Glomerular hydrostatic pressure (facilitates):	+50 mm Hg
Colloid osmotic pressure (opposes):	−25 mm Hg
Bowman’s capsule pressure (opposes):	−10 mm Hg
Net pressure favoring filtration:	+15 mm Hg

(1) Clinical assessment tool to determine renal function

(2) Definition: Volume of plasma cleared of a given substance per minute (may be determined by using endogenous creatinine)

(3) GFR equation

where

x = a substance freely filtered through the glomerulus and not secreted or reabsorbed by tubules (e.g., creatinine)

P = plasma concentration of x

V = urine flow rate (ml/min)

U = urine concentration of x

(4) Normal adult GFR: 125 ml/min or 180 L/day

(5) Normal adult urine volume: 1 to 2 L/day, reflecting greater than 99% reabsorption of filtrate

(6) Factors affecting GFR

a) Changes in glomerular hydrostatic pressure

1) Secondary to changes in systemic blood pressure (BP)

2) Caused by variation in afferent or efferent arteriolar tone; increased afferent arteriole resistance decreases GFR; increased efferent arteriole tone increases GFR

b) Alterations in oncotic pressure due to dehydration, hypoproteinemia, or hyperproteinemia

c) Alterations in Bowman’s capsule pressure due to urinary tract or nephron destruction, or interstitial edema of kidney

ii. Tubular functions of reabsorption, secretion, and excretion comprise the following steps in urine formation (Figure 5-3):

FIGURE 5-3 Transport of water and some solutes in the proximal tubule. TF/P, Tubule fluid to plasma ratio. (From Maude DL: Kidney physiology and kidney disease, Philadelphia, 1977, Lippincott.) Lippincott

(a) Conversion of 180 L of plasma filtered per day to 1 to 2 L of excreted urine

(b) Absorption and secretion by two processes:

(1) Passive mechanisms: Solute moves without the expenditure of metabolic energy

a) Diffusion: Solute following either a concentration or an electrical gradient

1) A solute moves from a solution of higher concentration through a semipermeable membrane to a solution of lower concentration

2) Selectivity of the membrane’s permeability and electrical gradient determine diffusion of the solute

3) The electrical gradient causes a solute to passively migrate to the oppositely charged compartment (e.g., Na⁺, a positive ion, migrates to a negatively charged compartment, whereas Cl⁻, a negative ion, moves toward a positively charged compartment)

b) Osmosis: Water following an osmotic gradient

1) Water normally moves from an area of low concentration to an area of higher concentration

2) An osmotic agent, such as sodium or mannitol, normally remains within a single compartment

(2) Active mechanisms:

a) Ion transport requires energy; adenosine triphosphate [ATP]) permits ions to move against the concentration gradient

b) Maximal tubular transport capacity: Active reabsorption mechanisms in the tubule have limited capacity for reabsorption of certain substances such as glucose. Plasma glucose level of 375 mg/min (transport maximum [Tm]), results in no excretion in urine; plasma glucose level above 375 mg/min results in glucose excretion in urine. Tm for glucose can vary from one nephron to another; as a result, glucose can sometimes spill into the urine at lower serum levels.

(1) Reabsorbs 60% to 80% of filtrate, which remains isotonic to plasma

(2) Major function is active reabsorption of sodium chloride (NaCl) with passive reabsorption of water

(3) Also reabsorbs glucose, amino acids, phosphates (PO₄³⁻), uric acid, potassium ion (K⁺)

(4) Regulates acid-base balance through reabsorption of carbonic acid (H₂CO₃) and bicarbonate (HCO₃⁻) and secretion of hydrogen ions (H⁺)

(5) Secretes K⁺, ammonium ion (NH₄⁺), organic acids, bases, foreign substances (e.g., drugs)

(d) Loop of Henle

(1) Variations in length depend on the type of nephron (i.e., juxtamedullary with long loops or cortical with short loops)

(2) Has two distinct segments

a) Descending segment, the thin limb, is permeable to water and impermeable to Na⁺

b) Ascending segment, the thick limb, has active NaCl pump and is impermeable to water; target site for loop diuretics

(3) Major function is concentration or dilution of urine, accomplished by a countercurrent mechanism that maintains hyperosmolar concentration in the interstitium of the renal medulla

(e) Distal convoluted tubule

(1) Receives hyposmotic (or hypotonic) urine from the ascending loop of Henle

(2) Major functions

a) Reabsorption of water, NaCl, and sodium bicarbonate

b) Secretion of K⁺, NH₄⁺, and H⁺ ions

c) Regulation of composition, tonicity, and volume

(3) Water permeability here is controlled by antidiuretic hormone (ADH); Na⁺ reabsorption is determined by aldosterone

(f) Collecting duct

(1) Receives urine, which is isotonic to plasma, from the distal convoluted and collecting tubules

(2) Functions with the distal convoluted tubule; affected by ADH and aldosterone

(3) Final urinary adjustments for composition, tonicity, and volume made here before urine enters the renal pelvis and progresses to the ureter and bladder

2. Renal hemodynamics: Normal blood flow patterns

a. Renal vasculature

i. Specialized arrangement of renal blood vessels reflects interdependence of blood supply with kidney function

ii. Pathway of blood supply

(a) Kidney: Aorta→segmented renal arteries→interlobar artery→arcuate artery→interlobular artery→(nephron)→interlobular vein→arcuate vein→interlobar vein→renal vein→inferior vena cava

(b) Nephron: Afferent arteriole→glomerular capillary→efferent arteriole→ peritubular capillary→vasa recta adjacent to tubules→interlobular vein→renal vein→inferior vena cava

iii. Juxtaglomerular apparatus: Site of renin synthesis

(a) Specialized cells composed of juxtaglomerular cells and macula densa

(1) Juxtaglomerular granular cells: Smooth muscle cells containing granules of inactive renin

(2) Macula densa: Portion of the distal tubule making contact with afferent arterioles of its respective glomerulus

(b) Responds to arterial BP in afferent and efferent arterioles and to sodium in distal tubule

b. Renal blood flow (RBF) parameters

i. Kidney receives 20% to 25% of cardiac output or 1200 ml/min, which translates to flow rate of 4 ml/g/min to the kidney

ii. Oxygen extraction from renal cells is high, but the amount is not significant enough to account for flow rate; rather, the flow is required to support normal renal function

iii. RBF is

(a) Higher in males than in females

(b) Increased with increasing age (until maturity), in the supine position, and in the afternoon

c. Distribution of RBF

i. Renal tissue

(a) Cortex: Metabolically active region, receives most (80%) of the blood supply

(b) Medulla: Site of anaerobic metabolism, receives 20% of blood supply

ii. Nephrons: Receive 600 to 650 ml/min of renal plasma flow

d. Intrarenal autoregulation: General principles

i. Mean arterial pressure (MAP) is maintained in a range of 80 to 180 mm Hg to prevent large changes in GFR

ii. Major site of autoregulation is the afferent arteriole

iii. Increase in the renal arterial pressure causes afferent vasoconstriction; decrease causes efferent vasoconstriction, producing an increased GFR/RBF ratio

iv. Changes in vascular tone of the efferent arteriole (primarily vasoconstriction) complement efforts to maintain GFR by compensating for reduced blood flow

v. Autoregulation is essentially absent at an MAP of 70 mm Hg or below

e. Neural control

i. Route of nerve supply is along renal blood vessels; renal neurologic intervention is vasoconstrictive

ii. Hypotension decreases systemic arterial pressure, stimulating the carotid sinus and aortic arch baroreceptors to trigger the sympathetic response (release of epinephrine), which decreases RBF and GFR by vasoconstricting both afferent and efferent arterioles

iii. Other factors that stimulate increased sympathetic tone are stress, fear, and exercise

iv. This neuronal effect is not the primary factor in autoregulation; a denervated kidney can be transplanted and still be able to compensate for changes in BP

f. Hormonal modulation of RBF (see Renal Regulation of Blood Pressure)

i. Renin-angiotensin system: A mechanism to sustain systemic BP and plasma volume

(a) Responds to a decreased afferent arteriolar pressure by increasing angiotensin II levels

(b) Angiotensin II vasoconstricts renal blood vessels, particularly the efferent artery, which reduces RBF but increases GFR

ii. Renal prostaglandins: Modulate the effects of vasoactive substances, such as angiotensin II, on the kidney by causing vasodilatation

g. Pharmacologic effects

i. Epinephrine and norepinephrine: Cause efferent arterioles to vasoconstrict, which leads to a rise in the filtration fraction and a dose-related decrease in RBF

ii. Dopamine: Pharmacologic action on RBF is dose-related for renal vasodilatation and increased sodium excretion. Generally has a vasodilatory effect on renal vasculature at dosages between 1 and 4 mcg/kg/min intravenously (IV) (optimal dosage, 3 mcg/kg/min); dosages above 10 mcg/kg/min cause renal vasoconstriction, decreasing RBF and GFR. Dopamine therapy has no impact on the prevention of acute tubular necrosis.

iii. Furosemide and mannitol: Increase GFR initially by increasing blood flow to the kidney and later by decreasing intratubular pressure

iv. Calcium channel blockers: Relax renal arteriole and ameliorate renal failure related to renal transplantation and nephrotoxicity due to radiocontrast dyes or cyclosporine

v. Atrial natriuretic factor (atrial natriuretic peptide, or ANP): Improves function in oliguric acute renal failure (ARF), but not preventive

3. Body water regulation

a. Thirst: Regulator of water intake

i. Thirst center is located in the anterior hypothalamus

ii. Neuronal cells are stimulated by intracellular dehydration, which causes sensation of thirst

iii. Role is maintenance of satiety state (i.e., drinking exact amount of fluid to return body to normal hydration state)

b. ADH: Sodium osmoreceptor mechanism for control of extracellular fluid (ECF) osmolality and sodium concentration

i. ADH is synthesized in the paraventricular and supraoptic nuclei of the hypothalamus and travels along the axons of the supraopticohypophysial tract for storage or release from the posterior pituitary. The supraoptic area of the hypothalamus may overlap with the thirst center, providing integration of the thirst mechanism, osmolality detection, and ADH release.

