The Renal System

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CHAPTER 5

The Renal System

SYSTEMWIDE ELEMENTS

Physiologic Anatomy

1. Process of urine formation

    Urine formation occurs in the renal nephron and involves four processes—filtration, reabsorption, secretion, and excretion

a. Anatomic structures of the kidney: Most humans are born with two kidneys; a small number are born with one. The kidneys are located in the retroperitoneal space above the waist (Figure 5-1).

i. Cortical (outermost) layer

ii. Medullary (middle) layer

iii. Renal sinus, pelvis, and collecting system

iv. Nephron: Anatomic microscopic structure (Figure 5-2)

(a) Structural and functional unit of the kidney

(b) Approximately 1 million in each kidney

(c) Compensates for a significant degree of nephron destruction by

(d) Types of nephrons, based on location and function

(e) Functional segments of the nephron

(1) Renal corpuscle

a) Bowman’s capsule: Specialized portion of the proximal tubule that supports the glomerulus

b) Glomerulus: Capillary bed with semipermeable membrane

    1) Normally permeable to water, electrolytes, nutrients, wastes; relatively impermeable to large protein molecules, albumin, erythrocytes

    2) Composed of three cellular layers: Fenestrated endothelial layer, basement membrane, and epithelium podocyte cells that contribute to characteristic semipermeability of this membrane

    3) Characteristics of cellular layers: Endothelial cells contain fenestrations 50 to 100 nm wide, favoring the movement of water and solute; remaining layers are less porous, with openings 1500 nm thick, which may explain the impedance of macromolecules

    4) Major factor influencing filtration is molecular size

    5) Ionic charge also affects filtration

(2) Renal tubules

b. Physiologic processes

i. Glomerular ultrafiltration is the first step in the formation of urine

(a) Characteristics of glomerular filtrate

(b) Filtration is determined by the glomerular pressure and presence of a normal semipermeable glomerular membrane

(c) Glomerular filtration rate (GFR)

(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

image

    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

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

(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

b) Osmosis: Water following an osmotic gradient

(2) Active mechanisms:

(c) Proximal convoluted tubule

(d) Loop of Henle

(e) Distal convoluted tubule

(f) Collecting duct

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

iii. Juxtaglomerular apparatus: Site of renin synthesis

b. Renal blood flow (RBF) parameters

c. Distribution of RBF

d. Intrarenal autoregulation: General principles

e. Neural control

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

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

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:

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

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)

(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:

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

(c) Aldosterone (provides feedback mechanism for maintenance of K+ in ECF)

(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)

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

(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

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

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

b. Creatinine: A waste product of muscle metabolism

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

b. Hydrogen ion secretion

c. Renal buffers of hydrogen ions

i. Buffers that are filtered by the glomerulus

ii. Buffers produced by the kidney tubule

d. Summary of renal responses to acidemia

e. Summary of renal responses to alkalemia

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

a. Maintenance of volume and composition of ECF

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

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

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

9. Aging kidney

a. Age-related changes can occur as early as 20 to 40 years of age. Changes include a decrease in tubular length and, at and over age 40 years, a progressive decrease in the percentage of glomeruli. Generally, renal function is diminished by 10% at age 65; may diminish further with aging.

b. Renal response in the elderly

Patient Assessment

1. Nursing history

a. Patient health history

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

ii. History of specific signs and symptoms

(a) Signs and symptoms of urinary tract disorders

(1) Dysuria

(2) Abnormal appearance of urine

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

(4) Polydipsia

(5) Patterns of urine output

(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:

c. Social history and habits