Only $35.99/year

Kidney Structure and Function

Terms in this set (22)

1. Excretion of metabolic waste products, foreign chemicals, drugs, and hormone metabolites- urea, creatinine, uric acid, end products of hemoglobin breakdown i.e. bilirubin, and metabolites of various hormones. These waste products must be eliminated from the body as rapidly as they are produced. Also eliminates most toxins and other substances like pesticides, drugs, and food additives. Excretion of Metabolic Waste Products, Foreign Chemicals, Drugs and Hormone Metabolites
primary means for waste product elimination; waste products must be eliminated as rapidly as they are produced
urea - from amino acid metabolism
creatinine - from muscle creatinine
uric acid - from nucleic acids
end products of hemoglobin breakdown - bilirubin
metabolites of various hormones
toxins - produced by body or ingested (pesticides, drugs or food additive

2. Regulation of water and electrolyte balances- excretion of water and electrolytes must precisely match intake. Kidneys adjust their excretion rates to match the body's intake. The capacity of the kidneys to alter sodium excretion in response to changes in sodium intake is enormous. Regulation of Water and Electrolyte Balances
For maintenance of homeostasis
If intake exceeds excretion, the amount of substance in the body will increase

3. Regulation of arterial pressure- plays a role in regulation of arterial pressure by excreting variable amounts of sodium and water. Also contribute to short-term arterial pressure regulation by secreting hormones and vasoactive factors, or substances (renin) that lead to the formation of vasoactive products (angiotensin II). Regulation of Arterial Pressure
Kidneys play dominant role in managing arterial pressure by excreting variable amounts of sodium and water
Kidneys contribute to short term arterial pressure regulation by secreting hormones and vasoactive factors (renin)that lead to formation of vasoactive products (angiotensin II)

4. Regulation of acid-base balance- the kidneys are the only means of eliminating from the body certain types of acids, such as sulfuric and phosphoric acid generated by the metabolism of proteins. Regulation of Acid-Base Balance
Kidneys work with lungs and body fluid buffers by excreting acids and by regulating body fluid buffer stores
Kidneys are only means of eliminating sulfuric and phosphoric acid (generated by metabolism of proteins)

5. Regulation of erythrocyte production- kidneys secrete erythropoietin which stimulates the production of red blood cells by hematopoietic stem cells in the bone marrow Regulation of Erythrocyte Production
Kidneys secrete erythropoietin which stimulates the production of RBCs by hematopoietic stem cells in the bone marrow
Hypoxia can stimulate the kidneys to produce erythropoietin
People with renal disease or on dialysis have decreased levels of erythropoietin

6. Regulation of 1,25-dihydroxyvitamin D3 (calcitriol)- the kidneys produce an active form of calcitriol by hydroxylating this vitamin at the "number 1" position. Calcitriol is essential for normal calcium deposition in the bones, and calcium reabsorption by the GI tract. Regulation of 1,25-Dihydroxyvitamin D3 Production
Kidneys produce this active form of vitamin D (calcitriol) by hydroxylating this vitamin at the number 1 position
Calcitriol is essential for normal calcium deposition in bone and calcium reabsorption in the GI tract

7. Glucose synthesis- the kidneys synthesize glucose from amino acids and other precursors during prolonged fasting, a process referred to as gluconeogenesis. The kidney's capacity to add glucose to the blood during prolonged periods of fasting rivals that of the liver. Glucose Synthesis
Kidneys synthesize glucose from amino acids and other precursors during fasting (process known as gluconeogenesis)
Also able to add glucose to blood during fasting (similar to capabilities of the liver)
Hall pages 303-304

List the functions of the kidneys. Guyton and Hall p 303-304
Renal Pyramids - 8-10 triangular structures located in the medulla of each kidney
Renal Cortex - granular, forms a shell around medulla. The tissue dips into the medulla between renal pyramids forming renal columns
Renal Capsule - The tissue that surrounds the kidney, tough and fibrous, and protects the kidney's inner structure
Medulla - Composed of conical masses of tissue called renal pyramids
Renal Pelvis - A funnel shaped continuation of the upper end of the ureter. Located inside the renal sinus, subdivided into 2 or 3 tubes called the major calyces. Major calyces are subdivided into minor calyces.
Nephron - The functional unit of the kidney.
The internal structure of the kidney is divided into two main areas: a light outer area called the renal cortex, and a darker inner area called the renal medulla.
Medulla is divided into 8-10 cone shaped masses known as Renal Pyramids. The base of each pyramid originates at the border between the cortex and medulla and terminates in the Papilla, which projects into the Renal Pelvis.

The outer border of the renal pelvis is divided Major Calyces (open ended pouches) that extend downward and divide into Minor Calyces (collect urine from the tubules of each papilla.

The walls of the Calyces, Pelvis and Ureter contain contractile elements that propel urine toward the Bladder, where urine is stored until it is emptied.