ii. Release of ADH occurs with the following:

(a) Increased serum osmolality stimulates osmoreceptor cells in the hypothalamus that transmit along the neurohypophysial tracts, leading to ADH release from the posterior pituitary; normal serum osmolality is 285 to 295 mOsm/L

(b) Volume contraction states reverse the inhibitory effect on ADH release; controlled by stretch receptors in the left atrium that activate the ADH mechanism

iii. In the presence of ADH, water reabsorption occurs in the distal tubule and collecting ducts, which results in a hypertonic urine, hypotonic medullary interstitium, and eventual correction of contracted ECF

iv. ADH secretion is inhibited when serum osmolality decreases (water intoxication). When this occurs, the distal tubule and collecting duct become relatively impermeable to water, so that large volumes of hypotonic filtrate are delivered to the collecting duct; this results in dilute urine and excess water loss (compared to extracellular solute concentration), which returns serum osmolality to normal limits.

c. Countercurrent mechanism of the kidney: Mechanism for the concentration and dilution of urine; adjusts urine osmolality from 50 to 1200 mOsm/L

i. Isotonic glomerular filtrate leaves the proximal tubule and enters the loop of Henle at 300 mOsm/L

ii. Descending limb of the loop of Henle is permeable to water only. Water is gradually drawn into the hypertonic medullary interstitium, which gradually increases the osmolality of the filtrate as it becomes dehydrated. At the hairpin turn of the loop, osmolality is dramatically increased by the removal of water and NaCl pump action; osmolality can reach 1000 to 1200 mOsm/L. Concurrently, the medullary interstitium becomes hypotonic.

iii. Thick ascending limb of the loop of Henle is permeable to NaCl but impermeable to water. The medullary interstitium becomes more hypertonic as its sodium concentration is increased by pumping action at the ascending limb.

iv. A dilute filtrate reaches the distal tubule. If ADH is absent, dilute filtrate is excreted unchanged, which results in dilute urine with water excretion in excess of solute. If ADH is present, the collecting duct reabsorbs water and concentrated urine is excreted.

4. Electrolyte regulation

a. Sodium regulation: Normal serum concentration is 136 to 145 mEq/L solute

i. Na⁺ is the major extracellular cation and osmotically active solute. Because variation in body sodium can be associated with an exchange of water between intracellular and extracellular compartments, sodium affects ECF volume.

ii. Renal reabsorption sites: Normal percentages of reabsorbed filtered sodium

(a) Proximal tubule: 65% of filtered Na⁺

(b) Loop of Henle: 25%

(d) Collecting duct: 2% to 4%

iii. Major factors that influence Na⁺ excretion include GFR, the sympathetic nervous system, aldosterone, the renin-angiotensin-aldosterone system, vasopressin (ADH), and ANP (a peptide hormone that plays a role in regulating and monitoring fluid, electrolyte, and cardiovascular balance)

iv. Sodium reabsorption increases at the renal tubules under the following conditions:

(a) Decreased GFR secondary to renal hypoperfusion (e.g., shock): Less sodium is delivered to the renal tubules, and less is excreted

(b) Secretion of aldosterone (a mineralocorticoid secreted by the adrenal cortex)

(1) Major effects are to increase renal tubular reabsorption of Na⁺ and to control selective renal excretion of K⁺

(2) Increases Na⁺ in ECF, which promotes water reabsorption; at the same time, K⁺ is secreted into the distal tubule and collecting duct to be excreted

(3) Regulated by K⁺ concentration in the ECF, the renin-angiotensin-aldosterone mechanism, total body sodium, and adrenocorticotropic hormone (ACTH)

(c) ANP action: Causes natriuretic, diuretic, and hypotensive effects secondary to its potent vasodilatory properties; the increased urinary excretion of Na⁺ is matched by an accompanying loss of K⁺ and PO₄³⁻

v. Sodium reabsorption decreases at the renal tubules under the following conditions:

(a) Increased GFR (excess ECF volume): Increases renal perfusion and GFR; more sodium is delivered to the renal tubules and more is excreted in urine

(b) Inhibition of aldosterone secretion, which results in renal Na⁺ excretion

b. Potassium regulation: Normal serum concentration is 3.5 to 5.5 mEq/L

i. Potassium is a major intracellular cation (K⁺) necessary for the maintenance of osmolality and electroneutrality of cells

ii. Renal transport sites: K⁺ is actively reabsorbed in the proximal tubule (60% to 70%) and thick ascending loop (10%); active and passive secretion in the distal tubule and collecting duct maintain the electroneutrality of urine. This electrical gradient is determined primarily by reabsorption of Na⁺ from urine.

iii. Factors enhancing K⁺ excretion

(a) Increase in cellular potassium via increased exchange with Na⁺ (K⁺ excreted in urine whereas Na⁺ is reabsorbed) or via acute metabolic or respiratory alkalosis (causes movement of K⁺ ions into cells)

(b) High-volume tubular flow rates in the distal portion of the nephron: Increase the number of available K⁺ ions and thus increase the excretion of potassium

(1) Elevation of serum potassium stimulates the secretion of aldosterone

(2) Aldosterone acts on the distal nephrons and collecting ducts, enhancing the retention of Na⁺ and excretion of K⁺

(3) Excretion of excess K⁺ eventually returns levels to normal

(d) Hydrogen ions: Alkalemia (associated decrease in H⁺) stimulates K⁺ secretion

(e) Diuretics: Loop and thiazide diuretics block NaCl and waste reabsorption, increasing tubular flow and secretion of K⁺

c. Calcium regulation: Normal serum concentration is 8.5 to 10.5 mg/dl or 2.20 to 2.60 mmol/L

i. Major functions of calcium ions (Ca²⁺): Generation of cardiac action potential and pacemaker function, contraction of cardiac and vascular smooth muscle, transmission of nerve impulses, blood coagulation, formation of bones and teeth, and maintenance of cellular permeability

ii. Total serum Ca²⁺: 40% bound to protein, 50% ionized, and 10% combined with carbonate, phosphate, citrate, and various ions

iii. Renal transport sites: 98% of filtered Ca²⁺ is reabsorbed. Reabsorptive pathways are similar to those for sodium transport. Most active reabsorption occurs in the proximal tubule. Other sites include the loop (20% to 25%) and the distal tubule (10%).

iv. Factors influencing Ca²⁺ reabsorption:

(a) Parathyroid hormone (PTH)

(1) Decrease in serum calcium stimulates secretion of PTH

(2) PTH stimulates tubular reabsorption of Ca²⁺ at the distal portion of the nephron, stimulates increased phosphate excretion, and mobilizes calcium and phosphate from bone

(b) Vitamin D: Calcium absorption from the small intestine depends on the presence of activated vitamin D (1,25-dihydroxycholecalciferol)

(1) Activation process: Absorption of ultraviolet light converts 7-dehydrocholesterol in skin to cholecalciferol. The liver hydroxylates vitamin D to form 25-hydroxycholecalciferol. The kidney further hydroxylates to the final activated form of vitamin D (1,25-dihydroxycholecalciferol) in the proximal tubule. PTH stimulates this activation process.

(2) Decreased serum calcium level reduces urinary Ca²⁺ excretion, so activated vitamin D must be available to absorb Ca²⁺ from the small intestine to maintain adequate serum calcium levels

(c) Corticosteroid effect: Large doses decrease Ca²⁺ absorption in the intestines; may influence the activation of vitamin D in the liver

(d) Diuretic effect: Diuretics can cause Na⁺ and Ca²⁺ excretion. Ultimate effect of reduced serum calcium is decreased excretion. A decrease in total body fluid volume leads to diminished GFR and reduced calcium excretion.

d. Phosphate regulation: Normal serum concentration is 3.0 to 4.5 mg/dl

i. About 90% of phosphate is found in bone, 10% in intracellular and extracellular fluid spaces. Phosphates (PO₄³⁻) play significant role in intracellular energy production and may also influence DNA, RNA, and genetic code information. Phosphates are used by the kidneys to buffer H⁺.

ii. Renal transport sites: Reabsorption of phosphate is an active process that occurs in the proximal tubule and requires Na⁺. Factors influencing phosphate excretion include the following:

(a) PTH secretion: Inhibits phosphate reabsorption (and thus promotes its excretion)

(b) Alterations in GFR: Increased GFR decreases reabsorption of plasma phosphates and vice versa

e. Magnesium regulation: Normal serum concentration is 1.5 to 2.2 mEq/L

i. The magnesium ion (Mg²⁺) is the second major intracellular cation and is a significant factor in cellular enzyme systems and biochemical reactions

ii. Mg²⁺ may have a role in the management of acute myocardial infarction (MI), because magnesium administration decreases the mortality rate in MI by 24% and improves ventricular function by 25%. Benefits may be attributed to magnesium’s ability to enhance coronary blood flow, conserve potassium, improve cellular function, and diminish dysrhythmias.

iii. Renal transport site: The reabsorptive process is similar to that of ca²⁺ and is linked to Na⁺ reabsorption along the renal tubules

iv. Factors influencing reabsorption include the availability of sodium (Na⁺ is necessary for reabsorption) and the availability of PTH (has minimal effect on Mg²⁺ reabsorption)

f. Chloride regulation: Normal serum concentration is 96 to 106 mEq/L

i. Renal transport sites: Reabsorbed with Na⁺ at all Na⁺ absorptive sites in the nephron

ii. Factors influencing excretion include acidosis (HCO₃⁻ reabsorbed whereas Cl⁻ excreted to maintain electrochemical balance) and alkalosis (HCO₃⁻ excreted as Cl⁻ reabsorbed)

5. Excretion of metabolic waste products: Excretion is a primary renal function. The kidney excretes more than 200 metabolic waste products. The products measured for interpretation of renal function are blood urea nitrogen (BUN) and serum creatinine.

a. Urea: Nitrogen waste product of protein metabolism filtered and reabsorbed along the entire nephron

i. Is an unreliable indicator of GFR, because urea excretion is influenced by

(a) Urine flow (decrease in urine flow rate may allow for reabsorption of urea)

(b) Extrarenal factors (e.g., hypoperfusion states or drugs such as corticosteroids)

