIDs), can overwhelm the kidney's ability to autoregulate. Early on autoregulatory mechanisms maintain GFR through afferent arteriole dilation and efferent arteriole vasoconstriction mediated by angiotensin II/prostaglandins (PGE1 and PGI2). Because of these characteristic changes associated with renal underperfusion, measurement of urinary volume, urinary sodium, and specific gravity is a simple method for determining the effect of management on renal perfusion.

Kidney Disease Improving Global Outcomes (KDIGO)

•Requires: at least 2 serum creatinine values within 48 hours •Requires: exclusion of urinary tract obstruction or other easily reversible causes •1st deliver adequate fluid resuscitation, as applicable Kidney Disease/Improving Global Outcomes (KDIGO) Serum creatinine: These criteria include an absolute and a percentage change in creatinine to accommodate variations related to age, sex, and body mass index and to reduce the need for a baseline creatinine level, but they do require at least two serum creatinine values within 48 h. Urine output: The urine output criterion was included based on the predictive importance of this measure but with the awareness that urine outputs may not be measured routinely in non-critical care unit settings. It is assumed that the diagnosis based on the urine output criterion alone will require exclusion of urinary tract obstructions that reduce urine output or of other easily reversible causes of reduced urine output. Clinical context: These criteria should be used in the context of the clinical presentation and after adequate fluid resuscitation when applicable. Many acute kidney diseases exist, and some may result in AKI. Because diagnostic criteria are not documented, some cases of AKI may not be diagnosed. Physiologic state: AKI may be superimposed on or lead to chronic kidney disease.

Hypertensive Nephrosclerosis

•Sclerotic lesions develop in renal arterioles and glomerular capillaries causing them to become thickened & narrowed. •Directly caused by high BP Systemic hypertension may result in a condition known as nephrosclerosis. This involves the development of sclerotic lesions in the renal arterioles and glomerular capillaries that cause them to become thickened, narrowed, and eventually necrotic. This can be benign or malignant. In benign nephrosclerosis, associated with chronic mild or moderate hypertension, renal impairment occurs over many years. Malignant nephrosclerosis, associated with malignant hypertension, can lead to permanent renal failure rapidly if BP is not immediately reduced. Because hypertensive nephrosclerosis is directly caused by hypertension, its incidence is greater in populations with a higher incidence of primary hypertension (eg, elderly people, African Americans). Patients often remain asymptomatic until extensive damage has occurred. BP control is essential, and often multiple antihypertensive medications are required.

History and Physical Examination when looking for an AKI

•Screen for history that indicates hypoperfusion and may lead to decreased renal perfusion -Acute MI, cardiovascular surgery, cardiac arrest, high fever, use of certain drugs, recent trauma •History of any diseases that affect the renal system -Renal artery stenosis (r/t i.e. atherosclerotic disease) -Lupus or vasculitis -Abdominal tumors •Fluid status By taking a detailed history, clues to the categorization and exact cause of the AKI can be obtained. Important indications in the history that suggest prerenal AKI include any event or condition that may have contributed to decreased renal perfusion (eg, acute MI, cardiovascular surgery, cardiac arrest, high fever, any shock state, and the use of certain drugs, such as NSAIDs). Also, a history of atherosclerotic disease may be a clue to renal artery stenosis, another precipitant of prerenal AKI. Clues to an intrarenal cause provided by the history include any prolonged prerenal event or condition as well as exposure to nephrotoxins, especially aminoglycoside antibiotics and radiocontrast media. It is also important to collectinformation about systemic diseasessuch as lupus or vasculitis,recent streptococcal infections,and causes of heme pigmenttoxicity, such as rhabdomyolysis(eg, a history of trauma or apatient found unconscious for anunknown amount of time). Inaddition, a history of cardiaccatheterization, anticoagulation,and thrombolytic therapyincreases the possibility ofatheroembolic intrarenaldiseases. Findings that maypoint to postrenal AKI includeany history of abdominal tumorsor calculi, and especially ahistory of benign prostatichypertrophy in elderly men. Afamily history of urolithiasis orbenign prostatic hypertrophy maybe contributory.