Interlobular Artery - delivers oxygenated blood at high pressure to glomerular capillaries
Renal Artery - Delivers oxygenated blood to the kidney. Arise from abdominal aorta, enters kidney through the hilum. Transports large volumes of blood (15-30% of cardiac output) to the kidneys when a person is at rest.
Renal Vein - Receives deoxygenated blood from the peritubular veins; Joins the inferior vena cava as it courses through the abdomen.
Interlobular Vein - Receives deoxygenated blood at lower pressure that it drains away from glomerular filtration and Loop of Henle.
Renal Hilum / Hilum - where various blood vessels, nerves, lymphatic vessels and ureter pass through

Renal Blood Supply - The Renal Artery enters kidney through the hilum (Renal Hilum) then branches progressively to form the Interlobular Arteries (also known as renal arteries) which lead to Glomerular capillaries - where large amounts of fluid and solutes are filtered to begin urine formation. The distal end of the capillaries form the efferent arteriole which leads to the peritubular capillaries (the kidney has two sets of capillaries). These eventually split into afferent arterioles (one of which serves the nephrons). The peritubular capillaries empty into the vessels of the venous system which run parallel to the arteriolar vessels. The blood vessels of the venous system form the Interlobular Vein, Arcuate Vein Interlobar Vein and Renal Vein, which leaves the kidney beside the renal artery and ureter. Guyton and Hall p304-305
Determinants of glomerular filtration rate:
a. Glomerular hydrostatic pressure (pressure wanting to push the fluid out of the arteriole into the bowman's capsule - promotes filtration), hydrostatic pressure in Bowman's capsule (wants to push the fluid in the arteriole - opposes filtration), and glomerular colloid osmotic pressure (wants to hold onto the fluids in the arteriole - opposes filtration).
Net filtration pressure (10 mm Hg) = Glomerular hydrostatic pressure (60 mm Hg) - Bowman's Capsule pressure (18 mm Hg) - Glomerular colloid osmotic pressure (32 mm Hg).
GFR = 125 ml / min
b. GFR = glomerular capillary filtration coefficient ( Kf ) x net filtration pressure.
- Kf - is a measure of the product of the hydraulic conductivity and surface area of the glomerular capillaries.
o Increasing Kf (increase the surface area for filtration) raises GFR and decreasing Kf (reduce the surface area for filtration or increase the thickness of glomerular capillary membrane - reduce hydraulic conductivity) reduces GFR.
- Kf = 12.5 ml/min per mm Hg, or 4.2 ml/min per mm/Hg / 100 gm (400 x greater than other capillaries of the body).
Table 26-2 (Hall p. 316) - Shows factors that can decrease the GFR.
Renal blood flow:
- Combined blood flow through both kidneys is about 22% of cardiac output.
- Oxygen and nutrients delivered to kidneys normally greatly exceeds their metabolic needs.
- Additional blood flow is to supply enough plasma for the high rates of GFR.
- The mechanisms that regulate renal blood flow are closely linked to the control of GFR and the excretory functions of the kidneys.

Factors that control GFR and RBF (Refer to Dr. Arbour's ppt slide 18 (summary of neurohormonal control of GFR and renal blood flow)
a. Sympathetic nervous system: constrict the renal arterioles and decrease renal blood flow [Severe sympathetic stimulation has a greater influence in pt's GFR and RBF compare to mild-moderate SNS stimulation]
b. Catecholamines (Epi & Norepi): constrict afferent and efferent arteriole à decrease GFR and decrease RBF
c. Endothelin: is a peptide that is released by damaged blood vessel which acts as a vasoconstrictor. It decreases GFR and RBF
d. Angiotension II: constricts efferent arteriole which increase glomerular hydrostatic pressure while decreasing RBF (constricting efferent arteriole à decreased flow through the peritubular capillaries àincreases reabsorption of sodium and water. Constricting efferent arteriole helps prevent decreases in glomerular hydrostatic pressure and GFR. Angiotension II has no change in GFR but decreases RBF.
e. Endothelial-derived nitric oxide or EDRF (endothelial-derived relaxing factor): protect against excess vasoconstriction. Helps increase GFR and RBF
f. Prostaglandins: hormone that causes vasodilation. Increases GFR and RBF.
g. Fever, pyrogens: increase GFR
h. Glucocorticoids: increase GFR
i. Aging: decrease GFR 10% / decade after 40 years
j. Hyperglycemia: Increase GFR (DM)
k. Dietary protein: high protein increase GFR, low protein decreases GFR
The Reabsorption process is highly variable and selective.

For a substance to be reabsorbed, (1) it must be transported across the tubular epithelial membranes into the renal interstitial fluid (either through transcellular path or paracellular path) and then (2) through the peritubular capillary back into the blood (figure 27-1 Hall p. 324).
· Transcellular path:
o Water and solutes can be transported through cell membranes themselves (transcellular path) by passive diffusion or active transport (Na+-K+ ATPase pump, Hydrogen ATPase, Hydrogen-potassium ATPase and Calcium ATPase)
§ Primary active transport of Na+: (Figure 27-2 p.325)
· Na+ diffused across the luminal membrane into the cell down electrochemical gradient
· Then transported in across the basolateral membrane against electrochemical gradient by the Na+-K+ ATPase pump
· Then Na+ and H20 and other substances is reabsorbed from the interstitial fluid by ultrafiltration.
o Secondary active transport (two or more substances with a specific membrane protein (a carrier molecule) and are transported together across the membrane). [ex. Sodium glucose co-transporters]
o Osmosis - water diffusion from a region of low solute concentration to one of high solute concentration
· Paracellular path:
o Substances transported between tubular cells by diffusion.