(d) Changes in protein intake or metabolism

ii. Elevation in BUN level without an associated rise in creatinine level (>25:1 ratio) suggests

(a) Volume depletion, low renal perfusion pressure

(b) Severe catabolic process or trauma with massive muscle injury (e.g., burns)

iii. Elevated levels of both BUN and creatinine (at a 10:1 ratio) indicate renal disease

b. Creatinine: A waste product of muscle metabolism

i. Amount produced daily is proportional to muscle mass, and production occurs at a constant rate

ii. Normal kidney excretes creatinine at a rate equal to RBF or GFR

iii. Creatinine is freely filtered, so its production normally equals its excretion, which makes it a reliable indicator of kidney function

iv. Elevated serum creatinine level is directly correlated with deterioration in renal function

6. Renal regulation of acid-base balance: The kidneys regulate acid-base balance by minimizing wide variations in body fluid balance in conjunction with retaining or excreting hydrogen ions. Acid-base balance is also regulated by the lungs and the body buffers (serum bicarbonate, blood, and plasma proteins)

a. Bicarbonate (HCO₃⁻) reabsorption

i. Primarily occurs in the proximal tubule with less in the distal tubule; occurs with reabsorption of Na⁺

ii. Occurs if the filtrate contains more than 28 mEq/L (Tm) as in acidemia, volume contraction

b. Hydrogen ion secretion

i. Passive secretion occurs in the proximal tubule; active secretion occurs distally in exchange for Na⁺

ii. Acid is buffered by ammonia (NH₃⁺) or phosphate (HPO₄²⁻) before excretion, which provides for hydrogen (H⁺) excretion without lowering pH

iii. H⁺ secretion is increased during acidemia and decreased during alkalemia

c. Renal buffers of hydrogen ions

i. Buffers that are filtered by the glomerulus

(a) HCO₃⁻ is completely reabsorbed (up to 28 mEq/L)

(b) Phosphate (PO₄³⁻) is secreted and then reacts with hydrogen

ii. Buffers produced by the kidney tubule

(a) HCO₃⁻ can be synthesized in the distal tubule when H⁺, excreted into urine as HCO₃⁻, is delivered by ECF with Na⁺. H⁺ and HCO₃⁻ both come from the distal tubule cell as a result of ionization of carbonic acid (H₂CO₃); thus

where CA is carbonic anhydrase

(b) Carbonic acid comes from hydration of carbon dioxide (CO₂) via CA:

(c) CO₂ is derived from either cellular metabolism or dissolved CO₂ in venous blood; thus new HCO₃⁻ can be made in the distal tubule from extraurinary sources

(d) Complete equation

d. Summary of renal responses to acidemia

i. H⁺ secretion is increased at the distal tubule with increased excretion of titratable acids (HPO₄²⁻)

ii. All HCO₃⁻ is reabsorbed in the proximal tubule

iii. Ammonium is produced to accommodate H⁺ excretion: NH₃⁺ + H⁺ E NH₄⁺

iv. Urinary pH can be as low as 4.5 for excretion of a more acid urine in the presence of acidemia

e. Summary of renal responses to alkalemia

i. H⁺ secretion in the distal tubule is decreased

ii. Excess HCO₃⁻ is excreted

iii. Production of NH₄⁺ is decreased

iv. Urine is alkaline, with a pH over 7

7. Renal regulation of blood pressure: Renal regulation of BP involves five mechanisms:

a. Maintenance of volume and composition of ECF

i. Normal plasma volume is essential for control of BP

ii. Alterations in plasma volume eventually affect BP. Reduction of plasma volume lowers arterial BP, leading to compensation by vasoconstriction. Expansion of plasma volume increases cardiac preload and, in accordance with Starling’s curve, raises BP.

b. Aldosterone–body sodium balance, which determines ECF volume: Aldosterone stimulates renal tubular reabsorption of Na⁺ in exchange for excretion of primarily K⁺ ions

c. Renin-angiotensin-aldosterone system: Preserves BP and avoids serious volume reduction

i. Juxtaglomerular apparatus: Granular cells contain inactivated renin. Factors that trigger juxtaglomerular cells to release renin reflect diminished GFR (e.g., reduced arterial BP in afferent and efferent arterioles, reduced Na⁺ content or concentration at distal tubule, sympathetic stimulation of kidneys).

ii. Renin, an enzyme, is released from juxtaglomerular cells into the afferent arteriole

iii. On entering the circulation, renin acts on angiotensinogen to split away the vasoactive peptide angiotensin I and convert it to angiotensin II. Requires the presence of angiotensin-converting enzyme (ACE), found primarily in the lung and liver but also in the kidney and all blood vessels. Angiotensin II is a potent systemic vasoconstrictor.

iv. Circulatory effect of angiotensin II on arterial BP

(a) Significant peripheral arteriole constriction with moderate venous constriction occurs, which results in the reduction of vascular volume

(b) Renal arteriolar constriction results in the renal retention of sodium and water; this expands ECF volume, thus increasing arterial BP

v. Fluid volume response to angiotensin II restores effective circulating volume in the following ways:

(a) Angiotensin II stimulates aldosterone release, which enhances Na⁺ reabsorption

(b) Vasoconstriction to further decrease GFR leads to Na⁺ reabsorption

d. Renal prostaglandins: Modulating effect

i. Major renal prostaglandins are prostaglandins E₂, D₂, I₂ (vasodilators) and A₂ (vasoconstrictor)

ii. Physiologic role is modulation, amplification, and inhibition. Vasoactive substances (angiotensin, norepinephrine, bradykinins) stimulate the synthesis and release of prostaglandins. Prostaglandins modulate the action of the vasoactive substances.

iii. Prostaglandins diminish arterial BP and increase RBF by arterial vasodilation and inhibition of the distal tubules’ response to ADH. Suppressed ADH response leads to sodium and water excretion, which ultimately decreases the effective circulatory volume.

iv. Pharmacologic prostaglandin inhibitors are the nonsteroidal antiinflammatory drugs (NSAIDs). In cases of compromised renal function avoid the use of NSAIDs (i.e., salicylic acid, ibuprofen [Motrin], indomethacin [Indocin], and naproxen [Naprosyn]).

v. Loop diuretics stimulate prostaglandin secretion, which leads to vasodilation and decreased preload

e. Kallikrein-kinin system: Renal kallikreins are proteases that release kinins and are excreted in the urine. Kinins stimulate both the renin-angiotensin and prostaglandin systems, appearing to link renal hemodynamics and fluid-electrolyte excretion.

8. Red blood cell synthesis and maturation

a. Erythropoietin secretion: Stimulates the production of erythrocytes in the bone marrow and prolongs the life of erythrocytes

b. Mechanism of erythropoietin synthesis and secretion

i. Renal cortical interstitial cells produce erythropoietin, a glycosylated, 165-amino-acid protein

ii. Renal erythropoietin production accounts for 90% of RBC production; the remaining 10% is produced by the liver

iii. Hypoxia stimulates renal erythropoietin production; the liver is not as responsive to hypoxia and therefore cannot support erythropoiesis in renal failure

c. Erythropoietin deficiency: Primary cause of anemia in chronic renal failure (CRF); bleeding is the second most common cause

9. Aging kidney

b. Renal response in the elderly

i. Decreased renal mass associated with a diminished number of nephrons

ii. Decreased GFR; diminished RBF secondary to age-related changes in vasculature

iii. Diminished creatinine production (10 mL/min/1.73 m² per decade) and diminished ability to excrete creatinine; therefore, change in serum creatinine level may not be evident. Uric acid levels are slightly increased.

iv. Decreased serum renin and aldosterone levels reduce the ability to conserve sodium, impair urinary water excretion, and limit urinary concentration

Patient Assessment

1. Nursing history

a. Patient health history

i. Previous health problems: Indicate the presence of or predisposition to renal disease

(a) Kidney and/or urinary tract disease

(b) Cardiovascular disease

(1) Hypertension: BP control and treatment may prevent or halt renal damage; hypertension develops in 70% to 80% of patients with advanced renal failure

(2) Heart failure with diminished renal perfusion

(3) Atherosclerosis

(d) Immunologic disorders, recent infections (streptococcal)

(e) Pulmonary disease (Goodpasture’s syndrome)

(f) Allergies, recent blood transfusions (history of incompatibility reaction)

(g) Other: Toxemia of pregnancy, renal transplantation, anemia, recent surgery, dialysis, exposure to drugs and toxins, renal calculi, azotemia, hematuria, exposure to chemicals or poisons

ii. History of specific signs and symptoms

(a) Signs and symptoms of urinary tract disorders

(1) Dysuria

(2) Abnormal appearance of urine

a) Hematuria (grossly bloody)

b) Pyuria (cloudy)

c) Biliuria or bilirubinuria (orange)

d) Myoglobinuria (usually clear; red-brown urine; Hematest positive)

(3) Urine frequency, urgency, incontinence, hesitancy; nocturia

(4) Polydipsia

(5) Patterns of urine output

a) Normal volume: Approximately 1500 ml/24 hr

b) Oliguria: Less than 400 ml/24 hr

c) Anuria: Less than 50 ml to no output over 24 hours

d) Polyuria: Excessive output exceeding 24-hour intake

e) Nonoliguria: Normal or excess urine volume in the presence of ARF

(6) Fever

(7) Pain in costovertebral angle, flank, or groin

(8) Pattern of weight gain or loss; dry weight is the ideal weight that minimizes symptomatology for a patient with renal failure as achieved by a dialysis treatment

b. Family health history: Genetic renal disease accounts for about 30% of azotemia. Genetically transmitted diseases that can cause or precipitate renal disease include the following:

i. Cardiovascular disease, hypertension

ii. Diabetes mellitus

iii. Gout

iv. Malignancy

v. Polycystic kidney disease and medullary cystic disease

vi. Hereditary nephritis (Alport’s syndrome)

vii. Renal calculi

c. Social history and habits

i. Social history: Sexual activity prior to renal disease and sexual dysfunction related to renal disease

ii. Habits

(a) Dietary habits

(1) Dietary and fluid restrictions; compliance or noncompliance with these restrictions

