Urinary System Anatomy and Physiology

Urinary System

Functions of the Urinary System

• The urinary system is a major excretory system.
• Kidneys filter blood to remove wastes, which are carried by ureters to the urinary bladder, and then emptied via the urethra.
• Urine consists of excess water, ions, metabolic wastes (urea), and toxic substances.
• Kidney functions:
  • Excretion of waste products from the blood.
  • Regulation of blood volume and pressure.
  • Regulation of blood solute concentrations.
  • Regulation of extracellular fluid pH (by secreting H^+).
  • Regulation of red blood cell synthesis (by secreting erythropoietin).
  • Regulation of vitamin D synthesis.

Kidney Anatomy and Histology

• Location:
  • Kidneys are bean-shaped and retroperitoneal (behind the peritoneum).
  • Lie on the posterior abdominal wall on either side of the vertebral column.
  • The lumbar vertebrae and rib cage partially protect them.
  • The right kidney is slightly lower than the left due to the liver.

External Anatomy:

• Renal capsule: fibrous connective tissue surrounding each kidney.
• Adipose tissue: surrounds the renal capsule, providing cushioning.
• Renal fascia: a thin layer of loose connective tissue that anchors the kidneys and surrounding adipose tissue to the abdominal wall.
• Hilum:
  • Renal artery and nerves enter.
  • Renal vein and ureter exit.
  • Opens into the renal sinus, a cavity filled with fat and loose connective tissue.

Internal Anatomy:

• Cortex: outer area.
• Renal columns: part of the cortical tissue that extends into the medulla.
• Medulla: inner area (surrounds the renal sinus).
  • Comprised of renal pyramids (cone-shaped structures).
  • Base is beside the cortex, apex is the renal papilla.
• Calyces:
  • Each renal papilla drains urine into a funnel-shaped minor calyx.
  • Minor calyces converge to form a major calyx.
  • Major calyces converge to form the renal pelvis.
• Renal pelvis: an enlarged chamber formed by major calyces, drains into the ureter, which exits at the hilum and drains urine to the urinary bladder.

Nephron - Functional Unit of the Kidney

• Regions of the nephron:
  1. Renal corpuscle
  2. Proximal convoluted tubule (PCT)
  3. Nephron Loop (Loop of Henle)
  4. Distal convoluted tubule (DCT)
• Juxtamedullary nephrons have nephron loops that extend deep into the medulla
• Cortical nephrons have nephron loops that do not extend deep into the medulla
• Path of urine produced by the nephron:
  • Collecting duct
  • Papillary duct
  • Minor calyx and beyond

Types of Nephrons

• Cortical nephrons: Nephron loops do not extend deep into the medulla.
• Juxtamedullary nephrons: Nephron loops extend deep into the medulla. (15% of nephrons)

The Renal Corpuscle

• The filtration part of the nephron is called the renal corpuscle.
• It consists of the glomerulus, a network of capillaries, and the glomerular capsule (Bowman's capsule), a double-walled chamber that surrounds the glomerulus.
• Blood flows from the afferent arteriole into the glomerulus and exits the glomerulus through the efferent arteriole.

Glomerular Capsule (Bowman's capsule)

• Double-walled chamber that surrounds the glomerulus.
  • Parietal layer: outer. Simple squamous epithelium (becomes cuboidal in PCT).
  • Visceral layer: inner. Specialized podocytes wrap around the glomerular capillaries.
• Fluid from the blood is filtered into the glomerular capsule, then passes into the PCT of the nephron.

Filtration Membrane

• Fluid from blood filters across the filtration membrane into the lumen of the glomerular capsule.
• Filtration membrane consists of:
  1. Glomerular capillary endothelium - fenestrated
  2. Basement membrane
  3. Filtration slits between podocyte cell processes

Characteristics of the Renal Corpuscle for Filtration

• Fenestrae of glomerular capillaries increase permeability (large proteins and blood cells cannot pass through).
• Filtration slits in the visceral layer of glomerular capsule allow substances to cross.
• High pressure - glomerular capillaries have a higher pressure because the efferent arteriole leaving the corpuscle has a smaller diameter than the afferent arteriole that enters the corpuscle.