Different rates of filtration, reabsorption and excretion of certain substances (Table 27-1 p. 324)
Most electrolytes (Na+, Cl-, K+, glucose - nutritional substance) reabsorbed. Waste products are poorly reabsorbed.

Concentration of solutes in different parts of the tubule depend on relative reabsorption of the solutes compared to water. [If water is reabsorbed to a greater extent than the solute, the solute will become more concentrated in the tubule. If water is reabsorbed to a lesser extent than the solute, the solute will become less concentrated in the tubule]

Proximal tubules: 65% of filtered load (permeable to water, Na+, K+, Cl-, certain organic solutes - glucose, amino acids and bicarbonate

Loop of Henle:
· Thin descending Loop of Henle: very permeable to water (solute will become more concentrated in the tubule)
· Thick ascending loop of henle: about 25% of filtered load. Permeable to electrolytes (Na+, K+, Cl-, bicarb, Calcium, and magnesium). NOT permeable to water (the tubule fluid will become less concentrated).

Early distal tubule: about 5% of filtered load (Similar function as thick ascending loop of henle)
· Permeable to Na+, Cl-, K+, and magnesium
· NOT permeable to water.
· NOT very permeable to urea

Late distal tubule and collecting tubule: permeability regulated by ADH
· Presence of ADH = H20 is reabsorb and permeable (tubular fluids more concentrated)
· Absence of ADH = H20 remain in the tubule (tubular fluids is less concentrated)
Tubule reabsorption and glomerular filtration are quantitatively large relative to urinary secretion for many substances, meaning a small change in either can potentially cause a large change in urinary secretion. Tubular reabsorption is also highly selective. Glucose and amino acids are almost completely reabsorbed in the tubules, leaving almost zero to be excreted in urine. Plasma ions such as chloride, bicarbonate, and sodium are reabsorbed based on the needs of the body, so their excretion rates vary. Waste products like urea and and creatinine are poorly reabsorbed, so excretion rate is increased. (Hall, p. 323-324)
Before a substance can be reabsorbed, it must be transported by either active or passive transport mechanisms. It is transported first across the epithelial membranes into the interstitial fluid, then through the peritubular capillary membrane back into the blood. (see Hall, figure 27-1)
In order to maintain a precise balance between tubular reabsorption and glomerular filtration, multiple hormonal, nervous, and local control mechanisms regulate and control through the following:
Glomerulotubular Balance - tubules increase their reabsorption rate in response to increased tubular load. Helps prevent overloading of the distal tubular segments when GFR increases.
Peritubular Physical Forces - Changes in peritubular capillary reabsorption influences the hydrostatic and colloid osmotic pressures of the renal interstitium, and in turn, the reabsorption of water and solutes from the renal tubules.
Hormones- Several hormones enable specificity of tubular reabsorption for different electrolytes and water. (Hall, table 27-3, p. 338)
Aldosterone - increases sodium reabsorption and stimulates potassium secretion.
Angiotensin II - increases sodium and water reabsorption.
Antidiurectic hormone (ADH) - increases water reabsorption
Atrial natriuretic peptide - decreases sodium and water reabsorption.
Parathyroid hormone - increases calcium reabsorption.
Sympathetic Nervous System - decreases sodium and water excretion by constricting the renal arterioles. Increases sodium reabsorption in the proximal tubule, Loop of Henle, and perhaps the renal tubules by activation α-adrenergic receptors on the renal tubular epithelial cells.
Arterial Pressure - small increases in arterial pressure can cause marked increases in urinary excretion of sodium and water, which is referred to as pressure natriuresis and pressure diuresis. Increasing arterial pressure effects the GFR, which in turn effects urinary output. Urine output is also increased by arterial pressure due to the decreased absorption of filtered sodium and water that is reabsorbed by distal tubules. Decreased Angiotensin II formation due to arterial pressure also leads to increased sodium reabsorption by the tubules.
Osmotic Factors - changes in osmotic pressure due to because of dilution of proteins in the renal interstitium decrease net reabsorption of fluid from the renal tubules. (Hall, p. 334-339)
Renal Glycosuria - transport mechanism for tubular reabsorption of glucose is greatly limited or absent, therefore large amounts of glucose pass into the urine daily.
Aminoaciduria - deficient reabsorption of amino acids due to failures in transport systems.
Renal Hypophosphatemia - failure of renal tubules to reabsorb phosphate ions when phosphate concentration is low. If untreated, may develop rickets.
Renal tubular acidosis - renal tubules are unable to secrete hydrogen ions due to a genetic disorder or injury of the renal tubules. Large amounts of sodium bicarb are lost in the urine, resulting in a metabolic imbalance.
Nephrogenic Diabetes Insipidus - renal tubule do not respond to ADH, and large amounts of dilute urine are excreted. Unless enough water is replaced, dehydration results.
Fanconi's Syndrome - failure to absorb amino acids, glucose, and phosphate due to a genetic defect or injury by toxins or ischemia.
Bartter's Syndrome - autosomal recessive disorder caused by impaired function of the 1-sodium, 2-chloride, 1-potassium co-transporter, or by defects in potassium or chloride channels. Volume depletion activates the renin-angiotensin-aldosterone system, leading to hypokalemia and metabolic acidosis.
Gitelman's Syndrome - autosomal recessive disorder of the thiazide-sensitive sodium-chloride co-transporter of the distal tubules. Similar to Bartter's Syndrome.
Liddle's Syndrome - autosomal dominant disorder resulting in various mutation of the amiloride-sensitive epithelial sodium channel in the distal and collecting tubules. Results in increased reabsorption of sodium and water, HTN, and metabolic alkalosis. (Hall, p. 408-409)
Plasma concentration of waste products like BUN and creatinine , urine specific gravity, urine concentrating ability, urinalysis strips which test for protein , glucose, etc. Biopsy, albumin excretion, renal scans, imaging methods such as MRI, PET , arteriograms, IV pyelography, ultrasound. Clearance methods (e.g. 24 hour creatinine clearance.