(2) Dietary intake: Number and nutritional value of meals

(b) Exercise

d. Medication history

i. Nephrotoxic agents: Radiocontrast dye and antibiotic therapy (tetracyclines, aminoglycosides, gentamicin, amphotericin B)

ii. Diuretics, antihypertensives

iii. Cardiac glycosides (digoxin), antiarrhythmic agents

iv. Electrolyte replacement therapy

v. Immunosuppressives

(a) Corticosteroids

(b) Azathioprine, cyclophosphamide, antithymocyte globulin (ATG), cyclosporine, monoclonal antibody (OKT3), tacrolimus (FK-506)

vi. Analgesics such as meperidine (Demerol)

2. Nursing examination of patient

a. Physical examination data

i. Inspection

(a) Diminished level of consciousness (lethargy, coma)

(b) Skin

(1) Abnormal color: Grayish tinge from anemia, yellowish tinge if retained carotenoids or urochrome pigments in uremia

(2) Capillary integrity: Easily bruised

(3) Skin turgor

(4) Purpura lesions: Present in some forms of renal failure

(d) Ear: Nerve deafness (Alport’s syndrome)

(e) Edema

(1) Significance depends on amount of water and Na⁺ retained

(2) Edema of renal failure often related to hypoalbuminemia

(f) Respiration: May see rate and pattern similar to Kussmaul’s respirations

(g) Muscle tremors, weakness, weight loss with uremic syndrome

(h) Tetany: Positive Chvostek’s and Trousseau’s signs; rarely observed; result from severe hypocalcemia or very rapid correction of acidosis

(i) Asterixis: Indicates progressive uremic state

(1) Ask the patient to face the examiner and raise the upper extremities in a fixed hyperextension position

(2) Palms (fingers separated) must be visible to the examiner

(3) Positive sign—irregular movements of the wrists, flapping movements of the fingers—occurs within 30 seconds

(j) Fatigue: Occurs with activities of daily living and exercise, and at rest

(k) Mobility: Extent and strength with ambulation

(l) Nutritional status

(1) Triceps skinfold thickness (normal is >25 mm for men, >15 mm for women)

(2) Anemia: Pale skin, weakness, shortness of breath

(3) Tolerance of diet: Nausea and vomiting; likes and dislikes

(4) Weight loss

(m) Arteriovenous access: Type, patency, signs of infection

ii. Palpation: To determine size and shape of the kidney and to check for tenderness, cysts, and masses

(a) Right kidney is easier to palpate because it is lower in the abdomen

(b) Palpate the bladder for urinary distention due to obstruction

(d) Palpate pulses for a baseline reading and to determine abnormalities

iii. Percussion

(a) At costovertebral angles to elicit pain or tenderness associated with

(1) Pyelonephritis

(2) Calculi

(3) Renal abscess

(4) Intermittent hydronephrosis

(b) At abdomen for the presence of ascites

iv. Auscultation: Listen for aortic and renal artery bruits (heard in flanks or intercostal regions of anterior abdomen)

b. Monitoring data: Intake and output (I&O), hemodynamics, body weight, central venous pressure (CVP) and/or pulmonary artery occlusion pressure to determine relationship between cardiac filling pressures and hydration status; correlate findings with daily weight

3. Appraisal of patient characteristics: Patients with acute, life-threatening renal problems come to critical care units with a wide range of biochemical, metabolic, and psychosocial clinical characteristics. During their stay, their clinical status may significantly improve or deteriorate, slowly or abruptly change, involve one or all life-sustaining functions, and be readily or nearly impossible to monitor with precision. Some attributes of patients with acute renal disorders that the nurse needs to assess are the following:

a. Resiliency

i. Level 1—Minimally resilient: Any patient with end-stage CRF on hemodialysis, who is septic with two other forms of organ failure, such as acute respiratory distress syndrome and cirrhosis

ii. Level 3—Moderately resilient: A 58-year-old patient on postoperative day 3 after uncomplicated coronary artery bypass graft surgery who received prophylactic intravenous therapy intraoperatively to prevent renal involvement but still developed and is recovering from nonoliguric ARF

iii. Level 5—Highly resilient: Any patient with an isolated episode of a prerenal ARF secondary to dehydration with no significant alteration in hemodynamics, receiving hydration

b. Vulnerability

i. Level 1—Highly vulnerable: A 65-year-old male diabetic patient with cardiovascular complications who has rejected his renal transplant and is unable to tolerate hemodialysis

ii. Level 3—Moderately vulnerable: A 24-year-old female with acute postrenal failure from infected renal calculi who is scheduled for surgery today

iii. Level 5—Minimally vulnerable: A 32-year-old single female with a urinary tract infection (UTI)

c. Stability

i. Level 1—Minimally stable: Any cardiogenic shock patient with oliguric ARF on intraaortic balloon pump and continuous renal replacement therapy

ii. Level 3—Moderately stable: An end-stage CRF patient with malignant hypertension whose BP is beginning to respond to a new therapeutic regimen of antihypertensive agents including ACE inhibitors

iii. Level 5—Highly stable: A 36-year-old patient with lupus nephritis in early stages of CRF who requires a protein-restricted diet and is compliant with the medical regimen

d. Complexity

i. Level 1—Highly complex: A 36-year-old elementary school teacher with chronic diabetic renal disease who decided to terminate dialysis treatment and is now in a uremic coma, and whose family does not agree with her decision

ii. Level 3—Moderately complex: A 21-year-old college student who is approaching end-stage renal failure and feels conflicted because two of his younger siblings are a tissue match and are both eager to donate a kidney

iii. Level 5—Minimally complex: A 46-year-old male with CRF who complies with his medical regimen, is dialyzed at home by his supportive wife, and is now admitted for an acute repair of his arteriovenous fistula

e. Resource availability

i. Level 1—Few resources: A 50-year-old Russian immigrant who has been in the United States 2 weeks when it is determined that he requires hemodialysis; he is not insured and is not eligible for state assistance, and his family cannot offer financial support

ii. Level 3—Moderate resources: A middle-aged patient who needs renal transplantation; he has four siblings who offered to donate but none is a tissue match, so he places himself on the cadaveric organ donor list

iii. Level 5—Many resources: Mrs. Jones, a well-respected elementary school nurse for the past 15 years, who has been effectively managing her own continuous ambulatory peritoneal dialysis for 5 years

f. Participation in care

i. Level 1—No participation: A 26-year-old quadriplegic with nephrotoxic acute tubular necrosis (ATN) secondary to carbenicillin administered for an antibiotic-resistant UTI requires 2 weeks of dialysis after which kidney function should return

ii. Level 3—Moderate participation: A blind man with diabetes is taught how to perform his own peritoneal dialysis at night with the assistance of his wife

iii. Level 5—Full participation: A patient who has had a successful renal transplant for the past 3 years makes a practice of visiting local hemodialysis units and teaching the benefits of transplantation as a treatment option

g. Participation in decision making

i. Level 1—No participation: A 70-year-old mentally retarded male patient with advanced chronic kidney disease is approaching the need for dialysis and lives with his 95-year-old mother, who has periods of senility

ii. Level 3—Moderate participation: A 32-year-old female recently diagnosed with renal cancer has a history of admissions for psychosis and is estranged from most of her family except her 29-year-old sister

iii. Level 5—Full participation: After running a marathon, the patient spends a week in the intensive care unit (ICU) recovering from an episode of ARF secondary to rhabdomyolysis; he is surrounded by his family, friends, and representatives from his community, who offer their support during his recovery at home

h. Predictability

i. Level 1—Not predictable: Any critically ill patient who develops ATN after an extensive period of hypotension and experiences repeated episodes of severe dehydration, systemic infection, and exposure to nephrotoxic agents during recovery

ii. Level 3—Moderately predictable: Any critically ill patient who develops contrast media–induced ATN, when renal involvement is identified early and hydration and loop diuretics are administered

iii. Level 5—Highly predictable: A critically ill patient with a relatively uncomplicated condition who develops nonoliguric ATN after a short episode of hypotension, easily reversed, and has an uneventful recovery period

4. Diagnostic studies

a. Laboratory

i. Blood

(a) Complete blood count: Reduced hematocrit and hemoglobin levels may reflect bleeding or a lack of erythropoietin

(b) Serum creatinine: To estimate GFR (normal level, 0.6 to 1.2 mg/dl)

(1) Creatinine excretion is proportional to its production

(2) A significant elevation in creatinine level is associated with renal disease and correlates with percentage of nephrons damaged

TABLE 5-1

Interpretation of Blood Urea Nitrogen (BUN) and Serum Creatinine Levels

(1) Prerenal problem: Ratio of BUN to serum creatinine equal to or greater than 25:1 suggests extrarenal problem (dehydration, catabolic state). Elevation in both BUN and creatinine results from decreased GFR.

(2) Renal failure: Caused by nephron damage

(d) Cystatin C: New test to determine GFR

(1) Cystatin C is a nonglycosylated basic protein continually produced by nucleated cells

(2) Freely filtered by glomeruli, metabolized by tubules

(3) Serum levels not affected by age, sex, or muscle mass

(4) More reliable indicator of renal function than creatinine

(5) Used to detect mild reductions in GFR, especially in renal transplant patients

(e) Serum chemistry tests (calcium, phosphate, alkaline phosphatase, bilirubin, uric acid, sodium, potassium, chloride, carbon dioxide, magnesium, glucose, cholesterol)

(f) Baseline arterial blood gas (ABG) levels, clotting profile

(g) Serum osmolality, total protein and albumin

ii. Urine

(a) Visual examination for color and clarity

(1) Clear and colorless in hyposthenuria

(2) Cloudy when infection is present

(3) Foamy when albumin is present

(b) Osmolality (50 to 1200 mOsm/kg)

(c) SG: Wide range of normal values (1.003 to 1.030); provides reasonable estimate of urinary osmolality; actually measures density

(1) Low normal (<1.010): Suspect diabetes insipidus, overhydration, or heart failure

(2) Above normal (>1.030): Occurs in proteinuria, glycosuria, severe dehydration, presence of x-ray contrast medium

(d) Creatinine clearance (C_cr): 24-hour urine collection

(1) Purpose: To determine the presence and progression of renal disease, estimate percentage of functioning nephrons, or determine specific medication dosages

(2) In 24 hours, the following occurs:

where

U_cr = amount of urinary creatinine excreted

V = urine volume per minute

P_cr = plasma creatinine level

(3) In average-size patients, a satisfactory 24-hour urine collection always has approximately 1 g of creatinine, regardless of the degree of renal function

(4) Cockcroft-Gault formula for estimation of C_cr: See Table 5-2

TABLE 5-2

Cockcroft-Gault Formula for Estimation of Creatinine Clearance Without Urine Specimen

Gender	Formula
Male	C_cr (in ml/min) = ([140 – age in years] × weight in kg) ÷ (P_cr in mg/dl × 72)
Female	C_cr (in ml/min) = ([140 – age in years] × weight in kg) ÷ (P_cr in mg/dl × 72) × 0.85

C_cr, Creatinine clearance; P_cr, plasma creatinine level.