The Juxtaglomerular Apparatus

• Juxtaglomerular apparatus: specialized structure near the glomerulus; also, the site of renin production.
• Consists of:
  • Juxtaglomerular cells: smooth muscle cells form a ring that surrounds the afferent arteriole.
  • Macula densa: specialized tubule cells of the distal convoluted tubule where it passes by the afferent arteriole.

Renal Tubules- Histology

• Proximal convoluted tubule: simple cuboidal epithelium with many microvilli.
• Nephron Loop:
  • Descending limb: first part similar to the proximal tubule, latter part simple squamous epithelium and thinner.
  • Ascending limb: first part simple squamous epithelium and thin, distal part thicker and simple cuboidal.
• Distal convoluted tubule: shorter than the proximal tubule. Simple cuboidal, but smaller cells with fewer microvilli.
• Collecting ducts: Larger diameter, simple cuboidal epithelium. Lead to papillae of renal pyramids.

Arteries and Veins of the Kidneys

1. Renal arteries from the abdominal aorta enter the hilum and branch.
2. Interlobar arteries ascend within renal columns toward the cortex.
3. Arcuate arteries arch over the base of the pyramids.
4. Cortical radiate arteries project into the cortex.
5. Afferent arterioles carry blood to the glomerular capillaries.
6. Glomerular capillaries are the sites of filtration.
7. Efferent arterioles exit the renal corpuscle.
8. Peritubular capillaries form a plexus around the proximal and distal convoluted tubules.
9. Vasa recta: a specialized part of peritubular capillaries that course into the medulla around nephron loops, then back toward the cortex.
10. Peritubular capillaries drain to cortical radiate veins.
11. Arcuate veins.
12. Interlobar veins.
13. Renal vein exits the hilum.

Urine Production

• Nephrons - major functional units; regulate body fluid composition.

Three major steps in urine formation:

• Filtration, tubular reabsorption, and tubular secretion.
• Filtration: Movement of materials across the filtration membrane into the Bowman capsule to form filtrate.
• Solutes are reabsorbed across the wall of the renal tubule into the interstitial fluid via transport processes like active transport and cotransport.
• Water is reabsorbed across the wall of the renal tubule by osmosis. Water and solutes pass from the interstitial fluid into the peritubular capillaries.
• Solutes are secreted across the wall of the renal tubule into the filtrate.

Steps:

1. Filtration: Blood pressure in the glomerular capillaries forces fluid and small molecules out of the blood. The filtered fluid is called filtrate. Filtration is nonselective and separates based only on size or charge of molecules.
2. Tubular Reabsorption: Cells in the renal tubules contain many transport proteins, which move water and some filtered molecules from the filtrate back into the blood in the peritubular capillaries. Most of the filtered water and useful solutes have been returned to the blood by the time the filtrate has been modified to urine, whereas the remaining waste or excess substances and a small amount of water form urine.
3. Tubular Secretion: Certain tubule cells transport additional solutes from the blood into the filtrate. Some of these solutes may not have been filtered by the filtration membrane.

Filtration Details

• Movement of fluid from blood in the glomerulus across the filtration membrane.
• Filtration membrane components:
  1. Fenestrated glomerular capillaries.
  2. Basement membrane.
  3. Filtration slits formed by podocytes of the visceral layer of the glomerular capsule.
• The pressure difference forces filtrate across the filtration membrane.
• Filtrate: water, small molecules, ions that can pass through the membrane.
• The filtration membrane prevents blood cells and proteins from entering the glomerular capsule.
• Some albumin and small proteins enter the filtrate but are reabsorbed by cells of the proximal convoluted tubule.
• Very little protein is normally found in urine.