Blood Tests
Serum Creatinine
Creatinine is a waste product that comes from the normal wear and tear on muscles of the body. Creatinine levels in the blood can vary depending on age, race and body size. A creatinine level of greater than 1.2 for women and greater than 1.4 for men may be an early sign that the kidneys are not working properly. The level of creatinine in the blood rises, if kidney disease progresses.
Glomerular Filtration Rate(GFR)
This test is a measure of how well the kidneys are removing wastes and excess fluid from the blood. It may be calculated from the serum creatinine level using your age, weight, gender and body size. Normal GFR can vary according to age (as you get older it can decrease). The normal value for GFR is 90 or above. A GFR below 60 is a sign that the kidneys are not working properly. A GFR below 15 indicates that a treatment for kidney failure, such as dialysis or a kidney transplant, will be needed.
Blood Urea Nitrogen (BUN)
Urea nitrogen comes from the breakdown of protein in the foods you eat. A normal BUN level is between 7 and 20. As kidney function decreases, the BUN level rises.
Imaging Tests
This test uses sound waves to get a picture of the kidney. It may be used to look for abnormalities in size or position of the kidneys or for obstructions such as stones or tumors.
CT Scan
This imaging technique uses contrast dye to picture the kidneys. It may also be used to look for structural abnormalities and the presence of obstructions.
Kidney Biopsy
A biopsy may be done occasionally for one of the following reasons:
to identify a specific disease process and determine whether it will respond to treatment
to evaluate the amount of damage that has occurred in the kidney
to find out why a kidney transplant may not be doing well
A kidney biopsy is performed by using a thin needle with a sharp cutting edge to slice small pieces of kidney tissue for examination under a microscope.
Urine Tests
Some urine tests require only a couple of tablespoonfuls of urine. But some tests require collection of all urine produced for a full 24 hours. A 24-hour urine test shows how much urine your kidneys produce in one day. The test also can give an accurate measurement of how much protein leaks from the kidney into the urine in one day.
Includes microscopic examination of a urine sample as well as a dipstick test. The dipstick is a chemically treated strip, which is dipped into a urine sample. The strip changes color in the presence of abnormalities such as an excess amount of protein, blood, pus, bacteria and sugar. A urinalysis can help to detect a variety of kidney and urinary tract disorders, including chronic kidney disease, diabetes, bladder infections and kidney stones.
Urine Protein
This may be done as part of a urinalysis or by a separate dipstick test. An excess amount of protein in the urine, called proteinuria. A positive dipstick test (1+ or greater) should be confirmed using a more specific dipstick test (an albumin specific dipstick) or by a quantitative measurement, such as albumin-to-creatinine ratio.
This is a more sensitive dipstick test, which can detect a tiny amount of protein called albumin in the urine. People who have an increased risk of developing kidney disease, such as those with diabetes or high blood pressure, should have this test if their standard dipstick test for proteinuria is negative.
Creatinine Clearance
A creatinine clearance test compares the creatinine in a 24-hour sample of urine to the creatinine level in your blood to show how much blood the kidneys are filtering out each minute.