(e) Culture and sensitivity: Check for infection

(f) pH (normal range, 4.5 to 8; average value, 6); alkaline urine is frequently seen with infection; in absence of infection, possibly indicates renal tubular acidosis if both alkaline urine and systemic acidosis are present

(g) Glucose: In urine when renal threshold for glucose exceeded

(h) Acetone: In urine with starvation or diabetic ketoacidosis; a false-positive result can occur in patients taking salicylates

(i) Protein: Expressed quantitatively as 1+ to 4+; diagnostic for the presence of glomerular membrane disease (nephritic syndrome) and allows the detection of myeloma proteins causing renal failure

(j) Spot urine electrolytes

(1) Measure urinary concentrations of Na⁺, K⁺, Cl⁻

(2) Screening test for tubular function; assess the kidney’s ability to conserve sodium and concentrate urine

(k) Urinary sediment

(1) Casts: Precipitations of protein in the kidney that take the shape of the tubules in which they are formed

a) Hyaline casts: Entirely protein; small amounts are normal in urine; if large amounts, suspect significant proteinuria such as albumin or myeloma protein in urine

b) Erythrocyte casts: Diagnostic for active glomerulonephritis or vasculitis

c) Leukocyte casts: Indicative of an infectious process and intrarenal inflammation

d) Granular casts: Small number, possibly the result of degenerating erythrocyte or leukocyte casts indicative of an infectious process or an allergic interstitial nephritis

e) Fatty casts: Abundant in nephrotic syndrome

f) Renal tubular casts: Seen in ARF

(2) Bacteria: Presence determined by Gram stain

(3) Erythrocytes: Small numbers normal; in abundance during active glomerulonephritis, interstitial nephritis, malignancies, and infection

(4) Leukocytes: Small numbers normal; present in infection and interstitial nephritis

(5) Renal epithelial cells: Rarely seen; present in abundance during ATN, nephrotoxic injury, and allergic reaction in the kidney

(6) Crystals: Seen in diseases of stone formation or following certain intoxications

(7) Eosinophils: Indicate allergic reaction in the kidney

(l) Nucleomatrix test: Noninvasive, quantitative, painless examination for transitional cell cancer of the bladder

b. Radiologic

i. Plain abdominal x-ray study: Determines position, shape, and size of the kidney and identifies calcification in the urinary system

ii. Intravenous pyelography (IVP)

(a) Visualizes the urinary tract for diagnosing partial obstruction, renovascular hypertension, tumor, cyst, congenital abnormality

(b) Complications include allergic reaction to dye, dehydration

(1) Poor renal function: Dye’s dehydrating effect and nephrotoxicity may further compromise function

(2) Multiple myeloma: IVP dye may precipitate myeloma protein in the kidney

(3) Pregnancy: Abdominal irradiation should be avoided

(4) Heart failure: Osmotic effect of dye can compromise cardiac function by expanding vascular volume

(5) Diabetes mellitus

(6) Sickle cell anemia: Dye’s elevation of renal oncotic pressure can promote renal tissue sickling, infarction

iii. High-excretion tomography: Indicated when kidneys cannot be readily visualized on IVP

iv. Renal scan: Determines renal perfusion and function; can provide information about obstructions and renal masses. Radioactive dye is taken up by normal kidney tubule cells. A decrease in uptake indicates hypoperfusion. Often used to assess renal transplants.

v. Retrograde pyelography: Used to examine upper region of collecting system

vi. Retrograde urethrography: Used to examine the urethra

vii. Cystoscopy: Detects bladder or urethral pathology

viii. Renal arteriography (angiography): Identifies tumors and distinguishes type of renal or renovascular disease. Potential complications can be serious:

(a) Allergic reaction to dye can cause same complications seen with IVP dye

(b) Puncture of a peripheral artery, with consequent hematoma, embolism, or thrombus formation, is the greatest technical risk

ix. Voiding cystourethrography: Identifies abnormalities of lower urinary tract, urethra, bladder to detect reflux and residual urine

x. Diagnostic ultrasonography: Identifies hydronephrosis, differentiates solid and cystic tumors, localizes cysts or fluid collections

xi. Computed tomography (CT): Identifies tumors and other pathologic conditions that create variations in body density (e.g., abscess or lymphocele); used in renal trauma to determine reason for acute flank pain

xii. Magnetic resonance imaging (MRI)

(a) Provides better tissue characterization than CT; provides direct imaging in several planes for detection of renal cystic disease, inflammatory processes, and renal cell carcinoma

(b) Detects alterations in blood flow (i.e., slow or absent flow)

xiii. Magnetic resonance urography: A form of magnetic imaging that offers results similar to those of an IVP, without the use of dye

xiv. Chest radiography: Identifies pulmonary edema, cardiomegaly, left ventricular hypertrophy, uremic lung, Goodpasture’s disease, and infection

c. Kidney biopsy: The most common invasive diagnostic tool

i. For renal disease that cannot be definitively diagnosed by other means

ii. Determines cause and extent of lesions; helpful in planning treatment

iii. Types of biopsy

(a) Open: For severe anatomic deformities or if a “deep specimen” is needed for diagnosis; contraindications to open biopsy include bleeding tendency, hydronephrosis, hypertension, cystic disease, and neoplasms

(b) Closed: A simple percutaneous procedure; used more frequently than open procedure

Patient Care

1. Overhydration: A state in which an individual experiences fluid retention and edema because kidneys are unable to excrete excess body water

a. Description of problem

i. Intake greater than output

ii. Weight gain with oliguria or anuria, low SG (≤1.015), dilute urine

iii. Elevated BP, bounding pulses, neck vein distention; elevated CVP, pulmonary artery pressure (PAP), and pulmonary artery occlusive pressure (PAOP), and muffled heart sounds

iv. Edema: Peripheral, anasarcal, ascitic, periorbital, pulmonary

v. Dyspnea, orthopnea, crackles on auscultation, pulmonary congestion

vi. Decreased (diluted) hemoglobin, hematocrit, and electrolyte values

vii. Anxiety, restlessness, stupor (seen with water intoxication)

b. Goals of care

i. Patient maintains dry weight

ii. BP, CVP, PAP, and PAOP are normal

iii. Patient is free of edema

iv. Breath sounds are clear bilaterally

v. I&O are balanced

c. Collaborating professionals on health care team

i. Critical care nurse

ii. Critical care intensivist or physician

iii. Nurse practitioner, clinical nurse specialist, or physician assistant

iv. Case manager

v. Dietitian

vi. Nephrology consultant

vii. Hemodialysis nurse (if dialysis indicated)

d. Interventions

i. Identify presence of common causes of fluid volume excess

(a) Expanded total body water volume secondary to renal failure with oliguria or anuria

(b) Expanded blood volume due to renal sodium retention

(d) Increased capillary permeability

ii. Document I&O; compare with daily weight; consider insensible losses—fluid losses via lungs, skin, and bowel (600 to 800 ml/day)

iii. Assess renal function

(a) Urine volume, urinalysis, creatinine clearance, and BUN/creatinine ratio

(b) Spot electrolytes, urine concentration (SG, osmolality)

iv. Restrict fluids in overhydration associated with impaired renal function, impaired cardiac function, or syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

v. Administer diuretics (preferably loop) if renal response is a GFR of 25 ml/min or higher

vi. Consider acute dialysis with ultrafiltration for rapid volume removal

e. Evaluation of patient care

i. 24-hour I&O balance is negative or zero

ii. There is no edema, as evidenced by absence of adventitious breath sounds and hypertension

2. Dehydration: A state in which an individual experiences vascular, cellular, or intracellular volume depletion due to active fluid loss. Dehydration may occur in the diuretic phase of ARF or as a result of aggressive diuretic therapy.

a. Description of problem

i. Output greater than intake

ii. Weight loss with elevated SG (≥1.020), concentrated urine, variable urinary output

(a) Polyuric phase: Large volume of dilute urine with low SG

(b) Dehydration with normal renal function: Oliguria, concentrated urine with an elevated SG

iii. Hypotension, increased pulse, decreased CVP

iv. Thirst, dry skin and mucous membranes, poor skin turgor

v. Increased body temperature

vi. Weakness, stupor (seen with severe hypovolemia)

b. Goals of care

i. Patient’s weight is normal and stable

ii. Vital signs and hemodynamic parameters are normal

iii. Fluid balance and urine output are within normal limits (WNL)

c. Collaborating professionals on health care team: See Overhydration

d. Interventions

i. Identify common causes of fluid deficit

(a) Renal water losses

(1) Diuretic abuse

(2) Salt-wasting nephropathies

(3) Diabetes insipidus (nephrogenic, central)