Filtration Pressure

• Filtration pressure: the pressure gradient responsible for filtration.
• Pressures that contribute:
  1. Glomerular capillary pressure (GCP): Blood pressure in the glomerular capillary tends to move fluid out of the capillary into Bowman's capsule. Higher than other capillaries (50 mm Hg instead of 30 mm Hg) because the diameter of the efferent arteriole is smaller than the afferent arteriole.
  2. Capsule hydrostatic pressure (CHP): the pressure of filtrate already in the lumen.
  3. Blood colloid osmotic pressure (BCOP): osmotic pressure caused by proteins in the blood. Favors fluid movement into the capillary. BCOP is greater at the end of the glomerular capillary because of fluid leaving the capillary (Colloid osmotic pressure in Bowman's capsule is normally close to zero because little protein filters).
• Filtration pressure = GCP (50 mm Hg) - CHP (10 mm Hg) - BCOP (30 mm Hg) = 10 mm Hg
• Net filtration pressure = 10 mm Hg → Direction of the force moves material out of the blood and into the glomerular capsule
• The blood pressure inside the glomerular capillaries. It is an outward pressure from blood pressing on the fenestrated capillary walls. The GCP forces fluid and solutes out of the blood into the glomerular capsule. This GCP is higher than that in other capillaries of the body. The higher GCP is due to the smaller diameter of the efferent arteriole compared to that of the afferent arteriole and glomerular capillaries.
• The CHP is an inward pressure that opposes filtration. CHP is due to pressure from the filtrate fluid in the capsular space. The CHP is about 10 mm Hg.
• The BCOP is also an inward pressure that opposes filtration. It is due to the osmotic pressure of plasma proteins in the glomerular capillaries. Through osmosis, these proteins draw fluid back into the glomerular capillary from the glomerular capsule. The BCOP is greater at the end of the glomerular capillary than at its beginning because there is a higher protein concentration at the end of the glomerulus. The average BCOP is approximately 30 mm Hg.

Glomerular Filtration Rate

• Renal fraction: part of the total cardiac output that passes through the kidneys. (~21%)
• Renal blood flow rate: rate of whole blood flow through kidneys.
• Renal blood flow rate = cardiac output × renal fraction; (~1176 mL/min)
• Renal plasma flow rate: renal blood flow rate x fraction of blood that is plasma: (~650 mL/min)
• Filtration fraction: part of plasma that is filtered. (~19%)
• Glomerular filtration rate (GFR): amount of filtrate produced each minute.
• GFR = renal\ plasma\ flow\ rate \times filtration \ fraction (~125 ml/min)
• Amounts to 180 L/day.
• Average urine production/day: 1 to 2 L. Most of the filtrate must be reabsorbed.

Regulation of Glomerular Filtration Rate

• Intrinsic mechanisms: autoregulation - involves changes in the degree of constriction of afferent arterioles.
  • Myogenic mechanism: as systemic BP increases, afferent arterioles constrict and prevent an increase in renal blood flow.
  • Tubuloglomerular feedback: increased rate of flow of filtrate past cells of macula densa, signal sent to juxtaglomerular cells, afferent arteriole constricts.
• Extrinsic mechanisms: sympathetic nervous system and hormones.
  • Occurs during severe conditions such as hemorrhage or dehydration.
  • Sympathetic stimulation constricts small arteries and afferent arterioles, decreasing renal blood flow and filtrate formation.
  • Renin secreted from juxtaglomerular cells results in the formation of angiotensin II, which stimulates vasoconstriction and maintains GFR.

Tubular Reabsorption: Overview

• Tubular reabsorption: transport of water and solutes from the filtrate back into the blood.
• Reabsorbed substances move from interstitial fluid into peritubular capillaries.
• Sodium, potassium, calcium, bicarbonate, chloride (overall 99% of filtrate is reabsorbed).
• Components of filtrate that are not reabsorbed end up in urine:
  • Urea, uric acid, creatinine, potassium, other substances.

Reabsorption of Solutes In the Proximal Convoluted Tubule

• PCT is the main site of reabsorption.
• Active transport of Na^+ across the basal membrane creates a gradient. Na^+ moves from filtrate into tubular cells across the apical membrane and is responsible for the secondary active transport of many other solutes from the PCT lumen into the cytoplasm of the tubule cells. Symported substances are ones that should be retained by the body.
• Water is reabsorbed from the filtrate by osmosis.
• ~65% of the filtrate volume is reabsorbed by the end of the PCT.
• The number of transport proteins limits the rate of transport. In untreated diabetes mellitus, glucose levels in the filtrate are so high that not all can be reabsorbed (the filtered load exceeds transport maximum). The excess glucose that remains in the filtrate becomes part of the urine (glucosuria).