Creatinine clearance is used to assess GFR. creatinine clearance is equal to creatinine excretion divided by creatinine concentration. Hall p. 341
According to Guyton & Hall, and the stimuli for thirst discussed on page 358 of the text, there are several causes for the feeling of thirst. One of the most important is:

· "Increased extracellular fluid osmolarity, which causes intracellular dehydration in the thirst centers", which stimulates the thirst response. In other words, the ECF is more concentrated with solutes and needs more water.
· "Decreases in extracellular fluid volume and arterial pressure also stimulate thirst"- this makes sense, doesn't it? If there is less fluid volume outside the cells, or the arterial pressure is higher, we need to cause some expansion via dilution by adding more water.
· "Dryness of the mouth and mucous membranes of the esophagus" will stimulate the thirst response - this one is pretty self explanatory.
· "GI & pharyngeal stimuli influence thirst"—That "full" feeling that we experience after drinking a big glass of water when we are really thirsty... you've probably felt that before, right? That is the body's way to help alleviate that thirst response. It may take up to 30-60 min for the water to be absorbed by the body, but if this reflex didn't occur in the GI tract, we would overwhelm our body with water - i.e. water intoxication, etc.

All of the above tends to make sense, right? Well, combine it with urine concentration now. So, if our urine is concentrated, would we be hydrated or dehydrated?? Most likely DEHYDRATED, right? Why? Because our body is trying to save water and it makes the urine more concentrated. Inversely, we have a less concentrated urine when we have a higher intake of water than is needed by the body. But this also occurs with alcohol intake as it blocks ADH and our body excretes excess water—this what causes "Hangover headaches" - dehydration. There are other reasons for more dilute urine as well, including diabetes insipidus, etc.
These are many factors that affect the urine concentrations. Normal kidneys have tremendous capability to vary the relative proportions of solutes and water in the urine in response to various challenges. For example, antidiuretic hormone controls urine concentration, where it regulates plasma osmolarity and sodium concentration that operates by altering renal excretion of water independently of the of solute excretion. When osmolarity of the body fluids become too concentrated, the posterior pituitary gland secretes more ADH, which increases the permeability of the distal tubules and collecting ducts to water. This permits large amount of water to be reabsorbed and decreases urine volume but does not markedly alter the rate of renal excretion of the solutes. (Hall, pg 345)
Vice versa, when there's excessive water in the body, the kidney will excrete high urine output by reabsorbing large amount of solutes and does not reabsorb water in the distal parts of the nephrons.
***Requirements for excreting a concentrated urine—HIGH ADH levels and hyperosmotic renal medulla. A high ADH increases the permeability of the distal tubules and collecting ducts of water, thereby allowing these tubular segments to avidly reabsorb water and a HIGH OSMOLARITY of the MEDULLARY INTERSTITIAL FLUIDS, which provides the osmotic gradient necessary for water reabsorption to occur in the presences of high levels of ADH. (Hall, 348)

Factors that affect the urine concentration because they affects the regulation of tubular reabsorption which were included in Dr. Arbour's lecture.
Glomerulotubular balance
Peritubular physical forces
Angiotensin II
Natriuretic hormones (ANF
Parathyroid hormone
Sympathetic Nervous System
Arterial Pressure (pressure natriuresis)
Osmotic factors- water is reabsorbed only by osmosis
(** Increasing the amount of reabsorbed solutes in the tubules decreases water reabsorption.

Overall, it depends the volume status of your patients. It your patient had a trauma or hemorrhages shock or dehydrated from days of nausea/vomiting and diarrhea (WATER DEFICIT) this causes
=è INCREASE extracellular osmolarity èINCREASE ADH secretion (posterior pituitary)è INCREASE plasma ADH è INCREASE H20 permeability in distal tubules, collecting ductsè INCREASE H20 reabsorptionè DECREASE H20 excreted. (Hall, pg. 355)
Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract. Obstruction may be anatomical or functional. It impedes flow proximal to the obstruction, dilates structures distal to the obstruction, increases risk for infection, and compromises renal function.

Common causes of upper urinary tract obstruction include stricture or congenital compression of a calyx or the ureteropelvic or ureterovesical junction; ureteral compression from an aberrant vessel, tumor, or abdominal inflammation and scarring; or ureteral blockage from stones or a malignancy of the renal pelvis or ureter.

Anatomic changes in the urinary system caused by obstruction are referred to as obstructive uropathy. The severity is based on location, completeness, involvement of one or both urinary tracts, duration, and cause.

Obstruction causes dilation of the ureter, renal pelvis, calyces, and renal parenchyma proximal to the site of urinary blockage.
Dilation of the ureter is referred to as hydroureter, and dilation of the renal pelvis and calyces proximal to a blockage lead to hydronephrosis (enlargement of the renal pelvis and calyces) or ureterohydronephrosis.
Dilation of the upper urinary tract is an early response to obstruction and reflects smooth muscle hypertrophy and accumulation of urine above the level of blockage (urinary stasis/retention). Unless the obstruction is relieved, this dilation leads to enlargement with tubulointerstitial fibrosis and apoptosis affecting the distal nephron and renal function.

Tubulointerstitial fibrosis is the deposition of excessive amounts of extracellular matrix. Deposition of extracellular matrix is a normal process of organ repair and maintenance, and the deposition of extracellular matrix is balanced by its breakdown under the influence of metalloproteinases.
Apoptosis is a normal process that the body uses to replace damaged cells with new ones.