(4) Osmotic or postobstruction diuresis

(b) GI losses

(1) Diarrhea, vomiting, nasogastric suction

(2) Fistula and wound drainage

(3) GI bleeding

(d) Third-spacing (ECF) phenomena

ii. Document I&O; compare with daily weight

iii. Administer fluid therapy

(a) Fluid challenge to increase RBF and urinary excretion

(b) Caution for fluid challenge: Monitor for pulmonary edema and renal failure unresponsive to volume expansion (i.e., no increase in urinary output)

iv. Assess renal function

(a) Urine volume, creatinine clearance, BUN/creatinine ratio

(b) Urinalysis; urine concentration (SG, urine osmolality), spot electrolytes

e. Evaluation of patient care

i. The 24-hour I&O balance is positive or zero

ii. Patient has stable, normal weight

iii. Vital signs and hemodynamic parameters are normal

iv. Urine volume and SG are normal

3. Malnutrition

a. Description of problem: Malnutrition is associated with increased morbidity in CRF, especially in the presence of hypoalbuminemia. Dietary protein intake is restricted to preserve kidney function in early stages of chronic kidney disease. Protein restriction can contribute to malnutrition.

b. Goals of care

i. Patient’s intake meets nutritional requirements

ii. Patient maintains stable baseline weight and adequate muscle mass

iii. Serum protein and albumin, BUN, and creatinine levels are normal

c. Collaborating professionals on health care team: See Overhydration

d. Interventions

i. Identify cause of inadequate nutritional intake; direct care there

ii. Teach appetite-enhancing measures

(a) Provide oral hygiene prior to meals

(b) Give small, frequent meals

iii. Teach the necessary elements of the renal patient’s diet

(a) Essential amino acids, adequate calories, vitamin and iron supplements (folic acid, multivitamins) as warranted

(b) Adjusted protein and electrolyte intake (Na⁺ and K⁺) to avoid uremic symptoms and electrolyte imbalances. Excessively diminished protein intake causes use of protein stored in muscles, which leads to body muscle wasting. Providing increased calories can help avoid this situation.

iv. Monitor pattern of changes in weight and nutritional intake

v. Assess for noncompliance with dietary instructions

e. Evaluation of patient care

i. Body weight and muscle mass remain WNL

ii. Serum protein, albumin, BUN, and creatinine levels are at or approach normal limits

4. Hypertension

a. Description of problem

i. In renal failure, the hypertensive state (diastolic BP >90 mm Hg, systolic BP >140 mm Hg) is usually created by fluid retention and/or stimulation of the renin-angiotensin mechanism; preexisting hypertension is common

ii. Clinical findings: See Chapter 3

b. Goals of care (see Chapter 3): Goal in CRF is systolic BP 130 mm Hg or lower and diastolic BP 80 to 85 mm Hg or lower

c. Collaborating professionals on health care team: See Chapter 3

d. Interventions (see Chapter 3): Treatment of hypertension in an aggressive manner with a diuretic, ACE inhibitor, β-blocker, and/or possibly calcium channel blocker has the benefit of slowing the progression of CRF

i. Administer diuretics, as ordered, to treat edema and hypertension

(a) General characteristics of diuretics

(1) Inhibit the active transport of sodium or chloride, resulting in an increase in urine output

(2) The diuretic effect reduces effective plasma circulating volume, thereby lowering BP

(b) Complications

(1) Volume depletion

(2) Hypokalemia, hyponatremia, hypochloremia

(3) Hyperkalemia, hyperuricemia, azotemia

(4) Metabolic alkalosis

(c) Types of diuretics: Used as single therapy to treat hypertension or with other antihypertensive agents to enhance their therapeutic effect

(1) Osmotic diuretic: A nonabsorbable solute (mannitol)

a) Exerts an osmotic effect, causing water diuresis in excess of NaCl

b) Side effects: Blurred vision, rhinitis, rebound plasma volume expansion, thirst, urinary retention, and fluid and electrolyte imbalance

(2) Loop diuretics: The most potent diuretics available (furosemide, indapamide, bumetanide, torsemide, and ethacrynic acid). The primary site of action is the thick segment of the medullary ascending loop of Henle.

a) Block the reabsorption of NaCl, thus contributing to a large diuresis of isotonic urine; potassium excretion also enhanced

b) Increase RBF by stimulating increased secretion of prostaglandin, which exerts a vasodilatory effect on renal vasculature leading to reduction in preload

c) Vasodilatory effect of loop diuretics can be minimized, if the cardiovascular effect is negative, by the administration of ACE inhibitors

d) Increase GFR even with a decrease in ECF volume, because the tubuloglomerular feedback mechanism is blocked

e) Side effects: Volume depletion, agranulocytosis, thrombocytopenia, transient deafness, abdominal discomfort, hypokalemia, hypomagnesemia, metabolic alkalosis, and hyperglycemia

f) Prolonged use without electrolyte replacement results in all other electrolyte imbalances

(3) Thiazides (hydrochlorothiazide, chlorthalidone, and metolazone)

a) Sodium reabsorption inhibited in the ascending loop of Henle and the beginning portion of the distal tubule

b) Increased potassium excretion occurs with a weak carbonic anhydrase inhibitory effect

c) Side effects: Rashes, leukopenia, thrombocytopenia, hypercalcemia, and acute pancreatitis

(4) Potassium-sparing diuretics (spironolactone, amiloride, triamterene): Aldosterone inhibitors

a) Promote Na⁺ secretion into the distal tubule and K⁺ reabsorption; cause mild diuresis and protect K⁺ level

b) Usually selected for patients receiving digoxin and diuretic therapy who cannot tolerate low serum K⁺ levels or when a mild diuretic effect is desirable

c) Side effects: Hyperkalemia, hyponatremia, headache, rash, nausea, diarrhea, urticaria, and gynecomastia or menstrual disturbances

(5) Carbonic anhydrase inhibitors (acetazolamide sodium)

a) Inhibit the enzyme carbonic anhydrase

b) Increase the excretion of Na⁺ by interfering with HCO₃⁻ reabsorption. Sodium bicarbonate is lost in the urine, which creates a hyperchloremic metabolic acidosis

c) Are beneficial when an alkaline urine is desirable, such as with metabolic alkalosis

d) Side effects: Hyperchloremic acidosis, renal calculi, rash, nausea, vomiting, anorexia, diminished renal function

(6) Other agents: Pharmacologic agents that increase both cardiac output and GFR contribute to diuresis (e.g., xanthines [theophylline, aminophylline] and digoxin)

(d) General nursing considerations in the administration of diuretics

(1) Collaborate with the physician to determine the weight and fluid balance desired at the conclusion of diuretic therapy

(2) Observe for fluid, electrolyte, and acid-base disorders

(3) Maintain I&O records; correlate with daily weights

(4) Monitor serum K⁺ levels, especially if the patient is taking digoxin (hypokalemia increases risk of digitalis toxicity)

(5) Administer potent or high doses of diuretics in the early morning or afternoon unless a Foley catheter is in place

(6) Monitor BP during aggressive diuresis because hypotension can indicate dehydration and impending circulatory collapse

(7) Advise the patient to report the onset of side effects such as difficulty hearing

(8) Be aware that a diminished response to diuretics may be related to electrolyte imbalances, particularly hyponatremia, hypochloremia, and hypokalemia

ii. Administer antihypertensive agents as ordered (see Chapter 3)

e. Evaluation of patient care: See Chapter 3

5. Metabolic acidosis: A condition commonly associated with renal failure caused by the inability of the kidney to excrete hydrogen ions (see Chapter 2)

6. Anemia: In renal disease, anemia is related primarily to a lack of erythropoietin synthesis and secretion by the kidney but can also be caused by actual blood loss (e.g., stress ulcer)

a. Description of problem: See Chapter 7

b. Goals of care: See Chapter 7

c. Collaborating professionals on health care team: See Overhydration; include hematology consult if the patient is unresponsive to therapies

d. Interventions

i. Identify common causes of anemia associated with renal failure

(a) Suppression of erythropoietin synthesis and secretion

(b) Actual blood losses

ii. Treat chronic anemia associated with renal failure

(a) Oral or IV iron unless the patient has excess body iron stores

(b) Folic acid and pyridoxine (vitamin B₆): Important, especially in dialysis patients, because these are dialyzable vitamins

(c) Epogen (recombinant human erythropoietin): Stimulates erythrocyte production and prevents the anemia of CRF; effect does not begin until 2 to 6 weeks, with peak results in 3 months after administration; as a result, it is not used in ARF

e. Evaluation of patient care

i. Patient maintains acceptable hematocrit level (usually 20% to 24% with traditional therapy and 33% to 36% with epoetin alfa therapy)

ii. Patient complies with pharmacologic and nutritional supplement therapy regimen

7. Uremic syndrome

a. Description of problem: Uremic state results from the kidney’s inability to excrete toxic waste products; uremic symptoms usually occur at BUN levels above 100 mg/dl or at a GFR below 10 to 15 ml/min (Table 5-3)

TABLE 5-3

Clinical Findings in Uremic Syndrome

b. Goals of care: BUN level is maintained below 100 mg/dl or at a level that minimizes uremic symptoms

c. Collaborating professionals on health care team: See Overhydration

d. Interventions: Based on minimizing azotemia and preventing dehydration

i. Restrict oral protein intake

ii. Remove blood if it is present in the GI tract because this is another protein source that can be metabolized to ammonia and urea. These metabolites cannot be handled by diseased kidneys.

iii. Consider dialysis to maintain BUN level below 100 mg/dl. In each patient, uremic symptoms develop at individual levels of BUN and creatinine. Identify these values, then strive to maintain BUN and creatinine below those levels.

e. Evaluation of patient care

i. BUN is below 100 mg/dl

ii. Uremic symptoms are absent or minimized

8. Infection

a. Description of problem: Major cause of death in patients with ARF and can seriously compromise patients with CRF (see Chapter 7)

b. Interventions: See Chapter 7

i. Keep in mind: Patients with renal failure have an impaired immune response from uremic toxins and reduced phagocytosis by the reticuloendothelial system

ii. Implement the following precautions

(a) Obtain a urine specimen for culture on admission: UTI may be asymptomatic

(b) Prevent introduction of microorganisms; avoid indwelling urinary catheters and unnecessary invasive monitoring procedures

(d) Maintain the BUN level at 80 to 100 mg/dl or lower to minimize susceptibility to infection