Reabsorption in the Nephron Loop

• The nephron loop descends into the medulla; interstitial fluid is high in solutes.
  • The descending limb is permeable to water and water moves out of the nephron. The volume of filtrate is reduced by another 15%.
  • The thick ascending limb is not permeable to water. In the thin segment, solutes diffuse out of the tubule into the interstitial fluid. In the thick segment, K^+ and Cl^- are symported with Na^+.

Reabsorption in the Distal Convoluted Tubule and Collecting Duct

• Water reabsorption in the DCT and CD is by osmosis.
• Permeability of DCT and CD walls to water is regulated by ADH.
• Urine can vary in concentration from low volume of high concentration to high volume of low concentration.
• Na^+ reabsorption in the DCT and CD is also under hormonal control, regulated by aldosterone.

Changes In the Concentration of Urea and Other Solutes In the Nephron

• Wastes - urea, uric acid, creatinine, sulfates, phosphates, nitrates - are only partially reabsorbed.
• Tubules are moderately permeable to urea (40 to 60% passively reabsorbed).
• As the volume of the filtrate decreases, the concentration of wastes increases (so their concentration is relatively high in urine).
• Toxic substances and wastes are eliminated.

Tubular Secretion

• Tubular secretion is the movement of nonfiltered substances from the blood into the filtrate (Active or passive).
• Substances include metabolic by-products, drugs, and molecules not normally produced by the body (E.g. para-aminohippuric acid (PAH)).
• Ammonia: produced by epithelial cells of nephron from deamination of amino acids and diffuses into the lumen.
• H^+, K^+, penicillin: actively secreted into nephron.

Urine Concentration Mechanism

• Kidneys can produce urine with varying concentrations (osmolarity).
• The ability to control the volume and concentration of urine depends on a medullary concentration gradient and hormonal mechanisms.
• Medullary concentration gradient: interstitial fluid of medulla has a high solute concentration compared to cortex.
• Maintenance of this gradient depends upon
  • Countercurrent mechanism
  • Urea cycling

Countercurrent mechanism and the Medullary Concentration Gradient

• Relationship between nephron loop and vasa recta.
• Nephron loop: increases solute concentration in the medulla.
• Vasa recta: maintains a high solute concentration in the medulla.

Urea Cycling and the Medullary Concentration Gradient

• Responsible for a large part of the high osmolality in the medulla.
• Urea flows in a cycle, maintaining a high urea concentration in the medulla.
• Collecting ducts are permeable to urea; some diffuses out into the interstitial fluid and reenters the thin segment of nephron loops.

Summary of Urine Formation

• In the average person, about 180 L of filtrate enter the proximal convoluted tubules daily.
• Glucose, amino acids, Na+, Ca^{2+}, K^+, Cl, water, and other substances move from the lumen of the proximal convoluted tubules into the interstitial fluid then enter the peritubular capillaries. Approximately 65% of the filtrate is reabsorbed here. The osmolality of both the interstitial fluid and the filtrate is maintained at about 300 mOsm/kg.
• As the filtrate continues to flow through the renal tubule, it enters the descending limbs of the nephron loops. This portion of the nephron loops is highly permeable to water and solutes. As the descending limbs penetrate deep into the kidney medulla, the surrounding interstitial fluid has a progressively greater osmolality. Water diffuses out of the nephron loops as solutes slowly diffuse into them. By the time the filtrate reaches the deepest part of the nephron loops, its volume has been reduced by an additional 15% of the original volume, at least 80% of the filtrate volume has been reabsorbed, and its osmolality has increased to about 1200 mOsm/kg.
• Both the thin and thick segments are impermeable to water, but solutes diffuse out of the thin segment, and Na^+, Cl, and K^+ are symported from the filtrate into the interstitial fluid in the thick segments. The movement of solutes, but not water, across the wall of the ascending limbs causes the osmolality of the filtrate to decrease from 1200 to about 100 mOsm/kg by the time the filtrate again reaches the kidney cortex.
• The volume of the filtrate does not change as it passes through the ascending limbs. As a result, the filtrate entering the distal convoluted tubules is dilute compared with the concentration of the surrounding interstitial fluid, which has an osmolality of about 300 mOsm/kg.
• The distal convoluted tubule and collecting duct are permeable to water when under hormonal regulation.
• Around 1% or less of the filtrate remains as urine when the body is conserving water.