The body is able to partially counteract the negative consequences of unilateral obstruction by a process called compensatory hypertrophy and hyperfunction.
The compensatory response is the result of two growth processes: obligatory growth occurs under the influence of somatomedins, and compensatory growth occurs under the influence of a hormone or hormones that have not yet be identified. These processes cause the contralateral (unobstructed) kidney to increase the size of individual glomeruli and tubules but not the total number of functioning nephrons (because the kidney cannot make new nephrons...what you have is what you have).

Relief of bilateral, partial urinary tract obstruction or complete obstruction of one kidney is usually followed by a brief period of diuresis called postobstructive diuresis.
It is a physiologic response and is typically mild, representing a restoration of fluid and electrolyte imbalance caused by the obstructive uropathy.

McCance and Huether, p. 1340-1342 and from the slides from lecture
Calculi, or urinary stones are masses of crystals, protein, or other substances that are a common cause of urinary tract obstruction in adults. Calculus formation is complex and related to: 1) supersaturation of one or more salts in the urine, 2) precipitation of the salts from a liquid to a solid state (crystals), 3) growth through crystallization or agglomeration (aggregation), and 4) the presence or absence of stone inhibitors. Supersaturation is the presence of a higher concentration of salt within the urine than the volume is able to dissolve. Human urine contains many positively and negatively charged ions capable of precipitating from solution and forming a variety of salts. The salts form crystals that are retained and grow into stones. Crystallization is the process by which crystals grow from a small nidus or nucleus to larger stones in the presence of supersaturated urine. Once the nidus has been formed, the urine doesn't need to stay supersaturated for the stone to form. Intermittent periods of supersaturation is sufficient for the stone to grow after the nidus has been formed.

Alkaline urinary pH significantly increases the risk of calcium phosphate stone formation, whereas acidic urine increases the risk of a uric acid stone. Cystine and xanthine precipitate more readily in acidic urine.

Potassium citrate, pyrophosphate, and magnesium are capable of crystal growth inhibition, reducing the risk of calcium phosphate or calcium oxalate precipitation in the urine and preventing subsequent stone formation.

Calcium stones account for 70-80% of all stones requiring treatment. Calcium oxalate accounts for about 80% of these stones and calcium phosphate about 15%. Genetic and environmental factors increase susceptibility. Hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, mild renal tubular acidosis, crystal growth inhibitor deficiencies, and alkaline urine are associated with calcium stone formation.

Struvite stones primarily contain magnesium-ammonium-phosphate as well as varying levels of matrix. Matrix forms in an alkaline urine and during infection with a urease-producing bacterial pathogen such as Proteus, Klebsiella, or Pseudomonas. Struvite calculi may grow quite large and branch into a staghorn configuration that approximates the pelvicaliceal collecting system. Women are at greater risk for struvite stones because they have an increased incidence of urinary tract infection.

Uric acid is primarily a product of biosynthesis of endogenous purines and is secondarily affected by consumption of purines in the diet. Persons who excrete excessive amounts of uric acid in the urine, such as those with gouty arthritis, are at particular risk for uric acid stones. Consistently acidic urine greatly increases this risk. Cystinuric or xanthine stone formation can occur due to genetic disorders of the cystine and xanthine amino acid metabolism.
(McCance & Huether, p. 1344-1345) See Also -Figure 38-3, p. 1345)
Neurogenic Bladder is:
- A general term for bladder dysfunction caused by neurologic disorders
- Types of bladder dysfunction are related to specific areas in the nervous system that control sensory and motor bladder function.
- Dyssynergia
· The loss of coordinated neuromuscular contraction
· Lesions that develop in upper motor neurons of the brain and spinal cord
o Causes overactive or hyperreflexive bladder function
Alterations of Renal and Urinary Tract Function are:
Detrusor Hyperreflexia
- Neurogenic disorders that develop above the pontine micturition center
- It is an upper level motor neuron disorder causing the bladder to empty automatically when it becomes full
~ The external sphincter still functions normally
- The pontine micturition center remains intact so coordination between detrusor muscle contraction and the relaxation of the urethral sphincter also remains intact
- Caused by:
· Stroke
· Traumatic brain injury
· Multiple sclerosis
· Dementia
· Alzheimer's
· Brain tumors
· Hydrocephalus
· Cerebral palsy
· Urine leakage
· Incontinence

Detrusor Hyperreflexia with Vesicosphincter (Detrusor Sphincter) Dyssynergia
- Neurogenic lesions that occur below the pontine micturition center and above the sacral micturition center (between C2 and S1)
· Upper motor neuron lesions
· There is loss of pontine coordination of detrusor muscle contraction and external sphincter relaxation
· Both the bladder and the sphincter are contracting at the same time.
~Causes a functional obstruction of the bladder outlet
- Caused by:
· Spinal cord injury (C2-T12)
· Multiple sclerosis
· Guillain-Barre syndrome
· Transverse myelitis
· Intervertebral disk problems
* Leads to Overactive Bladder Syndrome
- There is diminished bladder relaxation during storage with small urine volumes and high intravesicular (inside the bladder) pressures. Symptoms ( of overactive bladder syndrome)
· Urgency
· Frequency
· Urge incontinence
· Increases risk for urethral turbulence and urinary tract infection