Chronic Kidney Disease (CKD)

•Slow, progressive, irreversible deterioration of renal function •Results in kidney's inability to eliminate waste products and maintain fluid and electrolyte balances •Leads to end-stage renal disease (ESRD) CKD is a slow, progressive, irreversible deterioration in renal function that results in the kidney's inability to eliminate waste products and maintain fluid and electrolyte balance. Ultimately, it leads to end-stage renal disease (ESRD) and the need for RRT or renal transplantation to sustain life. Currently, there are more than 615,000 dialysis and renal transplant recipients in the United States, which is a 26% increase in prevalence since the year 2000. Among ESRD patients, incidence rates are higher in men than in women and are higher with increasing age. The incidence rates in the African American population are 3.4 times greater than in the white population. Hispanics and Native Americans also have higher incidence rates than whites, but the difference in rates is not as dramatic. Factors postulated to contribute to the increasing prevalence of ESRD include changes in the demographics of the population, differences in disease burden among racial groups, under-recognition and undertreatment of earlier stages of CKD, under-recognition of the risk factors for CKD, and increased survival of patients with ESRD. Increasing evidence shows that early detection and treatment of CKD may prevent, or at least delay, progression to ESRD. Consequently, it is important that opportunities to prevent and treat CKD are not lost secondary to under diagnosis or under treatment.

Pharmacologic Management: Potassium-Sparing

•Spironolactone inhibits the aldosterone mineralocorticoid receptor in the late distal tubule and collecting duct of the kidneys, causing potassium to be retained and sodium to be excreted.

Management of Fluid Balance in AKI

•Treat hypovolemia - crystalloids •Prevent hypervolemia •Use of diuretics •Fluid Restriction (in the setting of oliguria) •Diuretics •Dopamine (no longer recommended) •Dialysis or ultrafiltration Fluid Balance Changes in Acute Kidney Injury Therapy involves prompt administration of replacement fluids, such as blood and crystalloids. The replacement solutions used should reflect the type of losses (eg, for a patient with a hemorrhagic condition, blood would be the replacement fluid of choice). Often in AKI, even if signs and symptoms of intravascular volume deficits are not present, large boluses of IV fluids are given. Reversal of AKI after such a bolus is therapeutic as well as diagnostic of prerenal AKI. Fluid administration in AKI is also indicated for the prevention or alleviation of tubular obstruction seen in obstructive causes of AKI, including ATN and many postrenal etiologies. However, in any oliguric state, caution must be taken to prevent fluid overload. In a sustained oliguric state, such as the oliguric stage of ATN, fluid is restricted to the previous day's urine output amount plus 500 to 800 mL to account for insensible losses. Diuretics are often used in AKI to increase urinary flow and thereby help alleviate conditions of fluid overload or to prevent tubular obstruction. In states of fluid overload, such as pulmonary edema and heart failure, diuretics are also useful. Furosemide is administered every 6 hours, with the initial dose ranging between 20 and 100 mg. Dopamine is another agent that has been traditionally used in AKI because of its ability to theoretically cause renal vasodilation at "renal doses" (1 to 3 mcg/kg/min), thereby increasing renal perfusion. If fluid complications arise and cannot be controlled by fluid restrictions and pharmacologic agents, dialysis or isolated ultrafiltration may be necessary. This is often the case in oliguric patients who are receiving large amounts of IV fluids hourly in the form of medications and nutritional supplements. People in whom AKI develops secondary to hypoperfusion or tubular injury may have a delayed recovery time, necessitating maintenance dialysis until the tissue repairs itself and normal function returns. Daily Weight A less "high-tech" method but also important is a daily weight. The daily weight, combined with accurate intake and output monitoring, is a powerful indicator of fluid gains or losses over 24 hours. A 1-kg weight gain over 24 hours represents 1000 mL (1 liter) of additional fluid retention. Physical Assessment - Signs that suggest extracellular fluid depletion include thirst, decreased skin turgor, and lethargy. Signs that imply intravascular fluid volume overload include pulmonary congestion, increasing heart failure, and rising blood pressure. A patient with untreated AKI is edematous. The following factors contribute to this state: In critical illness, even though there is peripheral edema, and the patient may have gained 8 L of fluid over his or her "dry-weight" baseline, the patient may remain "intravascularly dry" and hemodynamically unstable because the retained fluid is not inside a vascular compartment and cannot contribute to maintenance of hemodynamic stability. A patient with AKI is assessed frequently for pitting edema over bony prominences and in dependent body areas.

Causes of CKD

•Two most common: -Diabetes (44%) and Hypertension (28%) •Other common causes include -Glomerulonephritis -Interstitial nephritis -Congenital malformations -Genetic disorders -Neoplasms -Hepatorenal syndrome -Obstructive uropathy -Microangiopathic The causes of CKD are numerous. By far, the two most common causes are diabetes mellitus and hypertension, which account for more than 44% and 28% of incident cases of ESRD, respectively. Other causes include glomerulonephritis (both primary and secondary to systemic diseases), interstitial nephritis, congenital malformations, genetic disorders, neoplasms, hepatorenal syndrome, obstructive uropathy, and microangiopathic etiologies, such as scleroderma and atheroembolic disease.