Regulation of Urine Concentration and Volume

• Filtrate reabsorption in the proximal convoluted tubules and the descending limbs of the nephron loops is obligatory and therefore remains relatively constant.
• Filtrate reabsorption in the distal convoluted tubules and collecting ducts is regulated and can change depending on body conditions.
• Regulation of urine concentration and volume involves hormonal mechanisms and the sympathetic nervous system.
• Hormonal mechanisms include the renin-angiotensin-aldosterone (RAA) mechanism and antidiuretic hormone (ADH) mechanism.

Renin-Angiotensin-Aldosterone Hormone Mechanism

• Mechanism initiated under low blood pressure conditions counteracts dropping blood pressure.
• Renin released by juxtaglomerular cells converts angiotensinogen to angiotensin I.
• Angiotensin-converting enzyme (ACE) in lungs converts angiotensin I to angiotensin II, a potent vasoconstrictor which also stimulates aldosterone secretion, sensation of thirst, and ADH secretion.
• Aldosterone acts on DCT and CD to increase sodium reabsorption and therefore water reabsorption.

Effect of Aldosterone on the DCT and CD

1. When blood pressure decreases, cells of the juxtaglomerular apparatuses in the kidneys secrete the enzyme renin. The kidneys detect low blood pressure when juxtaglomerular cells detect reduced stretch of the afferent arteriole. In addition, the macula densa cells signal the juxtaglomerular cells to secrete renin when the Na^+ concentration of the filtrate increases.
2. Upon secretion, renin enters the blood and converts angiotensinogen, a plasma protein produced by the liver, to angiotensin I.
3. Angiotensin-converting enzyme (ACE) is a proteolytic enzyme produced by capillaries of organs such as the lungs. ACE converts angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstricting hormone that increases peripheral resistance, causing blood pressure to increase. However, angiotensin II is rapidly broken down, so its effect lasts only a short time. Angiotensin II also increases the rate of aldosterone secretion, the sensation of thirst, salt appetite, and ADH secretion.
4. Aldosterone is a steroid hormone secreted by the cortex of the adrenal glands.
5. Aldosterone diffuses through plasma membranes and binds to nuclear receptors of tubular cells lining the distal convoluted tubules and the collecting ducts.
6. Binding of aldosterone to its receptor increases the synthesis of the Na^+/K^+ pumps in the basal membrane and other Na^+ transporters in the apical membrane. This results in increased Na^+ reabsorption and K^+ secretion.

Antidiuretic Hormone Mechanism

• Antidiuretic hormone (ADH) is produced by hypothalamic neurons and stored in the posterior pituitary.
• ADH is released if osmoreceptors in the hypothalamus detect increased osmolality of interstitial fluid.
• ADH is also released if blood pressure decreases substantially (detected by arterial baroreceptors).
• ADH acts on DCT and CD to increase water reabsorption by the insertion of aquaporins, countering any further decrease in blood pressure and/or increase in solute concentration.
• Insufficient ADH secretion = diabetes insipidus.