Detrusor Areflexia (acontractile detrusor)
-Lesions that involve the sacral micturition center (below S1)
~also called cauda equine syndrome
-May also be from peripheral nerve lesions
-Considered a low motor neuron disorder
-Results in an acontractile detrusor or atonic bladder with retention of urine and distention
· If the sensory innervation of the bladder is intact, the full bladder will be sensed but the detrusor may not contract
· This is an underactive bladder syndrome
- Caused by:
· Myelodysplasia
· Multiple sclerosis
· Tabes dorsalis
· Spinal injury (T12-S)
· Cauda equine syndrome
· Herpes simplex/zoster
· Peripheral polyneuropathies
An infection of one or both upper urinary tracts
-ureter, renal pelvis, kidney interstitium
-Common causes (see Table 38-4, p. 1352):
-kidney stones
-vesicoureteral reflux
-neurogenic bladder
-Female sexual trauma
Acute Pyelonephritis
-Rarely causes renal failure
-Associated microorganisms
-E.coli, proteus, Pseudomonas
-Proteus and Pseudomonas are more commonly associated with infections after urethral instrumentation or urinary tract surgery.
-These microorganisms also split urea into ammonia
-This makes alkaline urine that increases the risk of stone formation
-Infection is probably spread by ascending uropathic microorganisms along the ureters, but dissemination may occur by way of the bloodstream.
-The inflammatory process is usually focal and irregular, primarily affecting the pelvis, calyces, and medulla
-The infection causes medullary infiltration of white blood cells with renal inflammation, and purulent urine.
-In severe infections, localized abscesses may form in the medulla and extend to the cortex.
-Renal tubules are primarily affected.
-Glomeruli are usually spared and not affected
-Necrosis of renal papillae can occur
-After the acute phase, healing occurs with deposition of scar tissue, fibrosis, and atrophy of the affected tubules.
-Onset of symptoms is usually acute:
-fever, chills, flank or groin pain
-Symptoms characteristic of a UTI may precede systemic s/s
-frequency, dysuria, and costovertebral tenderness
-Older adults may have nonspecific symptoms
-low-grade fever and malaise.

-It is difficult to differentiate symptoms of cystitis and pyelonephritis by clinical assessment.
-Specific diagnosis is done by urine culture, urinalysis, and clinical signs and symptoms.
-White blood cell casts indicate pyelonephritis, however, these are not always present in urine.
Chronic Pyelonephritis
-Persistent or recurrent infection of the kidney leading to scarring of the kidney.
-One or both kidneys may be involved.
-The specific cause may be unknown (idiopathic) or associated with vesicoureteral reflux or renal stones
-Chronic pyelonephritis may be associated with recurrent infections from acute pyelonephritis
-Other causes, may be from drug toxicity from analgesics, such as nonsteroidal anti-inflammatory drugs, ischemia, irradiation, and immune-complex diseases.
-Chronic urinary tract obstruction prevents elimination of bacteria and starts a process of progressive inflammation, alterations of the renal pelvis and calyces, destruction of the tubules, atrophy or dilation and diffuse scarring and finally impaired urine-concentrating ability, leading to chronic kidney failure
-The lesions of chronic pyelonephritis are sometimes termed chronic interstitial nephritis because inflammation and fibrosis are located in the interstitial spaces between the tubules.
-Early symptoms are often minimal and commonly include:
-flank pain
-may include hypertension
-Progression of disease leads to:
-renal failure
(particularly in the presence of other risk factors: obstructive uropathy or diabetes mellitus)
-There is an inability to conserve sodium with loss of tubular function, and development of hyperkalemia and metabolic acidosis.
-Risk for dehydration must be considered if there is loss of the ability to concentrate urine.
-Intravenous pyelography
-Treatment is related to the underlying cause.
-Obstruction must be relieved
-Antibiotics may be given, with prolonged antibiotic therapy for recurrent infection.
The term acute kidney injury (AKI) is preferred to the term ARF because it captures the diverse nature of this syndrome. AKI commonly results from extracellular volume depletion, decreased renal blood flow, or toxic/inflammatory injury to kidney cells. Minimal to severe changes result.
See table 38-10, p.1360. McCance & Huether!
The etiologies described in three categories of AKI
-Renal hypoperfusion from reduced effective arterial blood volume. Most common cause and occurs rapidly. GFR ultimately declines because of decreasing filtration pressure. Poor perfusion can result in renal artery thrombosis, hypotension related to hypovolemia or hemorrhage, microthrombi, kidney edema.
2) Intrarenal
-Disorders involving the renal parenchymal or interstitial tissue. May result from ischemic acute tubular necrosis (ATN), nephrotoxic ATN, acute glomerular nephritis, vascular disease, graft rejection, drug allergy, infection, tumor growth.
- Ischemia is most common cause. Occurs most commonly after surgery.
3) Postrenal
-Rare. Usually occurs with urinary tract obstruction that affects the kidneys bilaterally; bilateral ureteral obstruction, bladder outlet obstruction- prostatic hypertrophy, tumors, neurogenic bladder, urethral obstruction.
-causes increase in intraluminal pressure upstream from site of obstruction with gradual decrease in GFR.
-hours of anuria with flank pain followed by polyuria.