Laboratory Studies

•Urinary Values - Urine sodium, osmolality, and specific gravity distinguish AKI from ATN •Fractional excretion of Na+ (FENa) (Look at picture) •Sedimentation •Serum Values •Diagnostic Studies -Acute kidney injury (AKI) is a sudden and temporary loss of kidney function, while acute tubular necrosis (ATN) is kidney injury characterized by acute tubular cell injury and dysfunction. Laboratory assessment, critical to the diagnosis and categorization of AKI, includes both serum and urinary values. For a basic comparison of laboratory values in prerenal AKI, postrenal AKI, and ATN. In addition to helping differentiate between prerenal, intrarenal, and postrenal AKI, blood and urine tests are also helpful for diagnosing the underlying etiology of the AKI. Urinary Values. The urine specimen should be obtained before a diagnostic challenge dose of diuretics is administered because these agents may alter the urine's chemical composition. The urine sodium concentration, osmolality, and specific gravity are especially helpful in distinguishing between prerenal AKI and ATN because these values reflect the concentrating ability of the kidney. In prerenal failure, the hypoperfused kidney actively reabsorbs sodium and water in an attempt to increase circulatory volume. Consequently, the urine sodium level and the fractional excretion of sodium (FENa) are low (less than 20 mEq/L and less than 1%, respectively), whereas the urine osmolality and concentration of nonreabsorbable solutes are high. In contrast, in ATN in which parenchymal damage affects the kidney, the tubular cells can no longer effectively reabsorb sodium or concentrate the urine. As a result, the urine sodium concentration is often greater than 40 mEq/L, the FENa is greater than 2%, and the urine osmolality is close to that of plasma. Unfortunately, there is a limit to the usefulness of these indices because of overlap in these values for prerenal AKI and ATN (ie, urine sodium concentration values in the 20 to 40 mEq/L range). Values at the extremes are thus the most useful. In prerenal AKI, the urinary sediment is normal with only a few hyaline casts, whereas in ATN, coarse, muddy-brown granular casts and tubular epithelial cells are typically found. In postrenal AKI, the sediment is often normal but can be helpful in diagnosing kidney stones.

Pathophysiology: Postrenal AKI

•Urine congestion causes retrograde pressure •Slows tubular fluid flow and lowers GFR •Increased reabsorption Na+, water, and urea •Prolonged pressure dilates collecting ducts which compresses and damages nephrons -Result is dysfunctional ability to concentrate and dilute urine

Pharmacologic Management: Dietary Phosphorus-Binding Medications

•Used in tandem with calcium supplements to achieve normal calcium levels is to reduce the level of phosphorus in the bloodstream -First generation: Aluminum salts (aluminum hydroxide) -Second generation: Dietary phosphorus-binding •Calcium salts including calcium carbonate or calcium acetate (PhosLo) Dietary Phosphorus-Binding Medications A second method used in tandem with calcium supplements to achieve normal calcium levels is to reduce the level of phosphorus in the bloodstream. (Test) ***Phosphorus is present in many foods, especially foods with a high protein content or food additives such as dairy products, processed meats, some carbonated drinks, and nuts. After eating these foods, free phosphorus passes from the gastrointestinal tract into the bloodstream and raises the serum level. Medications that bind dietary phosphorus in the gastrointestinal tract are administered orally or by NG tube. The binding agent must be taken at the same time as a meal. After the dietary phosphorus is bound to the binding substance in the bowel, it is eliminated from the intestine with stool. This lowers the serum phosphorus level. The original binders were aluminum salts (aluminum hydroxide) that bound dietary phosphorus effectively in the gastrointestinal tract but conferred aluminum toxicity because some of the aluminum metal was also absorbed. For this reason, aluminum binders have largely been abandoned. The second generation dietary phosphorus-binding agents that are widely prescribed use calcium salts including calcium carbonate or calcium acetate (PhosLo) to bind dietary phosphorus in the gastrointestinal tract. Calcium-based medications are safer, but elevated serum calcium levels and calcium deposits in other areas of the body (extraosseous calcification) are a problem. A third generation of nonabsorbable dietary phosphorus-binding medications is available. These are non-aluminum-based, non-calcium-based medications and include sevelamer hydrochloride (Renagel) and lanthanum carbonate (Fosrenol). These medications have a good safety profile and are frequently prescribed to lower serum phosphorus levels in patients with CKD.