Effect of ADH on Renal Tubule Water Movement

1. ADH moves from the peritubular capillaries and binds to ADH receptors in the plasma membranes of the distal convoluted tubule cells and the collecting duct cells.
2. When ADH binds to its receptor, a G protein mechanism is activated, which in turn activates adenylate cyclase.
3. Adenylate cyclase increases the rate of cAMP synthesis. Cyclic AMP promotes the insertion of aquaporin-2-containing cytoplasmic vesicles into the apical membranes of the distal convoluted tubules and collecting ducts, thereby increasing their permeability to water. Water then moves by osmosis out of the distal convoluted tubules and collecting ducts into the tubule cells through the aquaporin-2 water channels.
4. Water exits the tubule cells and enters the interstitial fluid through aquaporin-3 and aquaporin-4 water channels in the basal membranes.

Effect of ADH on Urine Concentration and Volume

• In the presence of ADH, the collecting duct is permeable to water and water is reabsorbed into the interstitial fluid. The result is the production of a small volume of concentrated urine.
• In the absence of ADH, the collecting duct is impermeable to water and water remains in the collecting duct. The result is the production of a large volume of dilute urine.

Atrial Natriuretic Hormone

• Atrial natriuretic hormone (ANH) is produced by cells in the right atrium of the heart when they are stretched more than normal, such as increased stretch due to high blood volume.
• ANH decreases blood volume by:
  • Inhibiting Na^+ reabsorption (therefore, less water is reabsorbed).
  • Inhibiting ADH production.
• Increases volume of urine produced.
• Venous return is lowered, volume in the right atrium decreases.

Regulation of Blood Pressure

• Homeostasis is maintained through a balance of blood volume and pressure, with various mechanisms responding to disturbances.
• Increased blood volume leads to elevated blood pressure, which is counteracted by:
  • Inhibition of ADH secretion, reducing water reabsorption.
  • Decreased aldosterone and increased ANH, leading to decreased Na^+ reabsorption.
  • Increased renal blood flow, increasing filtrate formation.
• Decreased blood volume leads to lowered blood pressure, which is countered by:
  • Vasoconstriction of renal arteries.
  • Increased aldosterone and decreased ANH, increasing Na^+ reabsorption.
  • Increased ADH secretion, increasing water reabsorption and thirst.

Urine Movement; Anatomy and Histology of Ureters, Bladder

• Ureters: bring urine from the renal pelvis to the urinary bladder. Lined by transitional epithelium.
• Urinary bladder: a hollow muscular container located in the pelvic cavity posterior to the symphysis pubis. Lined with transitional epithelium; the muscle part of the wall is the detrusor muscle.
• Trigone: the interior of the urinary bladder. Triangular area between the entry of the two ureters and the exit of the urethra. Area expands less than the rest of the bladder during filling.
• Internal urinary sphincter: in males, elastic connective tissue and smooth muscle keep semen from entering the urinary bladder during ejaculation.
• External urinary sphincter: skeletal muscle surrounds the urethra as it extends through the pelvic floor. Acts as a valve.
• The Male urethra extends from the inferior part of the urinary bladder through the penis.
• The Female urethra is shorter; opens into the vestibule anterior to the vaginal opening.

Urine Flow Through Nephron and Ureters

• Hydrostatic pressure moved urine through the nephron tubules.
• Peristalsis in ureters moves urine from the renal pelvis to the urinary bladder.
• Waves occur once every few seconds to minutes, frequency increased by parasympathetic stimulation and decreased by sympathetic stimulation.
• Ureters enter the bladder obliquely through the trigone. Pressure in the bladder compresses the ureter and prevents backflow.

Micturition Reflex

• The urinary bladder is a reservoir for urine; it can stretch to hold about 1 L due to folds of the wall, the transitional epithelium, and stretch of smooth muscle.
• Micturition reflex is activated when the urinary bladder is stretched.
  1. Stretch is detected by stretch receptors
  2. Action potentials are carried to the sacral region of the spinal cord by sensory neurons
  3. Parasympathetic action potentials cause the detrusor muscle to contract.
  4. Decreased somatic motor action potentials cause the external urethral sphincter to relax.
  5. Descending pathways can reinforce or inhibit micturition reflex through voluntary contraction of the external urethral sphincter.
• Urine flows when pressure is great enough to force urine through relaxed external urethral sphincter.