Phases of ARF
1) The initiation phase. Reduced perfusion or toxicity in which renal injury is evolving. 24-36 hrs. Prevention possible.
2) The maintenance phase/Oliguric. Established renal injury and dysfunction after the initiating event has been resolved. Weeks to months.
-UO lowest,
- CREAT, BUN, K+ serum levels increase.
-metabolic acidosis develops
-salt and water overload

3)The Recovery Phase. Interval when renal injury is repaired and nl renal function is reestablished.
-GFR returns toward normal
-decline serum creat and urea levels, increase creat clearance
McCance & Huether, P. 1360- 1361
Signs and symptoms of acute kidney failure may include:
Decreased urine output, although occasionally urine output remains normal
Fluid retention, causing swelling in your legs, ankles or feet
Shortness of breath
Seizures or coma in severe cases
Chest pain or pressure
Sometimes acute kidney failure causes no signs or symptoms and is detected through lab tests done for another reason.
Other symptoms include retention in the blood and ECF of water, waste products of metabolism, and electrolytes. Can lead to water and salt overload, which can lead to hypertension and edema. Excessive retention of potassium can be fatal. Patients with acute renal failure can also develop metabolic acidosis because the kidneys are unable to excrete sufficient hydrogen ions. Anuria may occur and the patient will die in 8 to 14 days unless kidney function is restored.

Patients with severe chronic renal failure almost always develop anemia due to the decreased renal secretion of erythropoietin, which stimulates the bone marrow to produce red blood cells.

The effect renal failure has on body fluids depends on water and food intake and the degree of impairment of renal function. Important effects include 1) generalized edema resulting from water and salt retention 2) acidosis resulting from failure of the kidneys to rid the body of normal acidic products 3) high concentration of the nonprotein nitrogens-especially urea, creatinine, and uric acid-resulting from failure of the body to excrete the metabolic end products of proteins; and 4) high concentrations of other substances excreted by the kidneys, including phenols, sulfates, phosphates, potassium, and guanidine bases. This total condition is called uremia because of the high concentration of urea in the body fluids.
CRF results from progressive and irreversible loss of large # of functioning nephrons. Serious symptoms often do not occur until the # of functional nephrons falls to at least 70-75% below normal. Electrolyte and fluid volumes maintained until # decreases below 20-25%.
Causes: Disorders of the blood vessels, glomeruli, tubules, renal interstitium, and lower urinary tract.
Metabolic disorders: DM, obesity, Amyloidosis
Renal vascular disorders: atherosclerosis, Nephrosclerosis-hypertension
Immunologic disorders: Glomerulonephritis Polyarteritis nodosa, Lupus
Infections: Pyelonephritis, TB
Nephrotoxins ( analgesics, heavy metals)
Urinary Tract Obstruction: Renal calculi, hypertrophy of prostate, urethral constriction
Congenital: Polycystic disease, renal hypoplasia) ( Hall 402)

Remaining nephrons are capable of compensatory hypertrophy and expansion or hyperfunction in their rates of filtration, reabsorption, and secretion and can maintain adaptive changes in solute and water regulation in declining GFR. Urine may contain abnormal amounts of protein and RBC or WBC but the major end products of excretion are essentially normal until advanced stages. .
The factors that contribute to the pathogenesis of CRF are complex and involve the interaction of many cells, cytokines, and structural alterations. Proteinuria and angiotensin II promote the pathologic changes of chronic renal injury. Glomerular hyperfiltration and increased capillary permeability lead to proteinuria.
-Proteinuria Contributes to tubulointerstitial injury by accumulating in the interstitial space and activating compliment proteins and other mediators that promote inflammation and progressive fibrosis.
Angiotensin II activity increases with progressive nephron injury.
Promotes glomerular HTN and hyperfiltration caused by efferent arteriolar vasoconstriction and also promotes systemic HTN.
Chronically high intraglomerular pressure increases glomerular cap permeability, contributing to proteinuria. ( McCance 1364-66. See table 38-12.)

Uremic syndrome is a proinflammatory state with the accumulation of urea and other nitrogenous compounds, as well as toxins and alterations in fluid, electrolyte, and acid-base balance that result from chronic kidney failure. All organ systems are affected and contribute to disease symptoms.
-accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes.
-Azotemia - increased serum urea levels and creat levels.
See Table 38-13, p.1365 McCance. For specific effects on each body system. Very detailed info!