(e) Implement isolation techniques for hepatitis antigen–positive patients receiving hemodialysis

c. Evaluation of patient care: See Chapter 7

9. Bone disease—osteomalacia, osteitis fibrosa: Chronic hypocalcemia can precipitate hyperparathyroidism, which leads to the mobilization of calcium from the bone and results in softening of the bone (osteomalacia)

a. Description of problem

i. History of chronic hypocalcemia, hyperparathyroidism, or both

ii. Bone pain, fractures, and radiologic examination of the skull, hands, and feet revealing signs of demineralization

iii. Activity intolerance with ambulation

b. Goals of care

i. Hypocalcemia remains within an asymptomatic range.

ii. No fractures or bone pain is present.

c. Collaborating professionals on health care team: See Overhydration

d. Interventions: See Electrolyte Imbalances—Calcium Imbalance: Hypocalcemia and Electrolyte Imbalances—Phosphate Imbalance: Hyperphosphatemia later in this chapter

10. Altered metabolism and excretion of pharmacologic agents related to renal failure

a. Description of problem

i. Kidneys unable to metabolize or excrete pharmacologic agents

ii. Unusual untoward effects may include enhanced sensitivity to drugs

iii. Active or toxic metabolites of a medication retained

iv. Increased azotemia due to elevation in metabolic wastes from drug usage

b. Goals of care

i. Patient tolerates pharmacologic therapy with no untoward drug effects

ii. Prescribed serum drug levels are adequate

c. Collaborating professionals on health care team: See Overhydration; also Pharmacologist

d. Interventions

i. Recognize alterations in the body’s use of drugs during renal failure

(a) Distribution of drugs in a uremic state

(1) Decreased stores of body fat affect distribution of lipid-soluble drugs

(2) Low cardiac output states reduce renal metabolism or excretion of drugs

(3) Acidemia alters tissue uptake of drugs

(4) Increased body water has a dilutional effect

(5) Decreased protein binding causes competition by various drugs for tissue binding sites, leading to a higher concentration of unbound drugs

(b) Uremic effects that can alter drug absorption

(1) Decreased GI motility and altered gastric pH

(2) Electrolyte imbalances, which may affect GI tract

(3) Inability of the kidney to excrete or metabolize drugs

(4) Diminished protein binding

ii. Follow general principles for drug administration during renal insufficiency

(a) Reduce drug dosage

(b) Increase intervals between doses

(d) Closely observe patients to recognize toxicity due to drug accumulation

(e) Report any untoward signs, especially elevated serum creatinine level, so the drug can be reconsidered, reduced in dosage, or discontinued

(f) Monitor serum drug levels, especially in situations requiring a specific drug concentration (e.g., antibiotics, digoxin, procaine)

(g) To ensure a more stable serum concentration, administer initial loading doses of drugs that have a long half-life (e.g., digoxin)

e. Evaluation of patient care: Patient tolerates pharmacologic therapy with no untoward drug effects

11. Ineffective patient and family coping (see also Chapter 10)

a. Description of problem

i. Insufficient, ineffective, or compromised support, comfort, assistance, or encouragement, usually by a supportive primary person (family member or close friend). The patient may need to manage adaptive tasks related to the stress of renal failure on the patient and the family.

ii. Signs of maladaptive patient coping

(a) Verbalization of the inability to cope or to ask for help

(b) Inability to meet role expectations and solve problems

(d) Destructive behavior toward self or others (i.e., suicide attempt)

(e) Failure to comply with the treatment regimen

iii. Signs of maladaptive family coping

(a) Patient communicates concern about the family’s response to his or her disease

(b) Family members demonstrate preoccupation with their own personal reactions—fear, anticipatory grief, guilt, anxiety

(c) Family has inadequate understanding of the patient’s condition, or therapy interferes with effective supportive behaviors

(d) Family withdraws from communication with the patient or demonstrates overprotective or underprotective behaviors

b. Goals of care

i. Patient demonstrates increased functional independence, compliance with treatment regimen, and participation in programs that enhance quality of life (e.g., exercise or rehabilitation program)

ii. Patient appropriately expresses ideas, feelings, and needs, participates in family activities, and accepts family support, as appropriate

iii. Patient and family adjust to any necessary role changes

iv. Patient resumes employment

c. Collaborating professionals on health care team (see also Overhydration)

i. Psychiatrist or psychologist

ii. Social worker

d. Interventions

i. Identify common causes of stress in the patient and family

(a) Life-threatening nature of renal disease

(b) Inability to perform activities of daily living

(c) Restrictions caused by a shunt, a fistula, or a Tenckhoff catheter; demands of dialysis schedule and other treatments

(d) Reversal in family roles, effects on sexual behavior and sexuality, and questions regarding ability to maintain or return to work

ii. Recognize that psychologic consequences of renal disease and its treatment include denial, depression, and dependency, and that the suicide rate among patients maintained with hemodialysis is believed to be 100 times that of the general population

iii. Assess the patient’s ability to cope with renal disease (see Chapter 10)

iv. Specific nursing interventions to support adaptation of the patient with renal failure

(a) Teach the patient about the various treatment alternatives and encourage participation in selection of the treatment method

(b) Link with support systems

(1) Visits with successfully adjusted patients

(2) Support for family members; patients with supportive families tend to have fewer physical complications, survive longer, and adjust more readily

e. Evaluation of patient care

i. Patient demonstrates the following:

(a) Participation in self-care, social and family activities, and use of adaptive coping mechanisms such as functional denial

(b) Increased self-esteem with acceptance of body image changes

ii. Family demonstrates the following:

(a) Decreased levels of anxiety, adaptive changes in family roles, and appropriate use of health care and community support systems

(b) Participation in patient care

SPECIFIC PATIENT HEALTH PROBLEMS

Acute Renal Failure

The ARF syndrome affects 5% to 7% of all hospitalized patients and 20% of the critically ill. Oliguria with ARF is associated with a 50% mortality rate in the critically ill and a 50% to 70% mortality rate in trauma or postoperative patients. Nonoliguria with ARF carries a better prognosis and a lower mortality rate of 26%. A mortality rate of 87% is seen in patients with ARF 24 hours after cardiogenic shock due to acute MI. These mortality rates in the critically ill have not improved in the last 45 years, so prevention of ARF remains the best intervention.

1. Pathophysiology

a. Prerenal conditions

i. Physiologic states diminish renal perfusion without renal tubular damage

ii. Effects of diminished kidney perfusion

(a) Decreased renal arterial pressure

(b) Decreased afferent arterial pressure (<100 mm Hg), which diminishes forces favoring filtration

b. Intrarenal conditions

i. Cortical involvement of vascular, infectious, or immunologic processes

(a) Causes renal capillary swelling and cellular proliferation, which eventually decrease the GFR

(b) Edema and cellular debris obstruct the glomeruli, which results in oliguria

ii. Medullary involvement after prolonged ischemia or hypoperfusion or nephrotoxic injury to the tubular portion of the nephrons (Figure 5-4, A)

FIGURE 5-4 A, Anatomy of intrarenal zones predisposed to hypoxic injury in acute renal failure. B, Potential mechanisms causing oliguria in patients with acute renal failure. (From Heyman SN, Fuch S, Brezis M: The role of indwelling ischemia in ARF, New Horiz 3(4):597, 1995.); (From Goldman L, Ausiello D, editors: Cecil textbook of medicine, ed 22, Philadelphia, 2004, Saunders, p 706.)

(a) Medullary hemodynamics: Hypoperfusion states and oxygen insufficiency disrupt the fine balance between limited oxygen supply and high oxygen consumption in the outer medullary region; may contribute to ARF from hypoxic medullary damage

(1) Conditions predisposing to hypoperfusion

a) Presence of endotoxin

b) Rhabdomyolysis

c) Hypercalcemia

d) NSAID use

e) Exposure to radiologic contrast agents

f) Antibiotic use (i.e., amphotericin, cyclosporine)

(2) Pharmacologic agents can also alter medullary hemodynamics, especially if administered in absence of volume depletion (i.e., furosemide, mannitol, dopamine). Other substances suspected of improving medullary hemodynamics are nitric oxide, which is normally produced by the macula densa to control glomerular blood flow and renin release, and ANP, an endogenous vasodilator.

(b) Tubular necrosis produced as localized damage in patchy pattern (actual necrosis) or in apoptosis as disruption of cellular function (usually in the distal tubules): Extent of the damage differs in nephrotoxic injury, ischemia or hypoperfusion, sepsis-associated states, and multiple organ failure

(1) Nephrotoxic injury affects the epithelial cellular layer (can regenerate)

(2) Ischemia and hypoperfusion alter renal tubular cells and damage the tubular basement membrane (cannot regenerate)

a) Cellular injury may involve several factors: ATP depletion, oxygen free radical formation, loss of epithelial cell polarity, and increased calcium levels; apoptosis causes DNA fragmentation and cytoplasmic condensation

b) ATP depletion: Begins 30 seconds after the kidney is hypoperfused; normal homeostatic benefits of cellular ATP (preservation of cellular volume, ionic composition, membrane integrity) are lost

c) Oxidative metabolism produces oxygen free radicals

1) Because these substances are highly reactive and volatile, intracellular mechanisms (enzyme systems and antioxidants) exist for their rapid breakdown and destruction

2) Left unopposed, as during ischemic events, these radicals disrupt cellular functioning (e.g., during ischemia, the renal cell is unstable and unable to protect itself from oxygen free radicals, which results in renal cell injury)

d) Loss of epithelial cell polarity: Ischemia alters the passage of water, electrolytes, and other charged elements through the tubule’s epithelial wall, which leads to a concentration defect

e) Increased calcium levels: Ischemic and hypoperfusion states lead to a rise in intracellular calcium levels that causes renal vasoconstriction and a decrease in GFR

(3) Systemic inflammatory response syndrome (SIRS): Released endotoxins significantly reduce renal perfusion, and renal vasoactive substances alter renal cellular metabolism and constrict renal vasculature (see Chapter 9)

(4) Multiorgan dysfunction syndrome results in rapid and progressive deterioration of renal function (see Chapter 9)

(c) Phases of recovery: Classic form of ARF has four phases, whereas nonoliguric form has only three; the nonoliguric phase seems to be synonymous with the diuretic phase, which suggests that nonoliguric ARF reflects less tubular damage so recovery is more rapid