Effects of Aging on Kidneys

• Gradual decrease in the size of kidneys, but only one-third of one kidney is necessary for homeostasis.
• The amount of blood flowing through gradually decreases.
• The number of glomeruli decreases, and the ability to secrete and reabsorb decreases.
• The ability to concentrate urine declines, and the kidney becomes less responsive to ADH and aldosterone.
• Reduced ability to participate in vitamin D synthesis contributes to Ca^{2+} deficiency, osteoporosis, and bone fractures.

Representative Diseases and Disorders of the Urinary System

• Inflammation of the Kidneys
  • Glomerulonephritis: Inflammation of the filtration membrane within the renal corpuscle, causing an increase in the filtration membrane's permeability; plasma proteins and blood cells enter the filtrate, which increases urine volume due to increased osmotic concentration of the filtrate
    • Acute glomerulonephritis: Often occurs 1 to 3 weeks after a severe bacterial infection, such as "strep throat"; normally subsides after several days
    • Chronic glomerulonephritis: Long-term, progressive process whereby the filtration membrane thickens and is eventually replaced by connective tissue; the kidneys become nonfunctional
  • Pyelonephritis: Often begins as a bacterial, usually E. coli, infection of the renal pelvis, which spreads to the rest of the kidney; the infection can destroy nephrons, dramatically reducing the kidney's ability to concentrate urine
• Renal Failure: Can result from any condition that interferes with kidney function
  • Acute renal failure: Occurs when damage to the kidney is rapid and extensive; leads to the accumulation of wastes in the blood; if renal failure is complete, death can occur in 1 to 2 weeks
  • Chronic renal failure: Caused by permanent damage to so many nephrons that the remaining nephrons are inadequate for normal kidney function; can result from chronic glomerulonephritis, trauma to the kidneys, tumors, or kidney stones

Acute Renal Failure Symptoms/Treatments

• Symptoms:
  • Decreased urine volume
  • Increased Na+ in urine
  • Decreased urine osmolality
• Treatments
  • Hemodialysis
  • Kidney transplant
• Organ System Effects:
  • Integumentary: Anemia causes pallor, and bruising results from clotting proteins lacking in the blood because they are lost in the urine.Accumulation of urinary pigments changes skin tone.High urea gives a yellow cast to light-skinned people, and white crystals of urea, called uremic frost, may appear on areas of the skin where there is heavy perspiration.
  • Skeletal: Bone resorption can result because of excessive loss of Ca^{2+} in the urine, Vitamin D levels may be reduced..
  • Digestive: Decreased appetite, mouth infections, nausea, and vomiting result from altered digestive tract functions due to the effects of ionic imbalances on the nervous system.
  • Respiratory:early during acute renal failure, the depth of breathing increases, and breathing becomes labored as acidosis develops because the kidneys are not able to secrete H+.Pulmonary edema often develops because of water and Na+ retention as a result of reduced urine production.The likelihood of pulmonary infection increases as a result of pulmonary edema.
  • Muscular: Neuromuscular irritability results from the toxic effect of metabolic wastes on the central nervous system and ionic imbalances, such as elevated blood K^+ levels.Involuntary jerking and twitching may occur as neuromuscular irritability develops.
  • Nervous: Elevated blood K^+ levels and the toxic effects of metabolic wastes result in the depolarization of neurons.Slowing of action potential conduction, burning sensations, pain, numbness, or tingling results.Also, decreased mental acuity, reduced ability to concentrate, apathy, and lethargy occur.Or in severe cases, confusion and coma occur..
  • Lymphatic: There are no major direct effects on the lymphatic system, except that increased lymph flow happens as a result of edema.
  • Cardiovascular: Water and Na^+ retention may cause edema in peripheral tissues and in the lungs, leading to increased blood pressure and congestive heart failure.Elevated blood K^+ levels result in dysrhythmias and can cause cardiac arrest.Anemia due to decreased erythropoietin production by the damaged kidney exists.
  • Endocrine: Major hormone deficiencies include vitamin D deficiency. In addition, secretion of reproductive hormones decreases due to the effects of metabolic wastes and ionic imbalances on the hypothalamus.