(d) Onset, or initial phase, precedes the actual necrotic injury and correlates with a major alteration in renal hemodynamics

(1) Associated with a decrease in RBF and GFR

(2) Most important factor altering RBF is decrease in cardiac output

(3) Other mechanisms contributing to decreased renal perfusion are increased sympathetic activity and renal vascular resistance

(4) A consistent increase in cardiac output during this phase will maintain an increase in RBF and protect the patient from impending ARF

(e) Oliguric phase reflects four processes (Figure 5-4, B)

(1) Obstruction of tubules by cellular debris, tubular casts, or tissue swelling

(2) Reabsorption or back-leak of urine filtration through the damaged tubular epithelium and into circulation

(3) Tubular cell damage with development of necrotic, patchy areas; the cell leaks ATP and K⁺, edema is present, mitochondria are altered, and calcium leaks into the cell

(4) Renal vasoconstriction continues and may contribute to the decreased GFR

(f) Nonoliguric phase reflects less tubular damage; symptomatology resembles that of the diuretic phase

(1) Urine output may exceed 1 L/hr

(2) Solute present in urine at approximately 350 mOsm/L

(3) Creatinine clearance is as high as 15 ml/min, and Na⁺ excretion is low

(4) Hyperkalemia remains a significant problem

(5) Phase of short duration; recovery phase reached in 5 to 8 days

(g) Diuretic phase: Signifies that tubular function is returning

(1) Tubular obstruction relieved, but cellular edema remains as scar tissue forms on necrotic areas

(2) Large daily urine output, sometimes exceeding 3 L; output due to the osmotic-diuretic effect of elevated BUN level and impaired ability of tubules to conserve Na⁺ and water

(3) Recovery phase

a) Occurs after gradual improvement of kidney function extending over a 3- to 12-month period

b) Residual renal impairment in GFR may result, with serum creatinine level remaining higher than previously

c. Postrenal conditions: Associated with obstruction of the urinary collecting system

i. Partial obstruction: Can increase renal interstitial pressure, increasing opposing forces of glomerular filtration; result is diminished urine output

ii. Complete obstruction: Impediment to urine flow accompanies bilateral kidney involvement; the “back-up” pressure of urine compresses the kidneys

2. Etiology and risk factors: See Table 5-4

TABLE 5-4

Common Causes of Acute Renal Failure

3. Signs and symptoms

a. Malaise, fatigue, lethargy, confusion

b. Twitching and/or weakness secondary to metabolic acidosis

c. Impaired mobility

d. Change in urine color and/or volume: Oliguria (<400 ml/24 hr); nonoliguria (excess, dilute urine); anuria (no urine output or <100 ml/24 hr); or hematuria

e. Cardiac involvement

i. Dysrhythmias secondary to electrolyte imbalance or heart failure

ii. Change in pulse rate (either tachycardia or bradycardia)

iii. Hypertension

iv. Cardiac friction rub, indicative of pericarditis

f. Skin changes: Dry skin, edema, pallor, bruising, uremic frost (rare), pruritus

g. Flank pain

h. Local or systemic infection presenting with shaking, chills, and fever

i. Abdominal distention secondary to enlarged bladder, obstruction

j. Uremic signs and symptoms: See Table 5-3

4. Diagnostic study findings

a. Laboratory

i. Prerenal

(a) Urinalysis

(1) Urinary sodium level less than 10 mEq/L

(2) SG greater than 1.020

(3) Minimal or no proteinuria

(4) Normal urinary sediment

(5) Urine osmolality higher than 400 mOsm/kg

(b) Serum BUN/creatinine ratio higher than 25:1

ii. Intrarenal—cortical disease

(a) Urinalysis

(1) Urinary sodium level less than 10 mEq/L

(2) SG variable

(3) Moderate to heavy proteinuria

(4) Hematuria

(5) Urinary sediment with erythrocyte casts, leukocytes

(6) Urine osmolality less than 350 mOsm/kg

(b) Serum BUN and creatinine levels elevated but remain in 10:1 ratio

iii. Intrarenal—medullary disease

(a) Urinalysis

(1) Urinary sodium level greater than 20 mEq/L

(2) SG 1.010

(3) Minimal to moderate proteinuria

(4) Urinary sediment with numerous renal tubular epithelial cells, tubular casts, and a rare erythrocyte

(b) Serum BUN and creatinine levels elevated

iv. Postrenal

(a) Serum BUN and creatinine levels elevated with complete obstruction

(b) Bacteriologic report showing significant positive results for a specific organism

v. Special

(a) Antistreptolysin O titer: To diagnose recent streptococcal infection (may cause poststreptococcal glomerulonephritis)

(b) Antiglomerular basement membrane titers: To diagnose Goodpasture’s syndrome, a devastating disease of pulmonary hemorrhage and renal failure

(d) Serum studies for complement components: A fall in complement levels is seen in active complement-mediated glomerulonephritis

(e.g., lupus nephritis)

(e) Serum electrophoresis for immunoglobulin levels: Abnormal proteins (as in multiple myeloma) can damage kidneys

(f) Hepatitis serologic tests: Hepatitis B and C cause kidney disease

b. Radiologic: To rule out obstruction as a cause of oliguria or anuria, because immediate treatment may reverse renal failure. Kidney size provides diagnostic information, because small kidneys imply chronic rather than acute renal failure (see Diagnostic Studies under Patient Assessment)

5. Goals of care

a. ARF is resolved

b. Normal renal function and urine output resume

6. Collaborating professionals on health care team

a. Critical care nurse, clinical specialist or physician assistant, case manager, hemodialysis nurse

b. Physicians: Intensivist, nephrologist (higher mortality when renal consult delayed >48 hours), hematology consult (if blood dyscrasias accompany ARF), vascular surgery consultant

c. Dietitian

d. Social worker

e. Pharmacologist

7. Management of patient care

a. Anticipated patient trajectory: Patients with ARF experience rapid decline, with recovery from 8 days for nonoliguric ATN and from 2 weeks to 3 months for oliguric ATN. Transfer or discharge varies with the stage of renal recovery. Expect patients with ARF to have needs in numerous areas:

i. Skin care: Impaired skin integrity due to uremia, malnutrition, immobility

(a) Assess for uremic effects on skin integrity (Table 5-3)

(b) Keep skin clean, dry, and intact to prevent infection

ii. Nutrition: ARF is associated with accelerated protein catabolism that contributes to negative nitrogen balance and uncontrollably high BUN levels usually indicative of a hypercatabolic state. Repeated elevations of BUN over 100 mg/dl despite routine dialysis correlate with evidence of rapid muscle wasting and indicate the need for higher levels of protein consumption, together with a continuous form of dialysis.

(a) Maintain protein intake at a minimum of 0.6 to 0.8 g/kg of body weight; administer higher amounts of protein during hypercatabolism

(b) Provide total calories of 30 to 35 kcal/kg/day of a carbohydrate and lipid combination while controlling glucose and triglyceride intake

(c) Be aware that hyperalimentation and daily dialysis have been associated with increased survival rates in ARF as well as promotion of renal tubular cell regeneration. Hyperalimentation requirements include consumption of large amounts of both essential and nonessential amino acids.

(d) Give IV glucose and lipid solution to augment caloric and nutritional intake, thereby reducing the need for protein in hypercatabolic states

(e) Maintain fluid restriction by limiting non–electrolyte-containing fluids

(f) Administer water-soluble vitamins. Avoid excessive doses of vitamin C (not exceeding 250 mg/day), which may exacerbate ARF. Be cautious with vitamin A, because excessive intake in the absence of renal excretion can lead to vitamin A toxicity.

(g) Monitor serum protein, albumin, hematocrit, and urea levels and weigh daily to assess the effectiveness of nutritional therapy

iii. Infection control: Uremia increases patient susceptibility to infection

(a) Assess for BUN levels over 80 to 100 mg/dl because these are associated with an increased risk of infection

(b) Monitor for early signs of septic shock (SIRS)

iv. Discharge planning

(a) Teach patient and family members or significant others the following:

(1) Etiology and course of the disease

(2) Dietary and fluid restriction requirements

(3) Dialysis machine operation, procedure, and schedule

(4) Prospects for recovery

(b) Assess and prepare the home for patient care and, if appropriate, for dialysis

(c) Make the patient and family aware of community resources (e.g., national or local kidney foundation [http://www.kidney.org], local dialysis center)

(d) Assist in patient transition to rehabilitation and/or home care

v. Pharmacology

(a) Use pharmacologic agents with adequate fluid replacement to reestablish or augment RBF. This does not protect the tubules from damage but may limit the extent of damage, creating nonoliguric ATN.

(1) Renal-dose dopamine: No longer the therapy of choice for prevention or treatment. Research (Kellum and Decker, 2001) reveals that dopamine has no benefit in treating ARF. Dopamine may actually compromise the kidney by moving oxygen to the renal medulla; can cause tachycardia and mesenteric ischemia and does not decrease mortality.

(2) Diuretics: Studies (Mehta et al, 2002; Singri, Ahya, and Levin, 2003) question their effectiveness in treating ARF

a) Commonly used agents

1) Traditional diuretics (mannitol, loop diuretics): Used to convert oliguria to nonoliguria

2) Mannitol: Protects the kidney by preventing the buildup of cellular debris, reducing tubular obstruction, and augmenting blood flow. Preserves mitochondrial function via osmotic effect; limits recovery ischemia and free radical production. Administer with caution; may precipitate pulmonary edema.

3) Furosemide (Lasix): Acts as both a diuretic and an augmentor of RBF; maximum dosage should not exceed 4 mg/kg/min

b) Diuresis encourages removal of sloughed tubular cells, eliminating tubular obstruction

c) Volume replacement needs to be a priority before administering diuretics; a trial of diuretics can be attempted but should be limited when effectiveness is in question

d) Monitor and report changes in urine output (onset of oliguria, nonoliguria, or anuria)

e) Obtain urine and blood specimens, analyze results

(b) Metabolism and excretion of pharmacologic agents may be altered in ARF (see Patient Care)

vi. Treatments

(a) Prevention modalities for ARF: Remain the best intervention; preservation of renal function is the desired outcome